Exam # 2 Flashcards

Question

What is petechia?

Answer 1

Hemmorhage within tissues that are (pl. petechiae): up to 1-2 mm in size. Especially found on skin, mucosal and serosal surface

Answer 2

Ecchymosis

Answer 3

Hemmorrhage within tissues, larger than petechia (up to ~1 or 2 cm). As seen in bruise (contusion) or small hematoma

Answer 4

Agonal Hemorrhages: Petechiae and ecchymoses associated with terminal hypoxia

Answer 5

Terminal hypoxia

Answer 6

• You can see this sometimes in slaughterhouses, the animal may be unconscious but heart may be alive for a few minutes.

Answer 7

Suffusive hemorrhage: larger than ecchymosis and contiguous. Serosal surface

Answer 8

Suffusive hemorrhage

Answer 9

Paint-brush hemorrhage: Looks like if red paint was hastily applied with a paint brush. Most common on mucosal and serosal surfaces. ◦ Can occur with inflammation of the rumen. ◦ Peritonitis

Answer 10

- Small amounts can be reabsorbed - Larger amounts require phagocytosis and degradation by macrophages

Answer 11

Central mass of fibrin & red blood cells surrounded by supportive vascular connective tissue -\> macrophages will eventually phagocytize this lesion.

Answer 12

Hemoglobin (dark red blue color) enzymatically converted to bilirubin (blue-green color) and eventually into hemosiderin (gold-brown color)

Answer 13

3rd stage -\> Hemosiderin (yellow to brown)

Answer 14

1st stage - Hemoglobin, red-blue

Answer 15

2nd stage- Bilirubin – blue-green

Answer 16

(arrest bleeding by physiological or surgical means). Normal hemostasis is a physiological response to vascular damage -\> Provides a mechanism to seal an injured vessel to prevent blood loss. It is the result of a complex and well-regulated process which maintains blood as a flowing fluid within the cardiovascular system.

Answer 17

* Thrombosis -\> clot ( forms w/in vessel) which is not injured or mildly injured. * Inappropriate activation of the normal hemostatic process. * Can cause many clinical issues, I.e embolism, death, severe neuro impairment, pain, ect.

Answer 18

1. Vascular wall (mainly the vascular endothelium) 2. Platelets 3. Coagulation cascade

Answer 19

* After initial injury, there is a brief period of vasoconstriction ( mostly reflex of neurogenic mechanisms) which is augmented by local secretion factors ( like endothelin which is a potent endothelium- derived vasoconstrictor). * Effect is transient, and bleeding would resume if not for activation of platelets/ coag factors. * Pre sx clotting profile ideal * thrombogenic - attracts platelets in blood

Answer 20

• platelets attracted to this area and to the von Willebrand factor. Has change in shape, starts aggregating, becomes flat and starts releasing granules that call more platelets to the area. This will cause hemostatic plug. This will attach to the ECM to stop bleeding.

Answer 21

• Will cause tissue factor 3 to be exposed to site of injury. Tissue factor is membrane bound pro coagulation glycoprotein synthesized by epithelium. It acts with factor 7 as way to activate clotting cascade. Eventually will create thrombin, thrombin will cleave circulating fibrinogen (in fluid state) into insoluble fibrin (solid), creating fibrin meshwork deposition. (Secondary Hemostatic plug) Thrombin will induce further platelet recruitment/ granule release. 2nd sequence lasts longer than initial platelet plug.

Answer 22

* goal of coagulation cascade is to convert fibrinogen to fibrin. * Fibrin and platelet aggregates form a solid permanent plug to prevent additional hemorrhage. This stage is counter regulatory mechanism ( they will produce substances that reverse process essentially)

Answer 23

 Endothelial cells are key players in the regulation of homeostasis, as the balance between the anti- and prothrombotic activities of endothelium determines whether thrombus formation, propagation, or dissolution occurs Endothelial cells primary release anticoagulant factors (to keep blood in fluid state), but injury will cause endothelial cells to release procoagulant factors (to repair injury).

