Pathology - Intro

Front 1

3 nuclear changes in irreversable cell injury are:

Back 1

PYKNOSIS (irrev. condens. of chr. in nucleus of cell undergoing necrosis or apoptosis)
KARYORRHEXIS
KARYOLYSIS

Front 2

Pyknosis

Back 2

Pyknosis, or karyopyknosis

irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis.

fyi: from Greek pyknono meaning "to thicken up, to close or to condense"

Front 3

What is KARYOLYSIS?

Back 3

loss of nucleus = KARYOLYSIS

Front 4

karyorrhexis

Back 4

karyorrhexis = fragmentation of nucleus
(follows pyknosis; or condens. of chr. in nucleus during apoptosis)

Front 5

Arthrogryposis

Back 5

Arthrogryposis: rare congenital disorder characterized by multiple joint contractures (shortened); can include muscle weakness and fibrosis; non-progressive disease.

* from Greek, literally meaning 'curved or hooked joints

Front 6

Chondrodystrophy

Back 6

any congenital disorder of cartilage formation (e.g. dwarfism)

literally, "cartilage mal-development"

Front 7

Encephalocele

Back 7

failure of neural tube to close characterized by sac-like protrusions of the brain and the membranes that cover it through openings in the skull.

Front 8

palatoschisis

Back 8

cleft palate

Front 9

T/F ATP depletion is consequence of both ischemic and toxic injury.

Back 9

True

ATP depletion is consequence of both ischemic and toxic injury.

Front 10

How can ATP depletion lead to cell injury?

Back 10

* Hypoxia attacks aerobic respir.- stoppage of ATP prod.-ATP decr. in cell membrane- causes Na pump failure results Na retention (Na enters cell and K diffuses out)-water gets in cell which results in cell swelling.
* also changes metabolism; accum. of lactic acid

Front 11

Reperfusion [tissue] injury refers to ?

Back 11

Reperfusion inj. refers to tissue damage caused when blood supply returns to the tissue after a period of ischemia; caused by oxidative stress

Front 12

Effects of increased Ca in the cell:

Back 12

Activates a number of enzymes with deleterious effects

Front 13

Name 4 examples of "deleterious" enzymes (released after intracellular Ca+ increase):

Back 13

1. Phospholipases - damage cell membr.
2. Proteases 3. ATPase - hasten ATP depl.
4. Endonuleases (e.g. DNase)

Front 14

What is a free radical? How do they cause cell injury?

Back 14

* single unpaired electron in an outer orbital
* unstable and extremely reactive and enters into reactions in cells with organic and inorganic chemicals.

Front 15

Sources of Ca+ rise?
(increased intracellular calcium)

Back 15

* Net influx of Ca across plasma membrane
* Release of Ca from mitochondria and ER

Front 16

Chemicals can induce injury in 3 ways:

Back 16

1. Binding to cell membrane causing increased membrane permeability and inhibition of ATPase dependent transport.
2. Direct cytotoxic effects.
3. Reactive free radicles.

Front 17

Continued ATP depletion and increased calcium influx in cell causes: (2)
1. damage to ?
2. affects pH, how? why?

Back 17

1. Extensive damage to plasma membrane. Cell membrane damage is central factor in irreversible injury.
2. Lower pH- injury to mitochondria and lysosomes (release enzymes)

Front 18

Is Acute Cellular swelling a form of Reversible cell injury?

Back 18

Yes

Front 19

Acute Cellular swelling usually seen in what tissues/organs?

Back 19

Usually seen in liver, kidney, muscles, glandular tissues, neurons, glial cells of brain and adrenals

Front 20

How does the physical appearance of these organs change (w/acute cellular swelling)? cells?

Back 20

Grossly - organ becomes pale, turgor., heavy.
Micro - Cytoplasm shows ground glass app., w/small vacuoles. Nuclear swelling.

Front 21

T/F In brain swelling is called ‘cytotoxic edema’. Swollen neurons fail to conduct nervous impulses and result in stupor or coma.

Back 21

True

Front 22

T/F Swollen epithelial cells in kidney impair absorptive and secretory function.

Back 22

True - Swollen epithelial cells in kidney impair absorptive and secretory function.

Front 23

T/F Endothelial cell swelling causes obstruction, worsening cellular hypoxia.

Back 23

True - Endothelial cell swelling causes obstruction, worsening cellular hypoxia.

Front 24

4 Forms of necrosis

Back 24

Depends on cause and tissue involved.
1. Coagulative necrosis
2. Liquifactive necrosis
3. Caseous necrosis
4. Fat necrosis

Front 25

Coagulative necrosis Caused by:

Back 25

type of accidental cell death typically caused by ischemia or infarction.
Also:
* Toxic product of certain bacteria- necrobacillus.
* Poison, burn, electricity, x-ray.
* Zenker`s necrosis-

Front 26

Gross appearance of tissue undergoing coagulative necrosis ?

