INFLAMASI, REPAIR AND HEMOSTASIS

Jawaban Ini Disusun untuk Memenuhi Ujian Inflamasi, Repair And Hemostasis

Dosen Pembimbing : Dr.dr. Udadi Sadhana, M.Kes, Sp.PA

Ashifa Quamila
22010119410003

BIOMEDICAL SCIENCE - FAKULTAS KEDOKTERAN

UNIVERSITAS DIPONEGORO
SEMARANG
2020
All of answer direct this picture.
1. Jelaskan kaitan antara inflamasi, repair dan hemostasis.
Answer :
Inflammation, hemostasis and repair are tight in a pathological process that certainly affects one
another. In this connection, inflammation leads to activation of the further hemostatic system
which also greatly affects inflammation and repair activities. Close interaction between the
immune and the haemostatic system is an attempt to restore normal tissue function after injury.
Local activation of the hemostatic system is a critical part of the body's defenses that are both
contagious and non-contagious. However, excessive and insufficient control of inflammation can
result in swelling of the disease. Following the current two instances of clinical inflammation in
which the joint interaction of healing responses between inflammation, hemostasis and repair
contributes greatly to pathogenesis and/or the development of the disease is an inflammatory
response to infection or sepsis and acute arteries as a result of broken atopsys and repair
mechanisms.

Once the activation of the hemostatic system occurs on inflammation and then inflammation,
increased hemostatic disorder can cause thrombosis and organ damage. The uncontrolled
activation of the hemostatic system can also reinforce the initial inflammatory reaction, resulting
in additional bodily injury. Like, the hemostatic system ACTS in conjunction with an inflamed
cascade creating a cycle of inflamed hemostatic where each process is activated promotes the
other and both systems of functions in a positive feedback loop¹.

The explained purpose is to restore or improve the integrity of tissues that are threatened or
damaged by pathogens or infections. Hemostatic, on the other hand, is a physiological defense
mechanism to stop bleeding from wall damage, activation by impact of a wall injury, the
hemostatic system composed of a complex network of individual components. Vascular
endothelial cells and platelets are the major hemostasis generating platelets. This process is
thwarted by an activation of cascade plasma coagulation, called secondary hemostasis that
triggers freezing. The result of hemostatic activation is a stable platelet mass. These processes
are regulated in detail by the anticoagulation mechanisms of physiology that continue to
accumulate the structure of the coagulation of the system under control and by the fibrinolytic
system which is responsible for the platelet-fibrin feed which has been in keeping with its
arbitrary function. Before going to that stage, however, the hemostatic and inflammatory process
must be completed successfully so that the repair process will go well even though the condition
of the body cannot undergo the formation of the original tissue as it did in ancient times. Surely
the quality of improvement also depends on the immune reaction processes in our bodies as well.

Resource:

Margetic, Sandra. (2018). Inflammation and haemostasis. Croatia.

2. Jelaskan proses inflamasi yang terjadi akibat bakteri, virus, jamur, mekanisme (trauma, sinar
UV, DINGIN, dll)

Answer :

Inflammation following as definition in causing about an inflammation such as infectious

organisms including Mycobacterium tuberculosis, protozoa, fungi, and other parasites that can
resist host defenses and remain in the tissue for an extended period. An autoimmune disorder in
which the immune system is sensitized to the normal component of the body and attacks healthy
tissue giving rise to diseases such as rheumatoid arthritis, systemic lupus erythematosus (SLE).
Recurrent episodes of acute inflammation. However, in some cases, inflammation is an
independent response and not a sequel to inflammation for example diseases such as
tuberculosis and rheumatoid arthritis¹.

Most of the features of inflammation continue as the inflammation becomes severe, including
expansion of blood vessels (vasodilation), increase in blood flow, capillary permeability and
migration of neutrophils into the infected tissue through the capillary wall (diapedesis).
However, the composition of the white blood cells changes soon and the
macrophages and lymphocytes begin to replace short-lived neutrophils. Thus the hallmarks of
chronic inflammation are the infiltration of the primary inflammatory cells such as macrophages,
lymphocytes, and plasma cells in the tissue site, producing inflammatory cytokines, growth
factors, enzymes and hence contributing to the progression of tissue damage and secondary
repair including fibrosis and granuloma formation¹.
Mechanism trauma, UV light, cold in inflammation will influence :

Nonspecific proliferative: Characterized by the presence of non-specific granulation tissue

formed by infiltration of mononuclear cells (lymphocytes, macrophages, plasma cells) and
proliferation of fibroblasts, connective tissue, vessels and epithelial cells, for example, an
inflammatory polyp-like nasal or cervical polyp and lung abscess¹.