Answer 24

- Prostacyclin: Vasodialation, inhibits platelet aggregation, anticoagulant - Nitric Oxide: Vasodialation, inhibits platelet adhesion and aggregation, anticoagulant - Tissue Plasminogen Activator (tPA): regulates fibrinolysis, anticoagulant - Thrombomodulin: anticoagulant activity, anticoagulant - Thromboplastin: Promotes blood coagulation, procoagulant - Platelt activating factor (PAF): activation of platelets and neutrophils, procoagulant von Willebrand Factor: promotes platelet adhesison and activation of blood coagulation, procoagulant

Answer 25

* Amplifying series of enzymatic conversions. Each step cleaves an inactive proenzyme into an activated enzyme, culminating in thrombin formation. * Conclusion of cascade, thrombin converts the soluble plasma fibrinogen to fibrin * Coag factors are plasma proteins mainly produced by liver.

Answer 26

Thrombosis: Formation or presence of a solid mass (thrombus) within the CV system Thrombus: • Form plugs: platelets, fibrin, and entrapped blood cells. • Can cause occlusion of vascular lumen and embolism. • Adhered to vascular wall as opposite to post mortem blood clot.

Answer 27

thrombus/ thrombosis

Answer 28

Pathogenesis of Thrombosis - Virchow triad • Endothelial injury - even alone can cause thrombosis • Alterations in blood flow ( turbulence or stasis) • Hypercoagulability ◦ Increase coagulation factors or increase sensitivity ◦ Decrease in coagulation inhibitors

Answer 29

DVT- Deep vein thrombosis

Answer 30

* Thrombus can appear anywhere in cardiovascular system. * HCM can cause spontaneous death in young cats. (usually underlying left sided CHF) * Mural thrombosis -attached to wall of heart

Answer 31

Mural thrombus, left ventricle -\> on the wall of the heart

Answer 32

Atrial thrombus, left atrium, cat with Cat Hypertrophic Cardiomyopathy (HCM).

Answer 33

• antemortem thrombi are usually attached to wall of endothelial cell, more pale in color, and dry/ friable looking - Post mortem clots -\> jelly clots

Answer 34

* Dogs with renal failure can develop pulmonary thrombosis ( antithrombin III in plasma can be lost with PLN ) * Many dogs with HWD can develop pulmonary thrombosis.

Answer 35

Seen in dogs with severe renal glomerular disease protein losing nephropathy  Significant loss of Antithrombin III, a major inhibitor of thrombin

Answer 36

Verminous thrombosis – thrombus formation in the cranial mesenteric artery of horses with Strongylus vulgaris infection

Answer 37

Verminous thrombosis

Answer 38

* Used to be quite common/ cause of colic. * More cases being seen with antihelminth resistance. * parasite makes it way through blood vessels and get lost and they produce damage in that area. Can be very prominent.

Answer 39

• Always check that artery during necropsy in horses. Can be in main branch of mesenteric artery, or in the branches (colic, cecum, ect)

Answer 40

Verminous thrombosis from stongylus vulgaris

Answer 41

• Pinpoint lesions are stronglyosis larvae

Answer 42

Saddle thrombosis, cat with HCM. Thrombus is located in the trifurcation of the abdominal aorta

Answer 43

* Saddle thrombus : increased turbulence is present, as well as hypercoagulability, and potential endothelial damage. * Happens in 30% of cats with HCM * You can see it in dogs with HCM but its more rare Signs: Extreme pain / panting/ respiratory distress, dragging hind legs in cats dogs can have partial saddle thrombus and still have use of legs.

Answer 44

* Lysis * Propagation (thrombus in there, starting to form and can cause obliteration of lumen) * Embolization (fragmentation of thrombus breaks off and can get stuck in other areas) * Organization/ recanalization (can become infiltrated by connective tissue/ macrophages and make small canals in the large clogged vessels)

Answer 45

Recanalization of an occlusive thrombus, cat

Answer 46

- If a piece breaks off then it would be called an embolism • Can end up in longs and cause pulmonary ischemia/ hypoxia/ infarct.