Back 26

Gross appearance of coagulative necrosis - Gray or white, firm and depressed.

Front 27

Microscopic appearance of coagulative necrosis?

Back 27

Microscopic appearance-
1. Outline of the necrosed cell is preserved,
2. Cytoplasm homogenous strongly acidophilic,
3. Nuclei show degeneration.

Front 28

What type of necrosis occurs in CNS (spinal cord lesions) and in abscess?
Causes?

Back 28

Liquefactive (colliquative) necrosis

Causes- same as for coagulative necrosis

Front 29

Gross appearance of tissue undergoing liquefactive (colliquative) necrosis ?

Back 29

Gross lesions- small or large cavity containing yellow white opaque fluid, the walls of the cavity are irregular and soft.

Front 30

What type of necrosis is caused by toxins of certain micro-organisms?

Back 30

All 4 including caseous and peritoneal fat necrosis - caused by toxins of certain microorganisms

Front 31

Where does caseous necrosis get its name?

Back 31

Because gross lesions- looks like “milk curd” or “cheese”
hence the name caseous. Necrosed tissue is dry, greasy and breaks easily.

Front 32

Cause: fat necrosis is often seen in what 2 places?

Back 32

A) Fat of peritoneal cavity- enzymic fat necrosis or pancreatic fat necrosis. Hard masses form on omentum, mesentery and peritoneum.; intestinal obstruction & clinical signs.
B) fat under the skin and pelvic canal- traumatic necrosis of fat.

Front 33

Which type of necrosis?
Mxscopic lesions- loss of cell line and normal arch. of tissue, necrosed tissue is granular and stains purple
~Inflamm. zone surrounds the necrosis ~calcif. is usually present in necrosed tissue.

Back 33

Caseous necrosis

Front 34

Which type of necrosis?
Gross lesions- lose shiny appearance, become opaque, whitish, solid or granular.

Back 34

Fat necrosis (necrosis of fat cells)

- fat becomes opaque

Front 35

Type of necrosis seen in young cattle fed on tall fescue (grass) infected with fungus (Acremonium coenophialum)?

Back 35

Peritoneal fat necrosis

“Summer fescue toxicosis” in cattle, sheep and horses.

Front 36

Refers to the death of single cells-through programmed ‘suicide’ path way.

Back 36

Apoptosis

Front 37

How are necrotic foci different from tissues undergoing typical apoptosis or post mortem autolysis? (4)

Back 37

Necrotic foci is often surrounded by inflammatory rxn; can cause 1. sloughing 2. liquefaction w/abscess or autolysis of foci, 3. encapsulation by fibrous tissue or 4. calcification

Front 38

Condition when necrosed tissue is invaded by putrifactive bacteria.

Back 38

Gangrene

Front 39

Three types of gangrene

Back 39

Dry gangrene.
Moist gangrene
Gas gangrene
--Area of gangrene are separated from healthy tissue by a line of demarcation- seen as red zone of inflammation.

Front 40

Type of apoptosis triggered by-
* irradiation
* virus infection
* certain toxins
* drugs

Back 40

Pathological apoptosis

Front 41

What is physiological apoptosis?
3 examples where might find it?

Back 41

* normal cell turn over (liver, kidney, epithelium)
* Hormone induced atrophy-
Involution of thymus
* remodeling of embryonic development
* tumors

Front 42

Chromatin condensation and fragmentation into seperate "bodies" is characteristic of apoptosis OR necrosis?

Back 42

APOPTOSIS
- Cell shrinkage
- Chromatin condensation and frag. into apoptotic bodies
- Phagocytosis of apoptotic bodies by tissue macrophages

Front 43

____ is caused by gradual cooling of carcass.

Back 43

Algor mortis: gradual cooling of carcass.

Front 44

____ is caused by gravitational pooling of blood to the down side of the animal.

Back 44

Livor mortis (hypostatic congestion): gravitational pooling of blood to the down side of the animal.

Front 45

____ is caused by contraction of muscles occurring after death, because of depletion of ATP in muscle.

Back 45

Rigor mortis; contraction of muscles occurring after death, because of depletion of ATP in muscle.

Front 46

Bile imbibition refers to what post mortem changes?

Back 46

Bile imbibition refers to yellow staining of tissues adjacent to gall baldder. Seen in 1-6 hours after death.

Front 47

Pseudomelanosis refers to what post mortem changes?

Back 47

Pseudomelanosis: blue green discoloration of tissues by iron sulfide (rxn of H2S from bacteria and Hb from RBC).

Front 48

Abnormal or excessive accumulation of fat within the cell (fat changes) common in what tissues?

Back 48

Fatty changes mostly occurs in LIVER, kidney and muscle.

Front 49

T/F: Digested fat arrives at liver from intestine in form FFA

Back 49

False: if from GI -> short chain FA

but if comes from fat tissue -> FFA

Front 50

Pathological glycogen deposition is occurs in what tissues? (4)

Back 50

Pathological deposition occurs in LIVER, kidney, leukocytes, cardiac muscle and less often in spleen, smooth muscle, brain and lymph nodes.

