Kuis Patologi Umum-gang. Sirkulasi

8/17/2019 Kuis Patologi Umum-gang. Sirkulasi

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KUIS PATOLOGI UMUMGANGGUAN SIRKULASI

Drh. Putri Pandarangga, MS15 Mei 201

Untu! "e"udah!an !a#ian $e#a%ar, &i#a!an $u!a 'e$&ite ini (a)htt*)++et.uga.edu+i-"+-ur&e&+/PAT5200+01-ir-u#atin+inde.*h*

Kasus 1.

Pada &aat !a"u "e#a!u!an ne!r*&i dan "ene"u!an #e&i &e*erti di$a'ah ini, "a!a -erita!an ha# a*a (ang $erada da#a" *i!iran andaMr3#gi diagn&a4Patgene&i& Pen(e$a$n(a (ang $erhu$ungan dengan %antung

A*a hu$ungann(a dengan dengan ga"$ar di $a'ah ini4 agi"ana"e!ani&"en(a &ehingga ha# ini $i&a ter%adi4

A*a!ah ti*e !nge&ti ini #-a# atau &i&te"i!4


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6$a $anding!ian dengan ti*e !nge&ti ini

Dan $anding!an dengan ga"$ar di $a'ah ini4 A*a!ah ini $enar7$enar#e&in atau *eru$ahan *&t"rte"4

A*a *er$edaann(a dengan ga"$ar di $a'ah ini4 8e#a&!an"e!ani&"en(a4


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Kasus 2

Se$ut!an !e"ung!inan (ang da*at &e$a$!an #e&in ini Serta

"e!ani&"en(a

Se$ut!an dan %e#a&!an %eni&7%eni& he"ragi *ada ga"$ar di $a'ah ini(hemoragi per diapedesis)

eri!ut ada#ah %eni& he"ragi (ang &*e&i9! :Te"u!an %a'a$an(a di)htt*)++et.uga.edu+i-"+-ur&e&+/PAT5200+01-ir-u#atin+he"rrhage+he"rrhage0;.ht"#


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(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)

• istended lymphatics are often visible in edematous lesions

• !t postmortem examination, edema is recogni"ed by the presence of clear yellow#

tinged fluid that distends loose connective tissues or accumulates in body cavities

such as the peritoneal, pleural, or pericardial spaces. The fluid may flow upon cuttingthrough the tissue or, if the vessels were damaged sufficiently that clotting proteins

accompanied the fluid, it may form a yellowish $ello#li%e clot.

&ere is a pig that was suffering from 'edema

disease,' which is due to a septicemia of certainstrains of E. coli . These bacteria produce a toxin

that acts on endothelial cells, allowing fluid to lea%

out.

Eyelid is a favored spot for this edema to be

manifest. This pig cant even open its eye becausethe lid is so swollen with edema fluid.


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Microscopic features of edema include:

• separation of tissue elements by spaces that are either clear (if the edema is protein

poor) or pin% (if the edema fluid has abundant protein).

• dilation of lymphatics

&istologically, edema fluid fills areas that

are not supposed to have fluid. &ere is asection of lung # protein#rich fluid has

lea%ed out of the vessels and is fillingalveoli and bronchioles ().

This is bad noo". *ant do no air exchange

if there is fluid in these spaces....

&ere is another photomicrograph of edema. +n

this case, the submucosa of the gut, which is

represented by the bottom two#thirds of thephoto, is mar%edly distended by fluid.

The arrowhead demonstrates a lymphatic

which is also way big. ith all this expansion,the nutrients and oxygen $ust have a hec% of a

time diffusing through to where they need togo.

Ka&u& ;

Pada &aat !a#ian "en%adi &erang d!ter he'an, &angat di$utuh!an!e*er-a(aan diri untu! "endiagn&a &uatu *en(a!it. Ta*i !e*er-a(aandiri itu a!an ter-i*ta $i#a dari &e!arang !a#ian "u#ai "e"*er!a(a diri!a#ian dengan *engetahuan ttg d!er he'an. O!, !ita "u#ai dari&e!arang (aeri!ut ga"$ar an%ing dengan *erut (ang "e"$e&ar. Ke"ung!inan(ang ter%adi ada#ah)


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-ld dog with heart failure develops pendulous abdomen 8e#a&!an *atgene&an(a

orphologic diagnosis # ascites

Jelaskan penyebab lain sehingga terjadi lesion seperti ini!