Answer 47

The size of the thrombus that was broken off. small piece -\> embolism larger piece -\> embolus

Answer 48

Fibrocartilaginous embolism, dog – spinal cord -\> results in spinal cord infarcts • Sometimes they are running around, and fine and then all of a sudden are in pain, have neurologic signs, and paralysis. • Usually you can see degeneration and necrosis in spinal cord. • Not very common

Answer 49

cartilage embolism

Answer 50

Fat Embolism  Could be a complication of long bone fractures - Image is of Bone marrow emboli in pulmonary artery, human –secondary to CPR efforts

Answer 51

• fat embolism is a complication of long bone fractures. 90 % of people with long bone fractures will get fat embolism but only 5 % have clinical signs. Sometime they could have it happen 3 days after injury. This can also cause neurologic disturbance (embolism to brain), difficulty breathing (to lungs), ect.

Answer 52

an infectious cause of thrombosis/ thromboembolism. Bacterial valvular endocarditis in cattle often involve the right AV valve and can give rise to septic emboli that will lodge in the pulmonary arteries inflammation/ abscess Formation (embolic pneumonia)

Answer 53

Thrombotic Meningoencephalitis (TME), steer, Noah’ Arkive Etiology: Histophilus somni infection – results in vasculitis and thrombosis

Answer 54

Disseminated Intravascular Coagulation (DIC). Signs of tissue hypoxia, infarction or/and hemorrhage are seen. * DIC -\> catastrophic systemic reaction, general activation of blood coagulation system * Caused by extensive tissue injury, neoplasia, systemic immunologic reactions ( anaphylaxis) and sepsis. * Can lead to consumptive coagulopathy and hemorrhage diathesis. * You will see fibrin thrombi within glomerular capillaries. * Stain: PTAH

Answer 55

Fibrin thrombi within glomerular capillaries ( Stain used: PTAH stain -\> DIC)

Answer 56

* Infarct: Caused by an area of ischemic necrosis in a tissue or organ caused by occlusion of either the arterial supply or venous drainage. * Venous infarct's are usually intensely hemorrhagic as blood backs up into affected tissue behind the obstruction.

Answer 57

Venous infarction, small intestinal volvulus, pig. Note the intensely congested loops of small intestine undergoing venous infarction. The twisting of the mesentery associated with the volvulus has resulted compression of the arteries and veins of the intestine. Because arterial pressure is higher than venous pressure, some blood can get into the gut but the compression of the thin-walled veins results in backing up and stagnation of blood in the gut

Answer 58

“Arterial infarcts are often initially hemorrhagic but become pale as the area of coagulation necrosis becomes evident”

Answer 59

Microscopically an infarct is a focal area of coagulation necrosis

Answer 60

Renal infarct. • Thrombus will cause obliteration of lumen of that artery and you will have a triangular shaped area of necrosis due to hypoxia.

Answer 61

* Shock is common pathway for number of potentially lethal events, including severe hemorrhage, extensive trauma, burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis. * Regardless of reason it will cause systemic hypoperfusion which is caused by either reduced cardiac output or by reduced effective circulating blood volume. * End results are hypotension, impaired tissue perfusion and cellular hypoxia. This may lead to DIC/ Multiorgan failure.

Answer 62

(failure of the heart to maintain normal cardiac output)

Answer 63

Fluid loss due to hemorrhage, vomiting, diarrhea

Answer 64

Anaphylactic (Type 1 hypersensitivity)  Neurogenic (neurological injury leading to loss of vascular tone and peripheral pooling of blood) - Sepsis

Answer 65

(results from the host innate immune response to infectious organisms that may be blood borne or localized to a particular site).

Answer 66

• Most caused by endotoxin producing gram negative bacilli.

Answer 67

Endotoxins are bacterial wall lipopolysaccharides (LPS) consisting of a toxic fatty acid (lipid A) core common to all gram-negative bacteria, and a complex polysaccharide coat (including O antigen) unique for each species. LPS and other microbial substances induce injury & activation of the vascular endothelium plus stimulate (“activate”) WBCs to release cytokines vasodilation & pro-thrombotic diathesis (DIC).

Answer 68

Brain & heart are very susceptible to tissue hypoxia.

Answer 69

- Abnormal deposition of Ca++ salts usually in form of phosphates and carbonates.

Answer 70

When the deposition of abnormal calcium salts occur locally in dying tissue.

Answer 71

Almost always result of hypercalcemia secondary to some disturbance in calcium metabolism.

