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KUIS PATOLOGI UMUM

GANGGUAN SIRKULASI
Drh. Putri Pandarangga, MS
15 Mei 2016
Untuk memudahkan kalian belajar, silakan buka website ini ya:
http://vet.uga.edu/ivcvm/courses/VPAT5200/01_circulation/index.php
Kasus 1.
Pada saat kamu melakukan nekropsi dan menemukan lesio seperti di
bawah ini, maka ceritakan hal apa yang berada dalam pikiran anda!
Morfologi diagnosa?
Patogenesis! Penyebabnya yang berhubungan dengan jantung!

Apa hubungannya dengan dengan gambar di bawah ini? Bagimana


mekanismenya sehingga hal ini bisa terjadi?

Apakah tipe kongesti ini local atau sistemik?

Coba bandingkian dengan tipe kongesti ini!

Dan bandingkan dengan gambar di bawah ini? Apakah ini benar-benar


lesion atau perubahan postmortem?

Apa perbedaannya dengan gambar di bawah ini? Jelaskan


mekanismenya?

Kasus 2
Sebutkan kemungkinan
mekanismenya!

yang

dapat

sebabkan

lesion

ini!

Serta

Sebutkan dan jelaskan jenis-jenis hemoragi pada gambar di bawah ini!


(hemoragi per diapedesis)

Berikut adalah jenis hemoragi yang spesifik (Temukan jawabanya di:


http://vet.uga.edu/ivcvm/courses/VPAT5200/01_circulation/hemorrhage
/hemorrhage03.html#hemorrhage3f) :

(hemo perikardium dan Hematuria (uterina) )

Edema is accumulation of excessive water in body cavities or interstitial tissues.


Definition of Edema = abnormal accumulation of water in tissues or body cavities

Gross characteristics of edema include:

Swollen, usually soft and doughy, distended tissue that tends to gravitate ventrally

Edematous tissue pits on pressure and the indentations remain after the pressure is
removed

Edematous tissue is cool to the touch rather than warm (unless inflammation is also
present)

The edematous tissue is not reddened (not hyperemic) or painful (again, unless
inflammation is also present)

Distended lymphatics are often visible in edematous lesions

At postmortem examination, edema is recognized by the presence of clear yellowtinged fluid that distends loose connective tissues or accumulates in body cavities
such as the peritoneal, pleural, or pericardial spaces. The fluid may flow upon cutting
through the tissue or, if the vessels were damaged sufficiently that clotting proteins
accompanied the fluid, it may form a yellowish jello-like clot.

Here is a pig that was suffering from "edema


disease," which is due to a septicemia of certain
strains of E. coli. These bacteria produce a toxin
that acts on endothelial cells, allowing fluid to leak
out.
Eyelid is a favored spot for this edema to be
manifest. This pig can't even open its eye because
the lid is so swollen with edema fluid.

Microscopic features of edema include:

separation of tissue elements by spaces that are either clear (if the edema is proteinpoor) or pink (if the edema fluid has abundant protein).

dilation of lymphatics

Histologically, edema fluid fills areas that


are not supposed to have fluid. Here is a
section of lung - protein-rich fluid has
leaked out of the vessels and is filling
alveoli and bronchioles (*).
This is bad nooz. Can't do no air exchange
if there is fluid in these spaces....

Here is another photomicrograph of edema. In


this case, the submucosa of the gut, which is
represented by the bottom two-thirds of the
photo, is markedly distended by fluid.
The arrowhead demonstrates a lymphatic
which is also way big. With all this expansion,
the nutrients and oxygen just have a heck of a
time diffusing through to where they need to
go.