*ause # +ncreased hydrostatic pressure, due to heart bac%up,creating liver problems, resulting lea%age into abdominalcavity.

i#a &eandain(a da#a" *erut an%ing ini $eri&i -airan !e"ung!inan a!andi*er#eh dua ti*e -airan. Se$ut!an dan %e#a&!an *er$edaan -airan ini

Tran&udat :9$rin rendah= dan eudat :$n(a! "engandung &e# #eu!&it

dan 9$ringen tinggi, *rtein tinggi=

Le&i ini &angat $er$aha(a $i#a ter%adi *ada $e$era*a rgan. Se$ut!anrgan ter&e$ut dan a*a (ang di*engaruhi4


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Ka&u& >

Pada ga"$ar di $a'ah ini "erua*!an %antung dari d"$a (ang "ati

&e-ara "endada!. Se$ut!an "r3#gi diagn&an(a A*a hu$ungann(a#e&in ini dengan !e"atian "endada!4

Morphologic diagnosis: Serofibrinous pericardial effusion (at this stage of your training, Iwould also give you full points for hydropericardiu

"hat was the iediate reason for death# $ardiogenic shock % the heart could not pup

the blood around and so there was ultisyste organ failure due to lack of o&ygen'

In fact this lab had white uscle disease (lack of itain )*seleniu so there wasyocardial failure'

eri!ut ini "eru*a!an rgan dari ga%ah (ang di&unti!!an &e&uatu&ehingga "en(e$a$!an #e&in ini. 8e#a&!ah *atgene&i&n(a &ehinggater%adi ha# ini.


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Se$ut!an %eni&7%eni& *en(e$a$ !e"atian (ang "endada! *ada he'an(ang $erhu$ungan dengan &h-! 8e#a&!an "a&ing7"a&ing %eni& &h-!ter&e$ut

orphologic diagnosis/ 0aryngeal edema

1athogenesis2 !naphylactic reaction to in$ectedpharmaceutical. assive histamine release, extensiveoutpouring of fluid from affected vasculature, death due toasphyxiation

SHOCK

Definition of shock: Shoc% is failure of the circulatory systemto ade3uately perfuse vital organs.

+n shoc%, tissue perfusion and oxygen delivery are insufficientto meet the basal metabolic demands of tissues. hatever theinciting cause, shoc% is characteri"ed by low blood flow thatis usually accompanied by low blood pressure (hypotension).

Situations of inade3uate tissue perfusion result in a variety ofad$ustments to the circulatory system that are directed towardmaintaining normal arterial blood pressure and conservingbody water.

These compensatory mechanisms may maintain viability ofvital organs and sustain the life of the patient, a situation


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termed 'compensated shoc%'. hen the ad$ustments fail toreestablish and maintain perfusion sufficient to sustain vitaltissues, a condition of 'uncompensated shoc%' ensues whereprogressive circulatory collapse leads to increasingly severe

disruption of critical cellular metabolic pathways and death.

Clinically, the primary goal of therapy for shoc% is the rapid

restoration of systemic blood flow by replacement of intravascular

fluid and the use of drugs that increase vascular tone and supportcardiac function.

Causes !ypes and "atho#eneses of Shock

Shoc% is initiated by anything that severely and usually

relatively suddenly decreases cardiac output, blood volume,and4or peripheral vascular resistance. The types of shoc% canbe classified on the basis of the primary general cause/

Cardio#enic shock is caused by insults that negatively affectcardiac output (inhibit the heart5s ability to pump blood).*ardiac output = heart rate x stro%e volume, so anythingaffecting heart rate or contractility can decrease cardiacoutput.