Answer 72

Causes can be vitamin E / Selenium deficiency There will be areas of normal adipose tissue (labeled A) and abnormal calcification ( usually on left ventricle (labeled b)

Answer 73

You can tell when making your incision if there are calcium deposits because it will feel gritty in comparison to other areas. The calcium deposits are the dark red areas in this slide.

Answer 74

This is Metastatic calcification. Cases of Vitamin D toxicity can cause calcium deposition in organs causing metastatic calcification. You will see it most commonly in the intima of major vessels, and you will see raised, granular mineralization.

Answer 75

Vitamin D toxicity, access to plants that are carcinogenic, that contains vitamin D analogs which can cause hypercalcemia due to excessive vitamin D.

Answer 76

Uremic Gastritis

Answer 77

Uremic gastritis leading to gastric mineralization. In this image you can see the mineralization of the mucosa of the intestines. • You will feel hard tissue in the intestines, this would be deposition of calcium w/in intestinal lumen.

Answer 78

Metastatic Caclification.

Answer 79

You can see congestion and hemorrhage, and inflammation. When the stain (von Koda) is done you can see increased calcium deposits within the mucosa. Could be dystrophic due to vasculitis and ischemia which leads to necrosis, or it could be metastatic due to secondary hyperparathyroidism.

Answer 80

Metastatic calcification

Answer 81

* Renal failure -\> Secondary Hyperparathyroidism -\> Hypercalcemia. * Uremia induces vasculitis -\> this causes thrombosis in different tissues, including GI tract. This is called uremic gastritis. Sometimes this is the cause of lesions such as this in patients with renal failure. * This accumulation of urea, nitrogen products in blood of individual with renal failure will cause vasculitis in the mucosa of the stomach, mucosa of intestine, can lead to thrombosis/ ischemic damage to the tissue, which will cause degeneration/ necrosis and then dystrophic calcification. * Can also develop secondary hyperparathyroidism (which would lead to metastatic calcification.

Answer 82

• Renal Failure: ◦ Retention of phosphates-\> increased stimulation of parathyroid gland -\> increase in parathyroid hormone -\> stimulation of osteoclasts -\> increased calcium absorption ( increased calcium level (aka hypercalcemia)) This can lead to dystrophic/ metastatic calcification

Answer 83

* position of carbon particles is called anthrocosis * most common in lungs, bronchi, regional lymph nodes, ect. * From carbon deposition within these areas. Can be seen in areas with high air pollution. Can be seen on pleural surface. * Not clinically significant, but can be an indication of exposure to air pollution.

Answer 84

* tattoos used to identify animals. * these pigments are phagocytized by macrophages while others remain free in the Dermis without eliciting an inflammatory response.

Answer 85

Familial renal disease can show signs at 2 years old.

Answer 86

This term is usually applied to the inhalation of silica or asbestos (asbestosis) that may lead to significant pulmonary fibrosis. - Silica crystals are birefringent under polarized light. Mild will not show any clinical significance. You don’t see it often. (Sometimes when there is exposure of volcanic ash.

Answer 87

- Fat soluable pigements of plant origin * Can be seen by over abundance of certain vitamin A precursors. * Can be seen in the adipose tissue. Due to consumption of feed with high level of pigment. Seen in horses and cattle.

Answer 88

Carotenoid pigments.

Answer 89

Y ou can see this sometimes in patients with renal failure,. Their could be areas of subpleurital mineralization. This is considered to be both metastatic/ dystrophic depending on the cause. Can be found on the inside of the ribs

Answer 90

Exogenous (formed outside the body) Endogenous (formed inside the body) Hematogenous (blood origin)

Answer 91

Lipofuscin

Answer 92

- Carbon - Tattoos - Dusts - Carotenoids - Tetracyclin

Answer 93

The leptomeninges

Answer 94

Carbon is the most exogenous pigment. Portal entry is usually by inhalation and can lead to black lungs. This is common in areas with substantial air polution.

Answer 95

Dusts. The condition associated with the inhalation and retention inorganic dusts within the lungs is known as Pneumoconiosis

Answer 96

Ceroid -\> associated to vitamin E deficiency and the ingestion of unsaturated fatty acids –brown discoloration of the tunica muscularis.

