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Pathology 1 RUSVM > Block 5 > Flashcards

Block 5 Flashcards

1
Q

PULMONARY EDEMA

what is it and what is it associated with?

A

Accumulation of fluid in interstitium and alveoli of the lungs
Associated with Left-Sided Congestive Heart Failure (CHF)

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2
Q

PULMONARY EDEMA

Left-Sided Congestive Heart Failure (CHF)
why?

A

heart can’t pull blood back from lungs bc left side has failed.
-increased hydrostatic pressure
-transudate

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3
Q

Left-Sided Congestive Heart Failure (CHF)
Gross Appearance:

(yes is is gross btw)

A

Gross Appearance:
- Lungs are expanded, heavy and wet
- Froth in airways on cut surface
- Congestion of blood (reddish areas)

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4
Q

what is:

Most commonly will result from CHF

Resulting in thickness of the alveolar walls

Possible fibrosis (scar formation)

Presence of siderophages
- alveolar macrophages filled with hemosiderin
- *b/c RBc’s staying there and breaking down.
- Perl’s Stain

A

CHRONIC PULMONARY EDEMA

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5
Q

CEREBRAL EDEMA

what is it?
what does it look like?
what causes it?

A
  • Edema of the brain
  • narrow sulci and flattened gyri
    What could cause this?
  • inflammation
  • trauma
  • obstruction of venous outflow
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6
Q

CEREBRAL EDEMA

histology?
consequences?
hint what is cerebral coning, what is cerebral herniation?

A

Histology: Virchow-Robin spaces are expanded

Consequences:
Cerebellar coning - Herniation of the cerebellum
through the foramen magnum
Cerebral herniation - Herniation of caudal
cerebral cortex beneath the tentorium cerebelli

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7
Q

HYPEREMIA V. CONGESTION

increase of arteriole-mediated engorgement of
oxygenated blood
- active process

what is this?

A

Hyperemia

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8
Q

HYPEREMIA V. CONGESTION

venous engorgement of non-oxygenated blood
- passive process

what is this?

A

Congestion

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9
Q

HYPEREMIA V. CONGESTION

Physiological?
Pathological?

A

Physiological: Exercising, blushing (neurovascular), digestion
Pathological: Inflammation

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10
Q

GROSS APPEARANCE OF HYPEREMIA

Name 4

A

Reddening of tissue

Swelling

Warm to the touch

Tends to be localized

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11
Q

GROSS APPEARANCE OF CONGESTION

name 4

A

Darker in color - red/blue/black
(cyanotic)

Tissue is usually cooler in temperature

Well ooze blood when the surface is cut

Often wet

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12
Q

Acute congestion
vs
chronic congestion

what are the differences?

A

Acute: Engorged capillaries, +/- edema

Chronic:
hypoxia (decreased oxygen b/c deox blood staying in vessels. No room for oxygenated blood to come in), cellular atrophy, cellular degeneration/necrosis

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13
Q

Pulmonary ? no idea what crossing out the word congestion is supposed to mean?

so what is this picture?
what caused it?
what is the pathomecanism?
what do you expect to see under histology?

A

What could cause this? Left Sided CHF
What is the pathomechanism? Increased Hydrostatic Pressure
What do you expect to see under histology? Siderophages

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14
Q

HEPATIC CONGESTION

omg this is so nasty–check out the photo and…

What could cause this?
What is the pathomechanism?
What is another name for this appearance?

A

What could cause this?
Right Sided CHF
What is the pathomechanism?
Increased Pressure, Hypoxia and Necrosis
What is another name for this appearance?
Nutmeg liver

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15
Q

WHAT IS HEMORRHAGE?

define
what does external and internal refer to?
why is this NOT the same as hypermia/congestion?

A

Blood escapes from the vasculature

Can be external or internal - in other words,
within the tissue or body cavities

Remember this is NOT the same as
hyperemia/congestion - these are within the
vasculature

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16
Q

CLASSIFICATION

due to a small defect in
the vessel wall or RBCs passing through vessel wall due to
increased capillary permeability (ex. Inflammation)
Other examples: congestion, hypoxia,

what is this called?

A

Hemorrhage by Diapedesis:

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17
Q

CLASSIFICATION

due to a substantial tear in the
vasculature
Ex. trauma, blood vessel necrosis, neoplasia invasion into
the vessel

what is this called?

A

hemorrhage by Rhexis

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18
Q

HEMORRHAGE & CLASSIFICATION

which is internal which is external?