Front 51

3 possible causes of abnormal glycogen deposition?

Back 51

Causes:
a) Hyperglycemia (in diabetes m.)
b) Drug induced metabolic dz (corticosteroids) --> Glucocorticoid hepatopathy
c) Glycogen storage diseases**

Front 52

**Glycogen storage diseases (lead to glycogen deposition) are caused by ?

Back 52

GSD's are autosomal recessive inherited disorders characterized by deficiencies of various enzymes involved in the synthesis or degradation of glycogen.

Front 53

How many forms of GSDs are there in animals? "Numbers" associated with them?

Back 53

Many types in humans, but only of them in animals (Type 1, 2, 3, 4, 7, and PSSM)

Front 54

Type I ; occurs in what breeds?

Back 54

Type I ; occurs in toy breeds;

Front 55

Type I due to ____.

Back 55

Type I due to deficiency of glucose-6- phosphatase. Glycogen storage is more in the liver; hypoglycemia develops.

Front 56

type II glycogenosis also known as ?.....what animals occur in ?

Back 56

Type II = Pompe`s disease

* Reported in Brahman and shorthorn cattle calves, Corriedale sheep, Lapland dogs, cats, turkeys and Japanese quail.

Front 57

Pompe`s disease (type II glycogenosis) caused by ?

Back 57

Pompe`s disease (type II) = Deficiency of lysosomal acid maltase (glucosidase).

Front 58

type III glycogenosis known as ?.....what animals occur in ?

Back 58

type III = Cori`s disease

Reported in German Shepherd dogs.

Front 59

type III (Cori`s disease) caused by deficiency in ?

Back 59

Cori's dz = Deficiency of amylo 1,6- glucosidase, involved in breakdown of glycogen to glucose.

Front 60

Cori's dz (type 3) causes glycogen to accumulate in ?

Back 60

Glycogen accumulates in liver, nerve cells, heart, skeletal and smooth muscles.

Front 61

T or F: Dogs affected with Cori's Dz (type III) have hyperglycemia

Back 61

False: Affected dog develops hepatomegaly and hypoglycemia (low sugar in blood, b/c all in glycogen)

Front 62

Type IV glycogenosis occurs in ?

Back 62

Type IV glycogenosis occurs in Norwegian forest cats, and American painted / quarter horses

Front 63

Type IV glycog. in NF cats caused by ?

Back 63

Type 4 = Deficiency of glycogen branching enzyme;affected kittens die soon after birth or develop progressive muscle degen., if survive after 7-8 month.

Front 64

Type IV deposits appear in what tissues?

Back 64

Type 4 = Glycogen deposit in many tissues but more in skeletal and cardiac muscles.

Front 65

Type IV glycog. in horses caused by ?

Back 65

Inherited as autosomal recessive trait in quarter horses and American paint horses; Due to congenital lack of glycogen brancher enzyme.

Front 66

Symptoms of type IV glycog. in horses

Back 66

Affected foals are aborted, stillbirth or weak at birth.

Front 67

Type IV glycog. in horses appear in what tissues?

Back 67

Accum. of long un-branched chain of glucose within cardiac, skeletal myocytes, Purkinje fibers and to less degree in hepatocytes; that leads to abnormal glycogen formation and deposition.

Front 68

Type VII glycogenosis found in what breeds?

Back 68

Type VII glycogenosis
* Reported in English springer spaniel dog and American cocker spaniel.
*

Front 69

Type VII glycogenosis caused by deficiency in ?

Back 69

Deficiency of M type phosphofructokinase (PFK)

Front 70

Dogs with Type VII glycogenosis show what signs? (4)
Clinical problems? (4)

Back 70

* Affected dogs show hemolytic anemia, intravascular hemolysis and hemoglobinuria.
* Clinical signs- exercise intolerance, muscle wasting and muscle cramping.

Front 71

Type VII glycogenosis affects what tissues/cells?

Back 71

Affected dogs have 1-6% of normal Muscle PFK activity;
and 10-20% of normal RBC PFK activity,
(normal RBC PFK is 80-90% of M-type, so a lot missing). Glycogen accum. in muscles

Front 72

PSSM stands for ?

Back 72

Polysaccharide storage myopathy in horses

Front 73

PSSM manifests itself in what tissues ?

Back 73

Excessive glycogen storage in horses with PSSM involves skeletal muscle, which is 1.5 to 4 times greater than normal horses.

Front 74

What horse breeds get PSSM?

Back 74

A familial basis for PSSM has been reported in Quarter horses, Arabian morgan, Pony of Americas and draft related breeds.

Front 75

PSSM caused by ?
Not caused by ?

Back 75

* Clinical, histological and biochemical similarities to PSSM is PFK deficiency.
* Although PSSM is classified as GSD or glycogenosis, NO signif. enzyme deficiency has been demonstrated.