Answer 97

Hemoglobin is the normal red pigment of erythrocytes, responsible got oxygen transport. * Normal animal Pink MM * Cyanosis: Pale grey- Blue MM -\> Decreased O2, CO2 may be carried instead * Anemia: Pale pink - White - \> Decreased RBC count

Answer 98

Hemoglobin pigmentation

Answer 99

* Urinary bladder was filled with red urine ( patient with bovine babesiosis) * You can see increased bilirubin and since it is difficult to excrete it will accumulate in the tissues which gives the jaundice characteristic yellow color

Answer 100

• Black tracks on surface of the liver, this is exhaust from the trematods you can find cystic lesions with trematode clusters. This is the result of breaking down hemoglobin in the area.

Answer 101

When administered during the period of teeth development they will be it deposited in the mineralizing dentin, enamel and cementum, staining the teeth or portions of them yellow or brown.  high doses may induce enamel hypoplasia Avoid the administration during pregnancy!

Answer 102

Fluke exhaust. Parasite hematin.

Answer 103

Melanin Lipofuscin/ Ceroid.

Answer 104

Hemosiderin * can also be seen in the lungs of individuals with congestive heart failure. * when there is breakdown of erythrocytes, iron containing heme will stain.

Answer 105

Chronic pulmonary congestion and edema is occuring in a horse with CHF. Iron (Perl’s) stain can be used to find Hemosiderin-laden macrophages (“heart failure cells” -\> siderophages). These cells will stain blue.

Answer 106

Pigment normally present in the epidermis, responsible for skin color and hair color.  Produced by melanocytes.  Formed by the oxidation of tyrosine, which requires tyrosinase (copper-containing enzyme).  Lack of tyrosinase may lead to a general lack of melanin, a metabolic inherited defect known as albinism.

Answer 107

HE-stain, dark brown pigment within the cytoplasm of alveolar macrophages

Answer 108

Chronic pulmonary congestion and edema, horse with congestive heart failure, H&E stained section

Answer 109

The aging pigment

Answer 110

* Sometimes can be seen in young animals such as cattle/ pigs, sheep ect. You can also see it in the intima of the aorta, and in the brain. * This is presence of melanin in abnormal places. * Their is dark brown discoloration on the tissue. This is just accumulation of melanin outside the skin. No proliferation changes/ clinical significance.

Answer 111

This is icterus or jaundice. It is caused by an increase in the bilirubin in plasma.

Answer 112

Congenital Erythropoietic Polyphyria

Answer 113

- Pigment is excreted in urine that if allowed to stand in light, develops a port-wine color due to photic activation of porphyrins  Urine and tissues fluoresce blue-green in UV light

Answer 114

* can be found in an aging animal. Can be seen in cardiac muscle, cardiac myocytes. Brown yellow granular tissue, that is next to nucleus. * Wear and tear pigment. * Can cause the destruction of organelles over time. This is usually not concerning. But will indicate age.

Answer 115

In neuronal tissue, you can see lipofuscin as well.

Answer 116

Ceroid has a similar histochemical features to lipofuscin but is not age-related. Small intestine a bit brown, this is the presence of ceroids. This can be a sign of vitamin E deficiency.

Answer 117

Hemoglobin Parasite Hematin Hemosiderin Bilirubin Porphyrins

Answer 118

- Cyanide binds to cytochrome oxidase, the enzyme responsible for oxidative phosphorylation -\> leads to impaired cellular respiration within mitochondria -\> tissues are unable to use the oxygen carried by the blood hemoglobin causing rapid death. - The arterial and venous blood in the poisoned individual appears brightly red. - Smoke inhalation is a common cause of cyanide poisoning during fires.

Answer 119

In intravascular hemolysis Hb is released from lysed erythrocytes and stains the plasma pink.  It may be excreted by the kidney staining it dark-red and the urine red (hemoglobinuria)

Answer 120

• Fascilodis Minor ( fluke infestation)

Answer 121

Golden-brown granular iron-containing pigment (intracellular aggregates of ferritin) that originates from the breakdown of erythrocytes.  It develops within macrophages, particularly common in the spleen, liver or within foci of hemorrhage.