A

Hemothorax
left=external
right=internal

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19
Q

PETECHIAE

what are they?
describe

A

Small pin-point hemorrhages
~1-2 mm in size
Commonly seen on the skin, mucosal and serosal surfaces

left=smallintestine of cow
right=abomasum of cow

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20
Q

PURPURA

what are they
describe

A

Kidneys-dog
Larger in size than petechiae
~3mm-1cm in size
Commonly seen on the skin, mucosal and serosal surfaces

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21
Q

ECCHYMOSES

what is this?
describe

A

Larger in size than purpura
** ~1-2cm in size**
Seen in bruises or small hematomas

left=sucutaneous tissue
right=large intestine of cow

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22
Q

AGONAL HEMORRHAGES in Heart

what causes this appearance?

A

Terminal hypoxia

left=epicardium
2 right=endocardium

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23
Q

SUFFUSIVE & PAINTBRUSH HEMORRHAGE

what is this?
describe

A

left=suffusive
-continuous and larger than ecchymoses

right=paint-brush
looks like red paint was hastily applied by a paint brush

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24
Q

HEMATOMA

what is this?
describe

A

left=splenic hematome
right=ovarian hematoma
Accumulation or pockets of blood
Can be caused by trauma (ex. Spleen)
Surrounded by a capsule

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25
Q

HEMORRHAGIC DIATHESIS

what is this?
describe

A

Increased tendency to hemorrhage from insignificant injuries

-i.e. not trauma

Platelet disorders and coagulation disorders

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26
Q

SUBDURAL & EPIDURAL HEMORRHAGE

what is bleeding between the dura matter and skull

vs.

bleeding between the arachnoid matter and the dura matter

A

AH HA!
the first is epidural
the second is subdural

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27
Q

what do we call this?
what could cause this?

A

Hemoperitoneum

Incomplete detachment of trophoblasts
in uterus postpartum

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28
Q

what do we call this?
what can this lead to?

A

Hemopericardium

Cardiac tamponade 2 fatal complication from
pressure on the heart

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29
Q

What do we call this?
What could cause this?

A

Hemothorax

Spirocerca lupi - causes vasculitis and loss of
integrity of the vascular wall ĺ aortic rupture

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30
Q

identify and describe

A

Hyphema

Between the cornea
and the iris

Cat w/ FIP

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31
Q

identify and describe

A

Hem(blood)arthrosis(arthritis=joints)

In the joint space

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32
Q

identify and describe

A

Epistaxis
Bleeding from the
nose

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33
Q

identify and describe

A

Hem(blood)optysis(spitting)

Coughing up blood
Can be mixed with
mucus

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34
Q

identify and describe-poop terms

A

Hema(blood)tochezia(pooping)

Fresh blood in the
stool

Bright red
*lower GI tract b/c blood isn’t digested

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35
Q

what is Hematemesis

A

Hema(blood)temesis(vomiting)

Vomiting blood

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36
Q

identify and describe poop terms

A

Melena (black)

Tarry blood in the
stool

Very dark red

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37
Q

RESOLUTION OF HEMORRHAGE

What is resolution dependent on?

A

The amount of hemorrhage present
ex. Smaller hemorrhages have the ability to be reabsorbed
while larger hemorrhages will require phagocytosis and
degradation of RBCs

Organizing hematomas may form and contain a mass of
RBCs and fibrin encapsulated in connective tissue
- will eventually become phagocytized by macrophages

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38
Q

RESOLUTION OF HEMORRHAGE

what is this?

A

Aural Hematoma

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39
Q

RESOLUTION OF HEMORRHAGE

Bruising Colors:

purple=
green=
yellow/orange=

A

Bruising Colors: Hemoglobin (purple) is converted to bilirubin(green)
and eventually hemosiderin(yellow/orange)

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40
Q

Hemorrhage: Clinical significance

generally dependent upon…..?

explain hemorrhagic shock

A

(volume and rate)

Profuse blood loss –> acute anemia –>
hypovolemic shock –> death
- Anemia due to repeated small
hemorrhages. E.g.: parasites
*chronic anemia

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41
Q

Hemorrhage: Clinical significance

Determined by….?

explain compressive effects
when can it be fatal?

A

the location and severity

e.g.: - Hemorrhage in the brain or heart
(pericardium) can be fatal.
- Mechanical compression of organs
due to a hematoma

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42
Q

HEMOSTASIS

what is it?
hint: blood

A

Main physiological response to vascular damage
- helps prevent blood loss by sealing injured vessels
- keeps the blood fluid inside the vasculature (i.e. no clots!)

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43
Q

HEMOSTASIS

How does hemostasis work?

first step is….