Kasus 3
Pada saat kalian menjadi seorang dokter hewan, sangat dibutuhkan
kepercayaan diri untuk mendiagnosa suatu penyakit. Tapi kepercayaan
diri itu akan tercipta bila dari sekarang kalian mulai memperkaya diri
kalian dengan pengetahuan ttg doker hewan. Ok, kita mulai dari
sekarang ya!
Berikut gambar anjing dengan perut yang membesar. Kemungkinan
yang terjadi adalah:

Old dog with heart failure develops pendulous abdomen


Jelaskan patogenesanya!

Morphologic diagnosis - ascites


Jelaskan penyebab lain sehingga terjadi lesion seperti ini!

Cause - Increased hydrostatic pressure, due to heart backup,


creating liver problems, resulting leakage into abdominal
cavity.
Bila seandainya dalam perut anjing ini berisi cairan kemungkinan akan
diperoleh dua tipe cairan. Sebutkan dan jelaskan perbedaan cairan ini!

Transudat (fibrin rendah) dan exudat (bnyak mengandung sel leukosit


dan fibrinogen tinggi, protein tinggi)
Lesio ini sangat berbahaya bila terjadi pada beberapa organ. Sebutkan
organ tersebut dan apa yang dipengaruhi?

Kasus 4
Pada gambar di bawah ini meruapkan jantung dari domba yang mati
secara mendadak. Sebutkan morfologi diagnosanya! Apa hubungannya
lesion ini dengan kematian mendadak?

Morphologic diagnosis: Serofibrinous pericardial effusion (at this stage of your training, I
would also give you full points for hydropericardium)
What was the immediate reason for death? Cardiogenic shock - the heart could not pump
the blood around and so there was multisystem organ failure due to lack of oxygen.
In fact this lamb had white muscle disease (lack of Vitamin E/selenium) so there was
myocardial failure.

Berikut ini merupakan organ dari gajah yang disuntikkan sesuatu


sehingga menyebabkan lesion ini. Jelaskah patogenesisnya sehingga
terjadi hal ini.

Sebutkan jenis-jenis penyebab kematian yang mendadak pada hewan


yang berhubungan dengan shock! Jelaskan masing-masing jenis shock
tersebut!

Morphologic diagnosis: Laryngeal edema


Pathogenesis? Anaphylactic reaction to injected
pharmaceutical. Massive histamine release, extensive
outpouring of fluid from affected vasculature, death due to
asphyxiation
SHOCK
Definition of shock: Shock is failure of the circulatory system
to adequately perfuse vital organs.
In shock, tissue perfusion and oxygen delivery are insufficient
to meet the basal metabolic demands of tissues. Whatever the
inciting cause, shock is characterized by low blood flow that
is usually accompanied by low blood pressure (hypotension).
Situations of inadequate tissue perfusion result in a variety of
adjustments to the circulatory system that are directed toward
maintaining normal arterial blood pressure and conserving
body water.
These compensatory mechanisms may maintain viability of
vital organs and sustain the life of the patient, a situation

termed "compensated shock". When the adjustments fail to


reestablish and maintain perfusion sufficient to sustain vital
tissues, a condition of "uncompensated shock" ensues where
progressive circulatory collapse leads to increasingly severe
disruption of critical cellular metabolic pathways and death.
Clinically, the primary goal of therapy for shock is the rapid
restoration of systemic blood flow by replacement of intravascular
fluid and the use of drugs that increase vascular tone and support
cardiac function.

Causes, Types, and Pathogeneses of Shock


Shock is initiated by anything that severely and usually
relatively suddenly decreases cardiac output, blood volume,
and/or peripheral vascular resistance. The types of shock can
be classified on the basis of the primary general cause:
Cardiogenic shock is caused by insults that negatively affect
cardiac output (inhibit the hearts ability to pump blood).
Cardiac output = heart rate x stroke volume, so anything
affecting heart rate or contractility can decrease cardiac
output.

This is a
picture of
lymphosarco
ma in a cow
heart, so
heck, this
heart isn't
working so
well anymore.
With all these
tumor blobs,
the heart
can't function
so good, and
there is poor
cardiac
output.