Front 76

Lysosomal storage diseases are classified according to the major stored material; give 4 examples.

Back 76

LSD::
a) mucoplysaccharidosis
b) sphingolipidosis
c) glycogenosis d) mucolipidosis.

Front 77

Characterized by extracellular deposition of abnormal proteinaceous substance in tissues.

Back 77

Amyloidosis = extracellular deposition of abnormal proteinaceous substance in tissues.

Front 78

Amyloid is seen morphologically uniform in tissues, but chemically it consists of two major forms of protein.

Back 78

1. Amyloid light chain protein (AL)
2. Amyloid associated (AA) protein

Front 79

Amyloid light chain protein (AL) derived from ?

Back 79

Amyloid light chain protein (AL) derived from plasma cells, contains light chain immunoglobulin

Front 80

Amyloid associated (AA) protein, secreted by ?

Back 80

Amyloid associated (AA) protein, secreted by liver cells in response to various cytokines.

Front 81

5 types of Amyloidosis (Based on clinical settings, anatomic location and biochemical composition)

Back 81

1. Primary 2. Secondary
3. Heridofamilial 4. Amyloid of aging
5. Localized amyloidosis

Front 82

Lesions of amyloidosis common in what tissues? (3 + 7)

Back 82

Common sites- liver, spleen, kidney.
Other organs affected - pancreas, lymph gl., adrenals, heart, lung, brain and G.I..

Front 83

Lesions of amyloidosis in liver have what appearance grossly?

Back 83

Lesions:
Liver- grossly not-noticed in small lesions. In advanced cases liver becomes hard, pale, firm and enlarged. External and cut surfaces are waxy.

Front 84

Amyloidosis causes protein deposits where in liver?

Back 84

Deposition starts in space of Disse (or perisinusoidal space) and continue to sinusoids, pressing on hepatocyte, squeezing to death.

Front 85

What is the space of Disse ?

Back 85

Space of Disse (or perisinus. space) is in liver btw. hepatocytes and sinusoids; contains blood plasma. Microvilli of hepatocytes into space allowing proteins, etc. from sinusoids/plasma to be absorbed by hepatocytes. Fenestration of endothelium facilitates transport. Space may be obliterated in liver disease.

Front 86

Lesions of amyloidosis in kidney have what appearance grossly?

Back 86

Kidney: Large gray and firm, or reduced in size.

Front 87

Amyloidosis causes protein deposits where in kidney? in dogs? in cats?

Back 87

Deposit mainly in glomeruli in dogs and other species, but extend to peritubular tissue in cats.
"Glomeruli are affected in almost all cases of AA amyloidosis and in less than half of AL amyloidosis."

//source: www.kidneypathology.com/English_version/Amyloidosis_and_others.html

Front 88

Lesions of amyloidosis in spleen have what appearance grossly?

Back 88

Spleen: Depending on pattern of deposit- ‘sago spleen’ or ‘bacon spleen’. Organ in both cases is firm, pale, gray and waxy.

Front 89

Amyloidosis causes protein deposits where in spleen?

Back 89

Staining of amyloid: congo red stains it pink or red; toluidine blue stains blue.

Front 90

True or False: Most cases of amyloidosis found at autopsy, without clinical signs.

Back 90

True: Most cases of amyloidosis found at autopsy, without clinical signs.
But prognosis of amyloid patients is poor.

Front 91

Renal Amyloidosis causes what clinical problems/symptoms?

Back 91

Renal involvement causes proteinuria and loss of anti-coag.,which results into thrombosis (blood clots). Adv. cases lead to RF and uremia (abn. high level of nitrogen-type wastes in blood).

Front 92

Liver Amyloidosis causes ?

Back 92

Liver Amyloidosis causes metabolic derangement.

Front 93

Pancreatic Amyloidosis causes ?

Back 93

* Pancreatic involvement causes non insulin dependent diabetes mellitus ( common in cat)

Front 94

What are hyaline changes?

Back 94

Hyaline change is any alteration within cells or in extracellular spaces or structures that give homogeneous, glassy pink appearance in tissue sections stained with H&E.

Front 95

Example of intracellular hyaline change:

Back 95

Intracellular hyaline change:
-Intracellular hyaline change is seen in renal tubular epithelium in proteinuria.
--Proximal convoluted tubules in the kidney

Front 96

Example of extracellular hyaline change:

Back 96

Collagen fibrous tissue in old scar
*Hyalinization of glomeruli in chronic renal diseases
*Equine intimal bodies
*Hyaline membrane disease
*Hyalinization of arterioles in diabetes (humans)

Front 97

Is it normal to have deposition of calcium salts in tissues other than bone and teeth?

Back 97

nope

Front 98

What type of calcification is this?
* Deposition of Ca. salts in dead and degen. tissue!
* Not related to increased conc. of calcium in blood.(10mg/dl of blood-normal)

Back 98

Dystrophic calcification

This occurs as a reaction to tissue damage!