A
  1. Injury vascular endothelium leads to reflex vasoconstriction (via endothelin)
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44
Q

HEMOSTASIS

How does hemostasis work?

  1. Injury vascular endothelium leads to reflex vasoconstriction (via endothelin)
  2. second stage is….
A
  1. Primary Hemostasis: Platelets (thrombocytes) - Adhesion, activation and
    aggregation
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45
Q

HEMOSTASIS

How does hemostasis work?

  1. Injury vascular endothelium leads to reflex vasoconstriction (via endothelin)
  2. Primary Hemostasis: Platelets (thrombocytes)- Adhesion, activation and
    aggregation
  3. third stage is…..
A
  1. Secondary Hemostasis: Coagulation cascade - consists of the intrinsic and
    extrinsic pathways
    - Leads to thrombin formation
    - Thrombin converts fibrinogen into fibrin
46
Q

HEMOSTASIS

How does hemostasis work?
1. Injury vascular endothelium leads to reflex vasoconstriction (via endothelin)
2. Primary Hemostasis: Platelets (thrombocytes) - Adhesion, activation and
aggregation
3. Secondary Hemostasis: Coagulation cascade - consists of the intrinsic and
extrinsic pathways
- Leads to thrombin formation
- Thrombin converts fibrinogen into fibrin
4. fourth stage is….

A
  1. Fibrinolysis - breaking down the clot

*Coagulation factors are plasma protiens produced mainly by the liver

47
Q

HEMOSTASIS

What happens at the end of the cascade?

A
  • Clot is stabilized by fibrin
  • Contraction of fibrin-platelet clot
  • Reduces size of the clot to restore normal blood flow
48
Q

HEMOSTASIS

How can coagulation fail?

A
  • Hepatic diseases - Why? Liver is where coagulation factors are produced
  • Nutritional deficiencies - Vitamin K
  • Lack of clotting factors ex. Hemophilia
  • Toxins - Warfarin toxicosis(anti-coagulation meds–what I took)
  • Platelet defects - thrombocytopenia
  • Bacterial invasion during the formation of the clot - leads
    to prolonged healing
49
Q

THROMBOSIS

what is it?
where?

A

Inappropriate activation of the normal hemostatic
process:
- Solid mass (thrombus) is formed within the
cardiovascular system
- May occlude the vascular lumen

50
Q

THROMBOSIS

What makes up a clot?

A

RBCs, Platelets and Fibrin

51
Q

THROMBOSIS

What makes a thrombus different than a PM clot?

A

Adhered to the vascular wall, dry, firm and friable

  • know thrombus is adheredto vascular
52
Q

what is this?

A

THROMBOSIS

Pulmonary Artery - Cow

53
Q

what is this?

A

THROMBOSIS

Renal Artery - Cow

54
Q

VIRCHOW’S TRIAD

what does this refer to?

A

3 components contribute to the formation of a thrombus:

55
Q

who is the”Father of Modern Pathology”

A

Rudolf Ludwig Carl Virchow

56
Q

VIRCHOW’S TRIAD

3 components contribute to the formation of a thrombus:
what are they?

A
  1. Endothelial Injury
    Damage to the vessel wall: infectious (viral, bacterial, parasitic),
    neoplasia, inflammation
  2. Alterations in Blood Flow
    Turbulence or stasis
  3. Hypercoagulability
    Increase in coagulation factors OR decrease in coagulation
    inhibitors
57
Q

Pathogenesis

Alterations in vascular endothelium
what is * VASCULITIS

A
  • VASCULITIS (arteritis and phlebitis) caused by bacteria, viruses
    parasites, neoplasia or trauma
58
Q

Pathogenesis

Alterations in blood flow

what is * Stasis

A
  • Stasis
  • Congestion
  • Vessel occlusion e.g.. prolonged recumbency in surgery or post
    operatively
59
Q

Pathogenesis

Alterations in blood flow
what is * Turbulence

A
  • Aneurysms
  • Branching vessels
  • Cardiac developmental anomalies
60
Q

Pathogenesis

Alterations in blood constituents

what happens here?
hint: before surgery (me) they put me on blood thinners (warfarin) why?