Myocardial degeneration such


as might occur with vitamin
E/selenium deficiency in pigs
(mulberry heart disease),
monensin toxicity in horses, or
myocardial infarcts (which occur
much more commonly in
humans than in domestic
animals), can cause heart failure
and cardiogenic shock.
In this photograph, a big palecolored infarct is outlined by
arrows. Infarcts are areas where
the blood supply has been
compromised and we'll go into
way more detail very soon in this
course about what exactly they
are.

Cardiac tamponade, which


occurs when fluid (usually
blood) accumulates rapidly in
the pericardial space and
impinges on the ability of the
cardiac ventricles to dilate and
fill with blood, will cause acute
heart failure and resulting
cardiogenic shock.

Electrolyte imbalances (such a hyperkalemia in uremic


animals) that negatively affect heart rate, can lead to heart
failure and cardiogenic shock.
Hypovolemic shock is caused by a sudden severe loss of
blood volume. Causes include:
acute hemorrhage involving loss of greater than 1/4 to
1/3 of total blood volume. The blood may be lost
externally or into internal spaces such as the peritoneal
cavity or the alimentary tract.
loss of fluid (intravascular and extravascular), which may
occur with water deprivation, vomiting, diarrhea, etc.
increased vascular permeability leading to loss of
intravascular fluid, proteins, and sometimes blood cells.
These insults include infections, toxicities, and immune
reactions that injure vessels. Specific examples include
equine viral arteritis, African swine fever, hog cholera,
and the hemorrhagic fevers (e.g., simian hemorrhagic
fever, Ebola virus infection)

This horse died of


hypovolemic shock
because it lost all its blood
into the abdominal cavity
(hemoperitoneum). The
underlying reason was a
tumor in the spleen that
ruptured.

Distributive (or vasogenic) shock is caused by a sudden


severe decrease in peripheral vascular resistance that causes
extensive pooling of blood within the venous system and
subsequent decreased venous return to the heart.

Severe colonic edema in a


horse with endotoxic shock.
Much of the fluid formerly
within the vascular system is
now pooled within the
colonic tissues, leading to
functional hypovolemia
characteristic of distributive
shock.

There are some important examples of distributive


shock including
Septic shock (endotoxic shock, toxic shock) results from a
bacterial infection (localized or systemic) in which large
quantities of endotoxin are released into
circulation.Endotoxins are complex components of the cell
wall of gram-negative bacteria and then can really do a
number on the body, and especially on the vasculature.

Endotoxin is bad news for


endothelium.

Endotoxin is sometimes referred to as "lipopolysaccharide"


because the most toxic part of the complex is this type of
molecule. Less commonly, other types of toxins from grampositive bacteria can cause shock by a similar
pathogenesis. READ YER NOTEZ AND MAKE SURE YOU
UNDERSTAND THE PATHOGENESIS.
Anaphylactic shock is a systemic manifestation of an acute
hypersensitivity (allergic) response. This is an idiosyncratic
reaction that occurs in certain predisposed individuals upon
exposure to certain antigens (substances, usually proteins, to
which the individual is allergic) such as insect stings, foods,
medicines, etc.

We will discuss hypersensitivity reactions in more detail in


another section of this course, but for the present discussion
just remember that upon exposure to these allergens,
histamine and other chemicals are released from cells such as
mast cells. Histamine and the other substances bind to
receptors, causing vasodilation and increased vascular
permeability with loss of intravascular fluid. SAME HERE READ THE NOTES.
Neurogenic shock can occur following severe trauma, severe
pain, or occasionally following restraint. The pathogenesis
involves massive autonomic nervous system discharge which
disrupts vasomotor control and there is extensive venocapillary
pooling of blood. Which is bad. When all of the blood is in the
capillaries, it doesn't get moved around to vital organs.