Granulomatous inflammation: A specific type of chronic inflammation characterized by the

presence of distinct nodular lesions or granulomas formed with an aggregation of activated
macrophages or its derived cell called epithelioid cells usually surrounded by lymphocytes. The
macrophages or epithelioid cells inside the granulomas often coalesce to form Langhans or giant
cells such as foreign body, Aschoff, Reed-Sternberg and Tumor giant cells. There are two types¹:

Granuloma formed due to a foreign body or T-cell mediated immune response is termed as
foreign body granuloma, for example, silicosis.¹

Granuloma that are formed from chronic infection is termed as infectious granuloma, for
example, tuberculosis and leprosy¹.

Resource:

R. Pahwa, A. Singh, I. Jialal. (2018). Chronic Inflammation. StatPearls.

3. Bagaimana menurut saudara repair dapat terjadi, apa yang menyebabkan? Mempengaruhi?

Answer :

The description of the repair can happen because of two kinds: 1) the primary mechanism: in this
type of wound is a clear wound. Can be cured through simple epithelial regeneration, but it
doesn't involve tissue involved. Directly clinging to the surface no longer produces a prominent
tissue and the less complex surface of the epithelium regeneration. This healing also releases a
fluid tissue fragment that can temporarily seal a wound called primary scab healing. 2) the
secondary mechanism: is an open wound involving a conspicuous defect of the granulation
network. Each granulation has a newly formed blood vessel region surrounded by a young
connective network of some kind. Fixing the elements is also a predictive phenomenon of
granulation processes¹.

Things that affect the repair occur can be caused by 2 factors: 1) external factors, wound
conditions that can be caused by metrics, thermal, chemical, and electric. The wound itself would
describe as an open and closed wound. Even treatment can be affected by outside stimulation of
regenerative pathways that include infection, foreign bodies, air, light, temperature and humidity,
mechanisms and chemicals. 2) internal factors, a group of factors that explain a functional
activity to the network itself. Like himeria¹.

Resource:

Dutton, Mark. (2019). Dutton’s Orthopaedic : Examination, Evaluation and Intervention, Fifth
Edition. McGraw-Hill Education.

4. Jelaskan prinsip-prinsip hemostasis pada manusia.

Answer:
 This picture represented of coagulation system is a highly complex and organized interaction
of cells and plasma proteins. The coagulation system provides an immediate activation when a
bleeding (hemostasis) control is needed and limits his activity to the location of blood loss.
Otherwise, coagulation can occur throughout the circulatory system, which is not compatible
with life.
A major component of hemostasis is thrombocytes, endothelial cells (coating blood vessels),
other tissue factors (TF) - cells that contain coagulation factors, which are plasma proteins. The
end result of an active coagulation system is the creation of a complex molecule and cross-
platelet which ends in hemorrhaging injuries after injury. To keep balance well regulated
between prothrombotic and antithetic factors, coagulation systems are fully understood to
provide multiple control points (pictures 6 - 4).
Coagulation factors generally do not circulate actively. Most of them are enzymes (serine
protease) and remain active until they are needed. This is accomplished by having another
enzyme (another protease in the coagulation system) available that could cut off dormant factors
into active ones that all of the factors have Roman numerals, and off without an anconnotation
written (mis. , factor II, also known as prothrombin). The activated form is marked by the letter
"a" (for example, IIa factor, also known as thrombin).
Most coagulation factors are established by the heart, but the xiii comes from thrombocytes
and the viii factor is made by endothelial cells. Factors II, VII, IX, and X in particular important
factors, because they depend on the liver enzymes of carboxylase. Gamma carboxyase is
dependent on vitamin K, and oral warfarin anticoagulant ACTS by interfering with vitamin K.
two properties of anticoagulant proteins, S protein and C protein (see what follows), also
depending on vitamin K.

In general functional of body physiologist:

Hemostasis is divided into three main principles: primary hemostasis, secondary hemostasis,
and fibrinolysis.