Front 99

Which type of calcification is assoc. w/elevated levels of calcium in blood?

Back 99

Metastatic calcification:

Deposition of calcium salts in tissues as result of incr. level of calcium in the blood.

Front 100

True or False: Serum calcium levels may be low, normal, OR high in dogs with CRF.

Back 100

True; so treatment should adjusted accordingly

Front 101

Serum calcium levels are normally tightly regulated by ___ and ____.

Back 101

combined actions of calcitriol and
PTH

For example, calcitrol promotes intest. abs. of calcium

Front 102

Causes of Metastatic calcification? (name five)

Back 102

Causes:
1. Hyper-parathyroid activity 2. In RF, where phosphates retained in blood. 3. Hypercalcemia of malignancy
4. Granulomatous dz (TB and fungal diseases in dogs)
5. Feeding on plants rich in vitamin D or excessive medication and toxicity of Vitamin D.

Front 103

Lesions in pathological calcification mostly observed in what animals?

Back 103

Mostly observed in cattle (see pic), sheep and goat.

Front 104

Lesions in pathological calcification mostly observed in what tissues?

Back 104

Mostly deposited in aorta and muscular arteries

Front 105

What is gross appearance of Pathological calcification?

Back 105

Gross- White or gray irregularly round particles, which gives gritty sound when cut with knife.

Front 106

What is micro appearance of Pathological calcification?

Back 106

Micro- seen as small irregular granule.

Front 107

True or False: Dystrophic calcification is dangerous to body and metastatic is beneficial to the body.

Back 107

False:
Dystrophic calcification is beneficial to body and metastatic is dangerous to the body.

Front 108

Which type of calc. affects any tissue?

Back 108

Dystrophic
* Affects any tissue
* considered beneficial to the body

Front 109

Which type of calc. affects affects mainly the blood vessels and is harmful to body?

Back 109

Metastatic
*affects mainly the blood vessels
* Injury to tissue not a prerequisite
* Affects Mainly the blood vessels
* Harmful to the body

Front 110

Is metastatic calcification common in dogs and cats?

Back 110

Hypercalcemia in dogs and cats usually does NOT cause metastatic calcification in large blood vessels; but may see Ca+ deposits in epith. cells of kidney

Front 111

What is calcinosis?

Back 111

Calcinosis- calcification in or under the skin.

Front 112

Calcinosis- seen in two forms:

Back 112

1. Calcinosis cutis-
2. Calcinosis circumscripta

Front 113

Which calcinosis reported in large breeds; rare in cats. Deposit of calcium in CT of dermis, esp. at pres. points, and trauma?

Back 113

Calcinosis circumscripta

seen at points of trauma, hence, considered dystrophic form (check this).

Front 114

Which calcinosis occurs in dogs with hyperadenocorticism. char. by mineralization of dermal collagen, epid. and follicular basement membranes?

Back 114

Calcinosis cutis

occurs in dogs with hyperadenocorticism.

Front 115

Which calcinosis type can be either dystrophic or metastatic?

Back 115

Calcinosis cutis

but most common cause of metastatic calcinosis cutis in dogs is overproduction of adrenal hormones (corticosteroids or “steroids”). .

Front 116

What is gout?

Back 116

Gout = Deposit of uric acid and urates in tissues.

Front 117

Gout common in ?

Back 117

Common in birds, reptiles and occasionally in dogs and cats.

Front 118

Two forms of gout:

(where is each found?)
1+3

Back 118

1. Articular form- deposit in joints
2. Visceral form- serous membranes, liver, kidney

Front 119

Which might see around gout deposit (microscopically)?

Back 119

Microscopically-granulomatous reaction around the deposit.

Front 120

Exogenous pathological pigmentation formed by what compounds? (name 2 or 3)

Back 120

Exogenous- pigment formed outside the body like carbon, dust, metal etc.
- characterized by fibrosis of tissue around granulomas (because body cannot remove)

Front 121

Endogenous pathological pigmentation formed by what compounds? (name 2 or 3)

Back 121

Endogenous- pigment formed inside the body.
Like melanin (melanosis), blood pigments and lipogenic pigments.

Front 122

Five possible conditions which can lead to exogenous (dust, etc.) pigmentation?

Back 122

1. Pneumoconiosis (dust in lung)
2. Anthracosis- carbon particles.
3. Asbestosis- dust from asbestos factories.
4. Silicosis- silicon from rock factories
5. Siderosis- iron dust from mines

P-A-A-S-S

Front 123

Where might dog/cat get pneumoconiosis or anthracosis?

Which tissues?

Back 123

Dogs and animals exposed to <carbon particles> from coal mines and smoky cities. Mostly lungs, but anthracosis can be in lymph nodes also.

Front 124

Which exogenous pigmentation does not stain and does not dissolve in any solvent?