Kasus 5
Pelajari dan mengerti bagaimana terjadi pembekuan darah dimana
melibatkan platelet (hemostatis sementara) dan faktor koagulasi
(hemostatis permanen). Selain itu bagaimana platelet dihambat
kerjanya yang dikenal sebagai antikoagulasi!

Here are the factors that the endothelial cell produces and how those factors have a role in
anticoagulation:

Prostacyclin, also known as Prostaglandin


I2(PGI2), is constantly produced by endothelial
cells. This prostaglandin works to keep vessels
open (vasodilation).

It also prevents platelet aggregation by acting on platelets to increase cyclic AMP (cAMP)
that effectively reduces the amount of thromboxane A2 (which is made by platelets and
which we will cover shortly) which has procoagulant activities.
What happens if the endothelial cell is damaged? : Oops. Endothelial cells get

damaged and there is decreased PGI2. As a result, vessel constricts a bit, cAMP
in platelets decreases, causing a thromboxane increase, causing platelet
aggregation.

When the platelets contact the collagen,


they produce ADP, which further promotes
platelet aggregation, as pictured in the
diagram at the left.
The endothelium is capable of
producingadenosine diphosphatase that
degrades ADP.

The endothelium produces nitric oxide in response to ADP from activated platelets. This
nitric oxide works to keep the vessel open (vasodilation), which decreases the probability
of clotting.
Protein C is released from the endothelium in response to thrombin (a very important
molecule in the whole clotting thang and we'll hear about thrombin very soon). This Protein
C acts to inactive some of the clotting factors.
A heparin-like substance is produced on the surface of endothelial cells that acts to
inactivate thrombin.
Endothelial cells act to help clot dissolution by releasing plasminogen activators.
Plasminogen is a key molecule involved in breaking clots down after they have formed.
Okay, for review, here are the products of endothelial cells - How does each work to
decrease thrombosis?

prostacyclin

adenosine diphosphatase

nitric oxide

Protein C

heparin-like substance

plasminogen activators

Pelajari lebih detail di:


http://vet.uga.edu/ivcvm/courses/VPAT5200/01_circulation/endothelium
/endo01.html#hemostasis2a
Jelaskan mekanisme bahan-bahan di bawah ini sebagai antikoagulan:
1. EDTA
2. Warfarin (berhubungan dengan vitamin K)
3. Heparin

Kasus 6.
Jelaskan perbedaan lesio yang terjadi pada gambar di atas!
Mekanisme hingga terjadi lesio tersebut.

Venous thrombi are in veins.


This is a venous thrombus by virtue of its location in the
jugular vein of a horse. The horse had received repeated
injections in the jugular vein. The pale color is due to fixation.

Arterial thrombi are in arteries.


These are bilateral arterial thrombi in the pulmonary arteries
of a cat.

Jelaskan lesion yang terjadi pada gambar di bawah ini. Ini


merupakan ginjal dari kuda dimana nodul-nodul putih merupakan
tumpukan bakteri. Jelaskan mekanismenya sehingga terjadi nodul
tersebut.

What would be the most likely


etiologic diagnosis for the disease? actinobacillosis
Etiology? Actinobacillus equuli
Morphologic diagnosis on the kidney? Embolic nephritis
Pathogenesis? This organism gets in through the umbilicus at
the time of birth and disseminates, with emboli of bacteria
showing up in many organs, especially kidney and joints.
Sebutkan apa yang terjadi dengan ginjal di bawah ini!

Arterial infarcts result from obstructed arteries and are identified


primarily by sharp lines of demarcation that delineate the vascular
field of that particular artery.

If the tissue is solid, the


infarct may be pale with red
edges. If the tissue is more
spongy and has good
collateral circulation, the
lesion may be dark-red.

They are arterial infarcts because they are all very pale.
There is not much collateral circulation in the kidney and once
the arcuate arteries (found at the junction of cortex and
medulla) get blocked, the corresponding portion of the cortex
gets pale and ischemic.