Primary hemostasis involves vasoconstriction and adhesion platelets and activation at the
endotel injury site. Collagen and thrombin activate platelets, which lead to increases in
intracellular calcium, platelet secretion secretions, and activation of various delivery paths.
Secondary hemostasis is a process in which the fibers form. Classic coagulation, including
intrinsic, extrinsic, and common, koagulation paths, as tested by coagulation: partial activation
thromboplastin time (APTT) and prothrombin time (PT). Mobile-based coagulation models have
been replaced as a more accurate depiction of the coagulation in vivo (picture 6- 4). Secondary
hemostasis then split into three overlapping phases: initiation, amplification, and propagation.
The initiation takes place on the surface of the injured cell. It starts with the tf release by the
wounded cells. Tf, also called thromboplastin, is a lipid protein material that is exposed to
plasma after injury to blood vessel walls. This immediately active VII factors, forming tf-VIIa
complex, which is active both factor IX and factor X. along with factor X (ko) along with factor
X (Co, activated from V factor by factor Xa) on the surface of the injured cell Rombin, a serin
protease, cuts plasma proteins everywhere into a fibrinogen monomer, a small soluble protein
that can be polled to each other to form complex fibers; But the amounts of thrombin formed at
injured cell sites are insufficient to create enough fibers to stabilize the platelet plug.
Amplification, unlike the initiation phase, occurred on the surface of the platelets. During this
phase, thrombin is produced in the initiation phase where the platelets occur and coagulation
factors V, VIII, and XI are found on the platelet surface. VIII factor has usually been
complicated into the von will brand factor (VWF), a protein that allows platelets to adhere to the
endothel cell. Rombin activated VIII factor by releasing it from the VWF. It also activates V and
XI, which allows them to bind surface platelets. XIa factor then catalyzes IX activation to IXa,
giving an added factor ixa to the platelet surface.
Propagation active platelets recruit other platelets that circulate to the injury site and the
formation of two main complex: tenase and prothrothroase, which are critical for the
production of fibers. The VIIIa and IXa factors form a tenase complex on the surface of the
platelets in the presence of pl and calcium (VIIIa-IXa-ca 2+ -pl). Together, they activated the x
factor on the platelet surface. The Xa factors then form a prothrombinase complex with Va
factors on the surface of the platelet, again in the presence of pl and calcium (xa-va-ca 2+ -pl).
This complex catalyzed a cleavage from prothrombin (II) to trombin (IIa) to be able to convert
some molecules per complex. As the thrombocytes that activated, recruit more thrombocytes that
circulate to the location of injury, a critical mass of thrombocytes led to a surge in the throbin
generation. This was deflected, this discussion led to the formation of fibers sufficient to stabilize
a platelet stopper. This polymer is further compressed with cross-link chemicals catalyzed by a
XIIIa factor, which is itself activated by thrombin. The XIIIa factor also combines residers 2 -
plasmin into blops to protect him from the fibrinolytic protease.

Fibrinolysis involves a process in which the fiber is broken into its degradable products. Plasmin
is the primary catalytic enzyme in this process. Plasmin's a protease serum that divides fibrin, to
produce clotting and fibrin degradation inhibits thrombin. Thrombin, which works in a negative
feedback way, which actually helps catalyze the plasmin formation of the precursor off to
proteins, plasminogens. Plasminogen can also be fragmented by tissue plasminogen (t-pa)
activators to form plasmin; T-pa and a clinically linked protein are to break out clots to form in
coronary arteries in patients with new myocard infarction, as well as cerebral arteries in patients
with newly injured. Fibrinolysis inhibitors include plasminogen inhibitors and dual -antiplasmin
inhibitors.
Besides fibrinolysis pathways, a check on the coagulation system (that is, an anticoagulant
system) also includes feedback loops and inhibitors. A Xa factor binds others such as plasma
proteins (and lipid bound) called tissues factor pathway inhibitor (tfpi). Tfpi not only retards
further activity as the Xa itself but also prevents a Xa from ever engaging in thrombocytes, and a
combination of Xa and tfpi factors significantly impede the tf-VIIa complex. Further,
downstream prothrombinase activity can only be maintained if the initial injuries continue to
produce enimeric and VIIIa sufficient factors (in the complex form of tenase) to activate more x
factors on the platelet surface.
Other anticoagulants include a group of coagulation inhibitors. This process is composed of
antitrombin (at), S protein, and protein C (see further discussion). At is a protease inhibitor and
physically blocks the serine protease action in the coagulation system. His activity was increased
to 2000 times by heparin. Protein c, activated by thrombin, cuts va factors into inactive form so
the prothrombinase complex cannot break the prothrombin (II) into thrombin. C proteins require
s protein as a cofactor. It's complex also deactivates VIIIa factors.