Answer 122

• Blood will back up into the lungs, which will increase the hydrostatic pressure in the pulmonary vasculature. Left sided congestive heart failure patients can have dyspnea (especially at night), chest tightness.

Answer 123

* Left sided congestive heart failure, since there is an area with stagnated poorly o2 blood, you end up with hypoxic damage to the alveoli. Their is also little foci of hemorrhage (micro hemorrhage). * RBC that go into alveoli will be phagocytized by alveolar macrophages, this will leave behind these brown intracytoplasmic pigment. This is called /hemosiderin.

Answer 124

- normal major pigment found in bile  Derived from Hb but contains no iron (end product of heme degradation)  Yellow to brownish green pigment

Answer 125

no iron, end product is from eme degradation.

Answer 126

 Low concentrations are normal in plasma as a result of the breakdown of senescent red blood cells.  Bilirubin is conjugated in the liver and excreted in the bile

Answer 127

Excessive amount of bilirubin in plasma will lead to icterus (Jaundice) yellow staining of tissues.

Answer 128

- Pre-hepatic: IMHA ( common especially in dogs) Destruction of RBC. Will overwhelm the liver. - Hepatic Jaundice: Hepatosis dietetica - vitamin E/ selenium deficiency. In pigs this can be main presentation due to liver lesions. Jaundice is easily seen in the intima of the vessel wall. - Posthepatic: Any disease that occurs after the liver and causes impairment of function.

Answer 129

Congenital erythropoietic porphyria of calves, cats and pigs is a rare inherited disorder caused by deficiency of uroporphyrinogen III cosynthetase. It affects RBC precursors and results in anemia. The disease is refer to as “pink tooth” because porphyrins accumulate in dentin and bones resulting in reddish teeth in young animals and dark brown teeth in older ones.

Answer 130

Consists of blood, central pump, blood distribution (arterial (O2+ nutrients) and collection (venous (metabolites, products ect)).

Answer 131

Lymphatics that parallel the veins contribute to circulation by draining fluid from the extravascular spaces into the blood vascular system.

Answer 132

Capillaries (part of a whole)

Answer 133

Aorta Vena cava

Answer 134

◦ Vein: tunica externa, veins also have valves. ◦ Artery: tunica media ◦ Capillary would just be basement membrane with endothelial tissue.

Answer 135

- microcirculation is where metabolic exchange occurs due to slowing down of circulation.

Answer 136

- Provides anti thrombic and pro fibrinolytic in normal state and pro thrombotic and anti fibrinolytic during injury. • Hemostasis is the arrest bleeding by physiologic properties of vasoconstriction and coagulation or by surgical means. Bleeding can be stopped.

Answer 137

- Liquid state - anti thrombic, pro thrombic, anti fibrinolytic, fibrinolytic factors help with keeping the blood in a liquid state.

Answer 138

◦ Formation of fibrin is very important for formation of clot.

Answer 139

• Injury will cause prothrombotic, and antifibrinolytic which will help to repair the vessel.

Answer 140

• Leaking vessels after an injury, and endothelial cells will produce cytokines so WBC can go and repair the area. This makes the area more more able to absorb nutrients and bring cells to repair the area.

Answer 141

NO ( nitric oxide) relaxes and causes vasodilation. Endothelin causes vasoconstriction.

Answer 142

- Regulates traffic of inflammatory cells. - Produces pro-inflammatory cytokines - Control angiogenesis and tissue repair

Answer 143

Total Body Water: 65 % total body weight - Plasma 5% - Interstitial Fluid 15% - Intracellular Fluid 40% - Transcellular Fluid 5%

Answer 144

Age. Infant have increased water content in their blood. Fluid loss occurs with age, and that is why wrinkles occur.

Answer 145

* Interstitium: Space between tissue compartments. It is the medium through which all metabolic products must pass and is made up of ECM and supporting cells. * ECM: Collagen, reticulin, elastic fibers) ground substance (glycoproteins, ect)

Answer 146

* Hydrostatic: Pressure of fluid within the vasculature * Osmotic: Pressure based on presence of solutes, primarily proteins, albumin. * These control the amount of fluids that will be within the vasculature vs. in the third space.

Answer 147

Increased Filtration. Edema.