Back 124

anthracosis

I guess can try to treat pneumoconiosis with transtracheal wash?

Front 125

can get from mesotheliomas?

Back 125

mesotheliomas is cancer of mesothelium from asbestos exposure

(asbestosis is just pigmentation from asbestos exposure)

Front 126

Melanin and melanosis result from endogenous pigmentation and usually seen in ?

Back 126

Melanosis is pigmentation of melanocytes (bottom layer of epidermis) and is usually seen on lung, pleura, heart and meninges.

Front 127

melanosis is harmful?

Back 127

No, melanosis harmless; but tumors of melanocytes are life threatening.

Front 128

tumors of melanocytes (melanoma) seen what spp.?

Back 128

dogs and horses

e.g. melanoma on skin or liver

Front 129

CO poisoning causes problems how?

Back 129

CO is inhaled, combines with Hb forming ‘Carboxyhemoglobin’ which deprives tissues of oxygen.
(Blood on CO poisoning is bright cherry red.)

Front 130

Poisoning by nitrites, chlorate, to less extent with acetoaminophen, local anasthetics and copper poisoning and other conditions cause ?

Back 130

intravascular hemolysis and form methemoglobin, which is incapable of oxygen transport.

>ferrous iron (Fe-2) in hemoglobin is oxidized to ferric iron (Fe3) forming methemoglobin

Front 131

What is a porphyrin ?

Back 131

Organic compounds, many naturally occurring. but best known is heme group (if u take away iron), what you have left is a porphyrin
(porphyrin + iron = heme)

Front 132

Hemochromatosis is ?
Caused by?

Back 132

Build up of iron pigment (bluish) in the cytoplasm of hepatocytes and epithelial cells of kidney.
- diet def. in copper/cobalt and rich in iron is pointed as cause.

Front 133

Hemochromatosis reported in what animals? (5)

Back 133

Reported in cattle, buffalo, horse, goats and a few species of birds.

Front 134

Formalin pigment (brownish) formed body by?

Back 134

acid (low ph) and hemoglobin
e.g. usually seen in tissues fixed in acidic formalin.
(does not stain with iron stain whatever that means)

Front 135

Parasite hematin?

Back 135

believed to be excreted by parasites

Front 136

Jaundice is the result of ?

Back 136

either excess production (hemolytic condition) or reduced clearance of bilirubin such that it accumulates in the plasma.

Front 137

3 Types of jaundice

Back 137

1. Prehepatic
2. Hepatic
3. Post hepatic or obstructive jaundice

Front 138

Which type of jaundice caused by damage to hepatocytes and known as "toxic jaundice"?

Back 138

Hepatic jaundice - damaged liver cells are incapable of conjugation process, and swollen liver cells block the bile flow.

Front 139

Which type of jaundice char. by circulation of conjugated and unconjugated bilirubin?

Back 139

Hepatic jaundice - increase in both conjugated and unconjugated bilirubin circulating in blood.

Front 140

What does it mean that bilirubin is "conjugated"?

Back 140

conjugated in liver (glucuronidation) so that it can be excreted

Front 141

Laboratory tests for elevated bilirubin: (2)

Back 141

1) Icterus index-spectrophotometry (quantitative test)
2) van den berg reaction- a qualitative test to differentiate type of jaundice. Specially in animals differentiation requires full investigation of blood and its chemical values.

Front 142

In dogs and cats- conjugated bilrubinemia can occur in hemolytic jaundice. How is this possible?
(check this)

Back 142

Maybe if hepatocytes able to conjugate even high levels of heme/bilirubin being produced by hemolysis, but hepatic duct cannot excrete efficiently as other animals.

Front 143

Is bilirubin (in circulation) harmful?

Back 143

Not in small quantities, but excessive amount causes itching and related conditions (esp. in young animals)

Front 144

What is condition “porphyria”?

Back 144

* Elevated levels of a photosensitizing pigment
* condition develops as a result of action of sunlight on fluorescent pigment present in body.

Front 145

condition “porphyria” reported in what animals?

Back 145

All domestic animals except dogs
(congenital form in cats, pigs and cattle)

Front 146

What symptoms of “porphyria”?

Back 146

* Lesions are dermatitis, starting as erythema, edema, developing to necrosis and sloughing.
* Strong effects are on part of skin unprotected by pigment, hair or fleece.

Front 147

Types of photosensitization?

Back 147

1. Type I (primary photosensitization)
2. Congenital erythropoietic porphyria
3. Type II- Hepatogenous (secondary)

Front 148

Plasma flowing through kidneys stained dark red to reddish black and urine red, explain:

Back 148

Excessive intravascular hemolysis, hemoglobin stains plasma pink

Similar condition is observed in myogolobinuria

Front 149

methemoglobin?


myoglobin?

Back 149

* formed when ferrous ion is oxidized to ferric ion (poisoning by nitrites, acetaminophen, anesth., etc.)