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This is a

picture oflymphosarco

ma in a cowheart, sohec%, this

heart isntwor%ing so

well anymore.ith all these

tumor blobs,

the heartcant function

so good, andthere is poor

cardiac

output.

Myocardial de#eneration suchas might occur with vitamin

E4selenium deficiency in pigs

(mulberry heart disease),monensin toxicity in horses, or

myocardial infarcts (which occurmuch more commonly in

humans than in domestic

animals), can cause heart failureand cardiogenic shoc%.

+n this photograph, a big pale#

colored infarct is outlined byarrows. +nfarcts are areas where

the blood supply has beencompromised and well go into

way more detail very soon in this

course about what exactly theyare.


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Cardiac tamponade, which

occurs when fluid (usuallyblood) accumulates rapidly in

the pericardial space and

impinges on the ability of thecardiac ventricles to dilate and

fill with blood, will cause acuteheart failure and resulting

cardiogenic shoc%.

Electrolyte imbalances (such a hyper%alemia in uremicanimals) that negatively affect heart rate, can lead to heart

failure and cardiogenic shoc%.

Hypo$olemic shock is caused by a sudden severe loss ofblood volume. *auses include/

• acute hemorrhage involving loss of greater than 647 to

648 of total blood volume. The blood may be lostexternally or into internal spaces such as the peritonealcavity or the alimentary tract.

• loss of fluid (intravascular and extravascular), which mayoccur 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 immunereactions that in$ure vessels. Specific examples includee3uine viral arteritis, !frican swine fever, hog cholera,and the hemorrhagic fevers (e.g., simian hemorrhagic

fever, Ebola virus infection)


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This horse died ofhypovolemic shoc%

because it lost all its bloodinto the abdominal cavity

(hemoperitoneum). Theunderlying reason was a

tumor in the spleen that

ruptured.

Distributi$e %or $aso#enic& shock is caused by a suddensevere decrease in peripheral vascular resistance that causesextensive pooling of blood within the venous system andsubse3uent decreased venous return to the heart.

Severe colonic edema in a

horse with endotoxic shoc%.uch of the fluid formerly

within the vascular system is

now pooled within thecolonic tissues, leading to

functional hypovolemiacharacteristic of distributive

shoc%.

!here are some important e'amples of distributi$eshock includin#

Septic shock (endotoxic shoc%, toxic shoc%) results from abacterial infection (locali"ed or systemic) in which large3uantities of endotoxin are released intocirculation.Endoto'ins are complex components of the cellwall of gram#negative bacteria and then can really do anumber on the body, and especially on the vasculature.


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Endotoxin is bad news forendothelium.

Endotoxin is sometimes referred to as 'lipopolysaccharide'because the most toxic part of the complex is this type ofmolecule. 0ess commonly, other types of toxins from gram#positive bacteria can cause shoc% by a similarpathogenesis. READ YER NOTEZ AND MAKE SURE YOU

UNDERSTAND THE PATHOGENESIS.

(naphylactic shock is a systemic manifestation of an acutehypersensitivity (allergic) response. This is an idiosyncraticreaction that occurs in certain predisposed individuals uponexposure to certain antigens (substances, usually proteins, towhich the individual is allergic) such as insect stings, foods,medicines, etc.


14/20

e will discuss hypersensitivity reactions in more detail in

another section of this course, but for the present discussion $ust remember that upon exposure to these allergens,histamine and other chemicals are released from cells such asmast cells. &istamine and the other substances bind toreceptors, causing vasodilation and increased vascularpermeability with loss of intravascular fluid. SAME HERE -READ THE NOTES.

9eurogenic shoc% can occur following severe trauma, severepain, or occasionally following restraint. The pathogenesis

involves massive autonomic nervous system discharge whichdisrupts vasomotor control and there is extensive venocapillarypooling of blood. hich is bad. hen all of the blood is in thecapillaries, it doesnt get moved around to vital organs.