Answer 148

• Arteriole side has increase of hydrostatic pressure( increased in fluid exchange), venous side has increase in oncotic pressure. remaining fluid is drained by lymphatic system ◦ Arteriole: Favors filtration ◦ Veins: Favor absorption.

Answer 149

• Increased hydrostatic pressure or diminished plasma osmotic pressure within capillaries will cause extravascular fluid to accumulate. If capacity of lymph drainage is exceeded tissue edema will result.

Answer 150

Edema Hyperemia & Congestion Hemostasis Hemorrhage Thrombosis, Embolism, DIC Infarction Shock

Answer 151

* abnormal accumulation of excess extracellular fluid. * Fluid outside vascular compartment.

Answer 152

• Increased hydrostatic pressure ◦ (Right sided CHF, Tightly bandaged limb) ◦ Impairing venous return will increase hydrostatic pressure. • Decreased plasma colloidal osmotic pressure aka oncotic pressure ( decreased protein absorption, decreased protein synthesis, increased protein loss) ◦ (proteinuria can indicate protein loss via damage of glomeruli in kidneys. This can lead to generalized edema in an individual ◦ Starvation, hypoproteinemia, PLE, ect. • Lymphatic obstruction: Damage/ obstruction of lymphatics ◦ Tumor, surgery, inflammation ect. • Increased vascular permeability ◦ inflammation, cytokines will decrease vascular permeability, and cause localized edema.

Answer 153

* Diffusely swollen leg, this is due to lymphatic obstruction. * Some tumors of dogs (i.e melanoma which this dog had), can spread along the lymphatics)

Answer 154

Local lymphatics are distended (lymphangiectasia) and filled with neoplastic cells.

Answer 155

Horse Gastric wall edema

Answer 156

* Clear or pale eosinophilic staining depending on whether it is non-inflammatory or inflammatory edema * Spaces are distended * Blood vessels may be filled with RBC * Lymphatics are dilated * Collagen bundles are separated

Answer 157

• Edema can be classified as: ◦ Inflammatory: Increased vascular permeability, - Refers to "exudate" -\> high protein, high specific gravity, higher cellularity, less than 7,000 cells/uL ◦ Non Inflammatory: Edema of CHF, Edema of Liver failure) Referred to as a "transudate" -\> Low protein content, low specific gravity, low cellularity, less than 1500 cells/uL Inflammatory may indicate peritonitis.

Answer 158

Pitting edema

Answer 159

• Presence of fluid w/in the thoracic cavity - hydrothorax ◦ Can be seen with chronic pneumonia ◦ Something in the lungs that causes pulmonary hypertension. ◦ Resistance to blood being pumped into the lungs

Answer 160

Wet Gelatinous and Heavy Swollen organs Fluid weeps from cut surfaces May be yellow

Answer 161

• Mulberry heart disease - related to vitamin E selenium deficiency. ◦ Increased protein in fluid, fibrin strands and cloudy with high cellularity, kind of inflammatory conditions.

Answer 162

• Hydroperitoneum/ Ascites: Fluid ( transudate) within peritoneal cavity.

Answer 163

Ascites in a horse

Answer 164

Anasarca This can be seen typically in aborted fetus' with severe congenital heart malformations .

Answer 165

When pressure applied to an area depression or dent results as excessive interstitial fluid is forced to adjacent areas. Takes a few seconds for area to return to normal.

Answer 166

Bottle Jaw/ Submandibular edema

Answer 167

Protein losses (i.e protein loosing enteropathy, protein loosing nephropathy)

Answer 168

‣ Increase of hydrostatic pressure, increase amount of plasma within those blood vessels and this causes edema. ‣ Left sided CHF will eventually back up into the lungs and cause all of the same issues as you see above.

Answer 169

• Pericardial effusion: yellowish in color, contains a bit of an exudate • Mulberry heart disease - related to vitamin E selenium deficiency. ◦ Increased protein in fluid, fibrin strands and cloudy with high cellularity, kind of inflammatory conditions.

Answer 170

* Hydroperitoneum/ Ascites: Fluid ( transudate) within peritoneal cavity. * R sided heart-failure can lead to more diffuse edema.

Answer 171

Anasarca- Generalized edema with profuse accumulation of fluid within the subcutaneous tissue.