A
  • ↑ in coagulation factors (or ↑ sensitivity to) (surgery, stress,
    inflammation)
  • ↓ in coagulation inhibitors e.g protein losing nephropathies (loss
    of AT III)

*antithrombin 3 must have in order to prevent thrombin from turning fibrinogen–> fibrin clot

61
Q

CLASSIFICATION

Based on: name 4

A
  • Type of vascular involvement:
  • arterial, venous, lymphatic, capillary, cardiac
    Location:
  • wall (mural), valvular, lateral, canalizing (partial repair), occluding (intire endothelium)
  • Infection
  • septic: bacterial or parasitic (thrombi) involvement (w/parasites)
  • **aseptic: no involvement of bacteria or parasites
    ** Color
  • Red = venous (platelets, fibrin, leukocytes, Few rbc)
  • White = arterial (platelets, fibrin)
  • Mixed (pale and red thrombi
  • Laminated
62
Q

CLASSIFICATION

what are laminated thrombi?

A

alternating layers of pale and red constituents–> change in blood flow speed

63
Q

what is this?

A

Mural Thrombus - Cat

64
Q

what is this?

A

Pulmonary Thrombosis
- Dog w/ PLE

*seen in dogs with severe renal glomerular disease–>protein losing nephropathy–>significant loss of antithrombin III, a major inhibitor of thrombin

65
Q

what is this

A

Saddle Thrombus

  • Located in the distal aorta - trifurcation w/ external iliac a.
  • Occludes blood flow to the hindlimbs
  • Animals will present with hindlimbs that are cold to the touch and neurological deficits
66
Q

OUTCOMES OF THROMBI

what are the 4 outcomes?

A

Embolization - spreading of the clot to a different
area **know an embolus is clott free in blood stream

** Recanalization** - Blood flow able to rearrange itself
over the thrombus

** Epithelization** - epithelial cells wall off the
thrombus

** Fibrosis** - scarring and eventual contraction of
thrombus

67
Q

OUTCOMES OF THROMBI

what is this?

A

Recanalization Ǖ Blood flow able to rearrange itself
over the thrombus

68
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

which appears after death?

A

Pm Clot

69
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

which is initiated by thromboplastin

A

PM-Clot

70
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

  1. which is pale or white
  2. which is red
  3. wich is yellow(chicken fat) or red (currant jelly)?
A
  1. Arterial
  2. venus
  3. clot
71
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

which is elastic and moist

A

pm-clot

72
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

which is small size (may be mural)

A

Arterial

73
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

which is composed of:
1. platelets, fibrin
2. platelets, fibrin, and RBC
3. fibrin

A
  1. arterial
  2. venus
  3. pm clot
74
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

lamination is
1. present
2. not frequent
3. absent

A
  1. arterial
  2. venus
  3. pmclot
75
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

which one is not attached to intima (smooth surface)

A

pm-clot

76
Q

THROMBUS V. POST MORTEM CLOTS (arterial thrombosis, venus thrombosis, PM

which is
1. partially organized
2. organized
3. not organized

A
  1. arterial
  2. venus
  3. pm clot
77
Q

EMBOLISM

what happens to cause an embolus?

A

Fragments of a thrombus are able to break off and
lodge themselves at a distant site
- Embolus

78
Q

EMBOLISM

how do you get from lodging to necrosis?

A

Lodging –> Obstruction –> Local ischemia
–> Infarction –> Necrosis

79
Q

EMBOLISM

Emboli can be caused by other things as well!

what are they?
95% are….

A

Emboli can be caused by other things as well!
- Parasites, bacteria, fat embolism, neoplasia, gas
- 95% of etiologies are thrombus
thromboembolism

80
Q

EMBOLISM

what is this?

A

Fat Embolism
- complication of long bone
fractures, osteomyelitis or
surgery

81
Q

what is this?

A

Tumor Embolism
- tumors and neoplastic
cells can cause an embolism

82
Q

what is this?

A

Thrombotic Meningoencephalitis

(TME)
- Histophilus somni
- vasculitis and thrombosis

83
Q

what is this?

A

Parasitic Embolism
- Dirofilaria immitis

84
Q

DISSEMINATED INTRAVASCULAR

COAGULATION (DIC)

is it a primary disease?
systemic reaction to what?
what gets depleted?

A

NOT a primary disease - always secondary
- something else leads to this reaction!!
Systemic reaction resulting in generalized activation of the coagulation
cascade
- Leads to depletion of coagulation factors and severe uncontrolled
bleeding
Ex. Extensive tissue injury, anaphylaxis, sepsis, neoplasia

85
Q

DISSEMINATED INTRAVASCULAR COAGULATION (DIC)

3 Main Steps:

A

1. Increased blood coagulation: something has caused the body to go
into a hypercoagulable state
2. Decreased platelets, fibrinogen and prothrombin(fibrinogen all used up by non-necessary clots forming. see increased bleeding with injury and hemoragic syndrome): consumption
coagulopathy –> hemorrhagic syndrome
*diatheses (clinical disorders with increased bleeding tendencies) Diapedesis (when RBC’s leave through small holes in intact blood vessels)
3. Delayed fibrinolysis activation in response to fibrin clot formation
- leads to severe hemorrhagic syndrome

86
Q

INFARCTION

what is it, what causes it?