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Ka&u& 5

Pe#a%ari dan "engerti $agai"ana ter%adi *e"$e!uan darah di"ana"e#i$at!an *#ate#et :he"&tati& &e"entara= dan 3a!tr !agu#a&i:he"&tati& *er"anen=. Se#ain itu $agai"ana *#ate#et diha"$at!er%an(a (ang di!ena# &e$agai anti!agu#a&i

&ere are the factors that the endothelial cell produces and how those factors have a role in

anticoagulation/

"rostacyclin, also %nown as 1rostaglandin

+:(1;+:), is constantly produced by endothelial

cells. This prostaglandin wor%s to %eep vesselsopen (vasodilation).

+t also prevents platelet aggregation by acting on platelets to increase cyclic !1 (c!1)that effectively reduces the amount of thromboxane !: (which is made by platelets and

which we will cover shortly) which has procoagulant activities.

hat happens if the endothelial cell is damaged2 / -ops. Endothelial cells get

http://vet.uga.edu/ivcvm/courses/VPAT5200/01_circulation/endothelium/endo01a.htmlhttp://vet.uga.edu/ivcvm/courses/VPAT5200/01_circulation/endothelium/endo01a.html


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damaged and there is decreased 1;+:. !s a result, vessel constricts a bit, c!1in platelets decreases, causing a thromboxane increase, causing plateletaggregation.

hen the platelets contact the collagen,they produce !1, which further promotes

platelet aggregation, as pictured in thediagram at the left.

The endothelium is capable of

producingadenosine diphosphatase that

degrades !1.

The endothelium produces nitric o'ide in response to !1 from activated platelets. This

nitric oxide wor%s to %eep the vessel open (vasodilation), which decreases the probability

of clotting.

"rotein C is released from the endothelium in response to thrombin (a very important

molecule in the whole clotting thang and well hear about thrombin very soon). This 1rotei

* acts to inactive some of the clotting factors.

! 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 plasmino#en acti$ators.1lasminogen is a %ey molecule involved in brea%ing clots down after they have formed.

-%ay, for review, here are the products of endothelial cells # &ow does each wor% to

decrease thrombosis2

• prostacyclin

• adenosine diphosphatase

• nitric oxide


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• 1rotein *

• heparin#li%e substance

• plasminogen activators

Pe#a%ari #e$ih detai# di)htt*)++et.uga.edu+i-"+-ur&e&+/PAT5200+01-ir-u#atin+endthe#iu"+end01.ht"#


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*enous thrombi are in veins.

This is a $enous thrombus by virtue of its location in the $ugular vein of a horse. The horse had received repeatedin$ections in the $ugular vein. The pale color is due to fixation.

(rterial thrombi are in arteries.

These are bilateral arterial thrombi in the pulmonary arteriesof a cat.

8e#a&!an #e&in (ang ter%adi *ada ga"$ar di $a'ah ini. Ini"eru*a!an gin%a# dari !uda di"ana ndu#7ndu# *utih "eru*a!antu"*u!an $a!teri. 8e#a&!an "e!ani&"en(a &ehingga ter%adi ndu#ter&e$ut.


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hat would be the most li%elyetiologic diagnosis for the disease2 actinobacillosis

Etiology2 !ctinobacillus e3uuli

orphologic diagnosis on the %idney2 Embolic nephritis

1athogenesis2 This organism gets in through the umbilicus atthe time of birth and disseminates, with emboli of bacteriashowing up in many organs, especially %idney and $oints.

Se$ut!an a*a (ang ter%adi dengan gin%a# di $a'ah ini

(rterial infarcts result from obstructed arteries and are identifiedprimarily by sharp lines of demarcation that delineate the vascular

field of that particular artery.


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+f the tissue is solid, theinfarct may be pale with red

edges. +f the tissue is morespongy and has good

collateral circulation, the

lesion may be dar%#red.

They are arterial infarcts because they are all very pale.

There is not much collateral circulation in the %idney and once

the arcuate arteries (found at the $unction of cortex andmedulla) get bloc%ed, the corresponding portion of the cortexgets pale and ischemic.

Kuis Patologi Umum-gang. Sirkulasi

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