Answer 172

- Submandibular edema: bottle jaw is commonly associated with severe GI parasitism and hypoproteinemia in sheep. - Specifically can be seen with infestations of Haemonchus contortus (barber pole worm) . Translucent fluid. - Decreased oncotic pressure from hypoproteinemia from heavy parasitism.

Answer 173

Haemonchus contortus (barber pole worm)

Answer 174

 Non-inflammatory edema: e.g.: Associated to left-sided congestive heart failure (CHF).  Inflammatory edema: Damage to pulmonary capillary endothelium -\> e.g.: pneumonia

Answer 175

ARDS (Acute respiratory distress syndrome) Sudden, diffuse and direct- increase in vascular permeability: high fatality rate -\> Followed by pneumonia if animal survives

Answer 176

• Pulmonary edema ◦ Lungs slightly enlarged, heavier, fluid coming out, you will see frothy material when you open sections of trachea, lungs, ect. ◦ Gelatinous material in the tissues.

Answer 177

• Macrophages with hemosiderin are indicators of micro hemorrhage/ pulmonary hemorrhage. ◦ these are considered heart failure cells or siderophages.

Answer 178

Hyperemia indicates increase of arteriole-mediated engorgement of the vascular bed. Blood is oxygenated (red). (i.e: exercise, inflammation)

Answer 179

Congestion indicates passive, venous engorgement. Blood is not oxygenated (blue). (i.e local obstruction, congestive heart failure)

Answer 180

Most commonly associated with cardiac failure  Alveolar walls become thickened -\> may lead to fibrosis  Congestion, micro-hemorrhages -\> and accumulation of heart failure cells

Answer 181

Gingivitis (pathologic hyperemia)

Answer 182

Bulbar and palpebral conjunctivitis, human

Answer 183

* GDV usually includes splenic involvement. * signs -\> abd pain, distention, ect. * Obstruction of gastric veins which will cause hypoxic damage due to the lack of blood-flow. Sepsis can occur, peritonitis, ect. * Can happen in swine as well when they get over excited. * Necrosis in the walls of vessel will cause blood to leak into abdomen after death.

Answer 184

Intestinal volvulus, horse

Answer 185

colonic torsion, horse

Answer 186

* L side of heart can cause pulmonary congestion/ edema and this can cause brownish accumulation on lungs. * Lungs will be enlarged, brown changes on lungs is deposition of heart failure cells and hypoxic damage (sign chronic pulmonary edema) * Lungs also wet looking

Answer 187

Digestion: Inc blood to GI Exercise: Inc blood to muscles To dissipate heat: Inc blood to skin to cool down Neurovascular: Involuntary inc blood in face as result of embarrassment/ emotional distress

Answer 188

Chronic hepatic congestion - \> likely the result of Right sided CHF Livers are enlarged and exhibit rounded edges

Answer 189

Chronic hepatic congestion: “Nutmeg liver"

Answer 190

Caused by an underlying pathological process – usually inflammation.  Arteriolar dilatation-\>secondary to inflammatory stimuli (inflammatory mediators).  Redness (“rubor”) is one of the 5 cardinal signs of inflammation : tumor (swelling), calor (heat), rubor (redness), dolor (pain) and loss of function. Swelling/ edema occurs

Answer 191

 Redness (“rubor”) is one of the 5 cardinal signs of inflammation : tumor (swelling), calor (heat), rubor (redness), dolor (pain) and loss of function.

Answer 192

Since the vascular beds are engorged with poorly oxygenated blood tissues are dark red to blue (cyanotic), depending on the degree of stagnation. Like other lesions it can be classified according to duration (acute or chronic) and its extend: localized (e.g. isolated area of venous obstruction); generalized: Systemic change like in CH

Answer 193

* Pulmonary Hypertension makes it hard for R side of heart to pump blood so R side will also start failure * Increase hydrostatic pressure, * Backup of poorly O2 blood will back up into liver and can show congestion in there. * Liver will be round, and enlarged, and you will see fibrosis/ discoloration due to backup of blood.

Answer 194

Chronic hepatic congestion -\> nutmeg liver • Poorly O2 blood/ increased around portal vein, and hypoxic damage due to poor oxygenation.