Resource:

Hammer, G. D., McPhee, S. J. (2018). Pathophysiology of Disease Eight Edition. An

Introduction to Clinical Medicine. McGraw-Hill Education.
5. Bagaimana menurut anda istilah hemostasis dengan Homeoastasis, jelaskan.

Answer :

Hemostasis is generally considered a complex process, but after that a major platelet reaction
triggered by a second reaction that leads to clotting blood. Early instances of adhesion may allow
for damage to the blood vessels on the wall, and there's growing evidence that these involve a
unique platelet reaction with a color until it's been dead-ended in the process of injury when
platelets adhere to collagen, they undergo drastic changes, including degranulation and the
release of certain contents, some of which have hemostatic meaning. Between the two
compounds that are released are Adenosine and Phosphate (ATP, ADP) which has the ability to
cause platelet aggregation, and this aggregation is considered responsible for enlarges platelet
deployment. At the same time, some ATP and ADP might escape to ambient plasma. If a platelet
count is attached to prevent passing blood from exiting the vessel, the nucleotides passing
through these platelets may circulate generally. It has been shown that an ADP can produce
thrombocytes circulating with thrombocytopenia formation, so a hated nucleotide like this can be
harmful. Another agent released by the thrombocytes on the hemostatic static is pro coagulant
phospholipid, a platelet factor 3 (pf3). This activity is not in the complete platelets, but is made
entirely acceptable¹.
A significant consequence of formation of a platelet cleft is the precipitation of a chain reaction
which leads to the blood coagulation. The role of thrombin formation this process may be
double: it serves to consolidated platelets by the nielets to change back the number of changes
that are collective known as viscous m 'they also produce a plasma clotting around the PKMG
that can cause expansion between the PKMG which lends permanence to the hemostatic
structure. One of the effects of blood thrombocytes on the blood platelets is to increase the
reactions mentioned above, increasing from the hemostatic platelets potential of in the anon, the
activities of clotting chain reactions introduced a new series of systemic effects if they are
allowed to affect the circulation. This can come from two sources: the affected areas, including
the wall of the blood vessels themselves, can release tissue factors that can directly activate X
factors in the presence of X factor called an extrinsic path to clotting; and and may contain
sequematic activation of the various plasma clotting factors forming the "intrinsic" path, through
broken tissue¹.
An additional series of systemic reactions can follow the activation of the xii factor, which also
seems to play a trigger role in a biochemical path other than freezing. The xii factor is involved
in forming a "plasma kinin," a material that gives pain in actual for injured skin, is a silk muscle
contract, and may contribute to increased vascular capacity¹.

Fig 1. Illustrated Blood Coagulation (Hemostatic homeoastasis)

Resource : Wikipedia common

In hemostatic enters circulation explained in picture, deactivation causes mences. One clear
mechanism is volume reduction with normal plasma, but plasma plays an active role beyond
settling. When ADP is added to poor plasma in platelet form, a person gradually loses the
platelets of the blood platelets. The ability of blood to sustain the spread of blood platelets in adp
is shown by the large amount of intravenous ADP needed to induce thrombocytopenia. Need to
understand carefully the platelets released from hemostatic could be inactivation by plasma
"anticoagulant." Coagulation factors compiled when unstable in the plasma or serum. Despite
pressor freezing is relatively stable but the activation will acquire the result of a progressive
inactivation. Various factors that occur in pictures XII, XI, VII, and pro thrombin are complex
processes, with some plasma components: some thrombin needs absorption to fibrin; And some
etrusons by heparin to act with co factor their proteins, some are slowly activated by different
anti thrombin, and other anti thrombin there may also be in clotting, on V and VIII factors. The
mechanism in which it originally occurred didn't work, but VIII inactivation can result from the
instability of thrombin's presence¹.
In my opinion, hemostatic homeostasis is a theoretical basis for blood coagulation as a
continuing generalization process. Viewed from the above perspective of the concept of
hemostatic - ostasis provides from the complexity of the coagulation process: because so many
steps are needed, various independent mechanisms are available to control it, and there's a safety
that's well-matched in a controlled mechanism and that can't be completely destroyed by some of
those paths.

Resource :

Dutton, Mark. (2019). Dutton’s Orthopaedic : Examination, Evaluation and Intervention, Fifth
Edition. McGraw-Hill Education.