* product of muscle break down

Front 150

Caused by ingestion of some plant or drugs which give rise to photodynamic pigment in the body.

Back 150

Type I (primary photosensitization):

Front 151

Is Liver damage is necessary in type I (primary photosensitization)

Back 151

No, liver damage is not necessary.

Front 152

It is inherited metabolic defect in the synthesis of normal heme pigment.

Back 152

Congenital erythropoietic porphyria (type of photosensitization):
inherited metabolic defect in the synthesis of normal heme pigment.

Front 153

Congenital erythropoietic porphyria seen in certain breeds of ?

Back 153

Congenital erythropoietic porphyria seen in certain breeds of cattle, swine and short hair and siamese cats.

Front 154

Cattle with congenital erythropoietic porphyria suffer from ?

Back 154

Cattle suffer from dermatitis and anemia

Front 155

Cats with congenital erythropoietic porphyria suffer from ?

Back 155

cats have anemia and red coloration of bone/teeth (osteohemochromatosis <- misnomer)

Front 156

Type II- Hepatogenous ( secondary photosensitization) seen in what animals?

Back 156

Type II- Hepatogenous PS is seen in ruminants

Front 157

Type II- Hepatogenous ( secondary photosensitization) caused by?

Back 157

In ruminants develops as metabolic byproduct (phylloerythrin) from plant pigment chlorophyll, is removed by liver. Damaged liver fails to remove pigment, hence circulates in blood.
Note: this is simplified explanation

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Known as wear and tear pigment; or pigm. of brown atrophy, imparts color to affected tissues; mostly KIDNEY, brain, heart, skeletal and smooth muscles.
Believed to be formed from fatty acids derived from membranes of autophagocytosed organelles.

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Lipofuscin (a lipogenic pigment)

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Because of its gross app. has been termed, "yellow fat dz” or “brown dog gut”.
Pigment is granular, yellow to brown in cell cytoplasm of heptocytes and in macrophages, fat cells, cardiac musc., smooth muscles of spleen and intestine.

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Ceroid pigment (a lipogenic pigment)

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Seen in wasting disease, senility or emaciation.

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Lipofuscin (a lipogenic pigment)

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* Stains positive for fat, but resistant to fat solvent
* Reported in dog, horse, cattle, pig and rat.

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Ceroid pigment (a lipogenic pigment)

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Pigment accumulation attributed to the deficiency of choline or vitamin E

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Ceroid pigment (a lipogenic pigment)

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Two types of extravascular fluid accumulation ?

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Transudate (edema)
Exudate (inflammatory)

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Two types of vascular clots ? (masses/abnormal constituents in the blood/blood vessels)

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Thrombus
Embolus

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Increase in volume of blood in tissues. It may be active/passive, local/general, acute/chronic.

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Hyperemia

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Abnormal accumulation of arterial Blood in an organ/tissue; can be physiological and pathological.
can be local and acute; affected organ/tissues are swollen and bright red.

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Active hyperemia:

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Accumulation of blood in veins and capillaries; may be local or generalized. may be acute or chronic; affected part is dark red/blue and swollen

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Passive hyperemia (passive congestion, congestion)

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Which type of hyeremia always pathological?

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Passive hyperemia (passive congestion, congestion)

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Local passive hyperemia cause ? (1+3)

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Cause: Obstruction of venous drainage due to:
a) organ misalignment (telescopy, volvulus (twisted on itself), torsion, herniation).
b) venous thrombosis or embolism.
c) compression.

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Effects of local passive hyperemia: (2)

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1. Edema because of increased venous pressure.
2. Anoxia- degeneration and necrosis.
Consequences depend on the organ involved.

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Intussusception is ?

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part of the intestine has invaginated into another section of intestine

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Causes of general passive hyperemia

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Causes:
1. Cardiac failure- valvular, myocardial disorders.
2. Impeded venous return- caval thrombosis, hydropericardium.
3. Increased pulmonary resistance- hydrothorax etc.

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Effects of general passive hyperemia (3)

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Effects of general passive congestion:
* reduced output (forward effect)
* increased venous pressure (backward effect)
* long term effects are in lungs and liver.

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area of tissue death (necrosis) due to a local lack of oxygen caused by obstruction of the tissue's blood supply

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Infarction

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Various terms used in connection with _____:
* _ by rhexis
* _ by diapedesis
* petechiae (1-2mm)
* ecchymosis (>1cm)
* purpura (bruise)
* hematoma

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hemorrhage

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Edema, abnormal accumulation of fluid in tissue spaces or body cavities, may be classified into what categories? (2&2)

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Edema, accum. of extravascular fluid, may be:
1. Inflammatory OR non-inflammatory
2. Local OR generalized

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Which type of edema caused by loss of (renal disease) or decr. formation of protein (nutritional edema)?

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Non-inflammatory edema
*renal diseases (renal edema)
*certain parasitic infections

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How can parasitic infections cause non-inflammatory edema?