A

A localized area of ischemic necrosis
- **Caused by occlusion of arterial blood supply **or venous drainage
- thrombosis, embolism or vascular occlusion

87
Q

INFARCTION

Where do we commonly see infarction?

A
  • Kidneys, lungs and intestines
88
Q

INFARCTION

Gross Appearance:

A
  • Wedge-shaped
  • Ill-defined and red (early)
  • Becomes lighter and paler with time
89
Q

INFARCTION

Characteristics differ with: name 4

A

Characteristics differ with:
Nature of the vascular supply
Oxygen content at the time of infarction
Rate of the development of the occlusion
Vulnerability of affected organ/tissue to hypoxia

90
Q

INFARCTION

what is it?

A

Renal Infarction - Cat

91
Q

INFARCTION

what is it?

A

Renal Infarction - Cow

92
Q

TYPES OF INFARCTS

name the 4 types

A
  1. Red Infarct
  2. Pale Infarcts
  3. Septic Infarct
  4. Venous Infarction
93
Q

TYPES OF INFARCTS

Red Infarct:
name 3 characteristics

A
  • Acute
  • Contains a lot of RBCs
  • Seen commonly in organs with dual blood supply
94
Q

TYPES OF INFARCTS

Pale Infarcts: name 3 characteristics

A
  • Does not contain RBCs
  • Red zone surrounding periphery
  • Starts red but gets paler over time
95
Q

TYPES OF INFARCTS

Septic Infarct: name 2 characteristics

A
  • Mostly from bacterial/septic infected thromboembolus
  • Can be opportunistic bacteria making its way into necrotic
    tissue
96
Q

TYPES OF INFARCTS

Venous Infarction: name 2 characteristics

A
  • From venous obstruction: commonly from twisting of vessels
  • Seen occasionally from obstruction of the vena cava or portal
    vein
  • Dogs: severe heartworm infection
    -Ruminants: rupture of hepatic abscesses
97
Q

TYPES OF INFARCTS

identify

A
98
Q

TYPES OF INFARCTS

identify

A
99
Q

TYPES OF INFARCTS

identify

A
100
Q

TYPES OF INFARCTS

identify

A
101
Q

Cardiovascular collapse
- Acute reduction of effective circulating blood
volume
- Inadequate perfusion of cells and tissues with
blood

what is it?

A

shock

102
Q

SHOCK

Regardless of pathology, hypoperfusion may be caused
by:

A
  • Decreased Cardiac Output
  • Decreased Blood Volume
103
Q

SHOCK

Leads to….

A

Leads to hypotension, impaired perfusion, hypoxia
and DEATH AQ

104
Q

TYPES OF SHOCK

name 4

A
  1. Cardiogenic Shock
  2. Hypovolemic Shock
  3. Blood Maldistribution
  4. Septic Shock
105
Q

TYPES OF SHOCK

  • inability of the heart to maintain adequate cardiac output

what is it called?

A

Cardiogenic Shock

106
Q

TYPES OF SHOCK

  • decreased blood volume usually due to fluid loss
  • blood, dehydration, vomiting and diarrhea

what is it called?

A

Hypovolemic Shock

107
Q

TYPES OF SHOCK

  • decrease in peripheral vascular resistance
  • results in pooling of blood in peripheral tissue caused by vasodilation

what is it called

A

Blood Maldistribution

108
Q

TYPES OF SHOCK

  • endotoxin producing gram negative bacteria activate complement and
    WBCs to produce cytokines ĺ leads to vasodilation, DIC and more
    complement activation

what is it called

A

Septic Shock

109
Q

STAGES OF SHOCK

-attemps to maintain adequate cerebral and coronary bloos supply–>blood redistribution is called

A

1-initial nonprogressive stage (compensated and reversible)

*body able to compensate

110
Q

STAGES OF SHOCK

-patient suffers other stress of risk factor besides the persistence of the shock–> progressive deterioration

A

2-progressive stage (decompensated)

*body unable to compensate can be ok with supportive therapy

111
Q

STAGES OF SHOCK

-severe cell/tissue injury -despite therapy and control of ethilogic agent–> no recovery
-irreversible shock leading to death

A

3- irreversible stage (decompensated)

*not even supportive therapy can help

Pathology 1 RUSVM (7 decks)

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