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* loss of protein (nutrional edema)
* obstr. to lymphatic drainage

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Retention of Na&H2O - seen in congestive HF, nephritis and nephrosis - causes local OR generalized edema?

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Retention of sodium and water causes 'generalized edema'

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What type of edema is confined to a particular organ, e.g. hydrocephalus, pulmonary edema?

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Local edema

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Generalized edemas DO have predilection sites in different spp., what organ in cat?

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cat - thoracic cavity (hydrothorax)

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Generalized edemas DO have predilection sites in different spp., what organ in dog?

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dog- peritoneal cavity (ascitis)

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Generalized edemas DO have predilection sites in different spp., what organ in sheep/cattle?

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sheep/cattle- sub-mandibular/peritoneum

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Generalized edemas DO have predilection sites in different spp., what organ in horse?

Back 184

horse- limbs

Front 185

Anasarca is ?

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generalized edema under the skin

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edema in peritoneal cavity

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Ascites

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edema fluid in scrotal layers

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Hydrocele

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What might one see microscopically w/appearance of edema?

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extracellular space is enlarged. It stains light pink homogenous.

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extravascular fluid with:
- low protein content
- low specific gravity (< 1.013)
- lack of inflammatory cells

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transudate

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extravascular fluid with:
- high protein content
- high specific gravity (>1.018);
- presence of inflammatory cells and clotting factors

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exudate
- high protein content
- high specific gravity

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a mass formed from constituents of the blood in blood vessels or heart during life

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Thrombus

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What will this cause? Name?
1) alteration in the vascular endothelium
2) alteration in blood flow
3) alterations in the constituents of blood.

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Virchow`s triad --> thrombosis

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Alterations in blood flow types/causes: (2)

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Stasis
Turbulence - sites of branching of arteries, in arteriosclerosis, venous valves and congenital heart diseases.

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What type (color) thrombi formed in rapidly moving blood- usually in heart and arteries?

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White or pale thrombi: fast blood

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What type (color) thrombi formed in slow moving blood- usually in large veins?

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red thrombi: in slow moving blood- usually in large veins.

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Mural thrombi:

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attached to a side of the vessel, not occluding the lumen completely.

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Occlusive thrombi:

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completely blocking the vessel.

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In cattle thrombi in the vena-cava results from ?

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the liver abscesses (skip until know other stuff)

Front 199

resolution of thrombi via ___

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fibrinolysin

Front 200

Laminations form in post mortem clots OR thrombi?

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Lamination of red and white thrombi; not PM

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Prevents blood from clotting normally. May cause excessive (thrombosis) or bleeding (hemorrhage) throughout body and lead to shock, organ failure, and death.

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Disseminated intra-vascular clotting

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Disseminated intra-vascular clotting occurs in ?

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DIC occurs in microvasculature.

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___ is solid material carried by blood from origin to distant site within circulation.

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embolism

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Types or examples of emboli

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Pieces of thrombus, fat, tumor cells, gas, bacteria and parasites.

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Effects of emboli:

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It mostly leads to infarction.

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Infarcation more common in arteries or veins?

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arteries (95% of cases)

both can in veins or both

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Infarctions cause what type of necrosis?

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coagulative necrosis

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clinical entity of body caused by inadequate perfusion of organs & tissue

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Shock

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secondary disorder (conseq.) resulting from large scale platelet activation a/o thromboplastin release for any reason (tissue damage)

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Disseminated Intravascular Coagulation:
if fibrolytic protein used up in tissue, may get coagulation elsewhere

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DIC usually seen in what tissues?

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microvasculature

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Another name for DIC?

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consumption coagulopathy
- if fibrolytic protein used up in tissue, may get coagulation elsewhere

Front 212

How to differentiate PM clot from thrombus?

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PM clot not attached to vessel wall (unlike thrombi)

Front 213

Clinical effects of DIC depend on balance btw. what 2 proteases?

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thrombin (clot forming) and plasmin (fibrolytic; favors bleeding)

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Shock often due to 1 of 3 events; list them:

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1. Cardiogenic: Reduced cardiac filling or emptying
2. Hypovolaemic (reduced BP; blood loss)
3. Vasculogenic

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3 causes of vasculogenic shock?

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1. neurogenic (dilation, deep anesth.)
2. endotoxic (infection)
3. anaphylactic (histamine)

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A piece of liver (from dead animal) floats when placed in formalin. What does this indicate?

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fatty changes

Front 217

What GSD is char. by deficiency in debranching enzyme?

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Type 3 (Cori's Dz)!!!
>Don't confuse with branching enz. (type 4); DEbranching enzyme = amylo 1,6 glycosidase

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what type of amyloidosis associated with long standing condition (e.g. chronic inflammatory dz)?

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secondary amyloidosis

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type of amyloidosis occurring with plasma cell dyscrasias (dysfunction) e.g. multiple myeloma and B cell prolif. disorders?

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primary amyloidosis