Block 2 Flashcards

Question 1

Q

WHAT IS CELL INJURY?

Answer

A

Disruption of homeostasis stress or stimulus was too intense to adapt

Question 2

Q

WHAT IS CELL INJURY?

is it reversible?

Answer

A

Reversible or Irreversible

Question 3

Q

WHAT IS CELL INJURY?
name 6 causes

Answer

A

Many Causes:
Bacteria, fungi, viruses (infectious)
Hypoxia or anoxia
Immune-mediated diseases
Genetics
Aging
Toxicity

Question 4

Q

WHAT IS CELL INJURY?

If normal cell is stressed, what happens?

Question 5

Q

WHAT IS CELL INJURY?
if a normal cell is affected by an injurious stimulous what happens?

Answer

A

cell injury

Question 6

Q

WHAT IS CELL INJURY?
is a stressed cell is unable to adapt, what happens?

Answer

A

cell injury

Question 7

Q

WHAT IS CELL INJURY?
if the cell injury is mild and transient what happens?

Answer

A

it is reversible

Question 8

Q

WHAT IS CELL INJURY?
if the cell injury is severe and progressive, what happens?

Answer

A

Not reversible

Question 9

Q

WHAT IS CELL INJURY?
if the cell injury is irreversible what are the possible outcomes?

Answer

A

cell death
necrosis
apoptosis

Question 10

Q

WHAT IS CELL INJURY?
label 1-12

Question 11

Q

EXAMPLES OF CELL ADAPTATION

What is atrophy

Answer

A

cells decrease in size or number

Question 12

Q

EXAMPLES OF CELL ADAPTATION
what is hypertrophy

Answer

A

Hypertrophy: increase in cell size
- cells can increase size of organelles and
cytoplasm
*non-dividing

Question 13

Q

EXAMPLES OF CELL ADAPTATION
what is hyperplasia

Answer

A

increase in cell number
*dividing

Question 14

Q

EXAMPLES OF CELL ADAPTATION
what is metaplasia
example?

Answer

A

change in phenotype
- Ex. Cuboidal cells change to squamous cells

Question 15

Q

EXAMPLES OF CELL ADAPTATION
what is dysplasia
what is it commonly associated with?

Answer

A

disorganized and abnormal cell
growth
- Commonly associated with neoplasia

Question 16

Q

ATROPHY
What is it?
are the cells dead?
what kind of change is it, when does this occur?

Answer

A

Cell decreases in size
Viable cells - NOT DEAD … just adapting
Physiological change : after birth

from slide:
* a dimunation in the size of the cell, tissue, organs or part that was properly developed.

Question 17

Q

What can cause atrophy?
name 6 causes

Answer

A

What can cause atrophy?
- Denervation (loss of nerve supply)
- Decreased workload
- Ischemia
- Hypoxia
- Aging
- Poor nutrition Ǖ emaciation

Question 18

Q

ATROPHY
what is Serous Atrophy of Fat?
what causes it?
what happens?
where does it happen in the body?
what does it look like?

Answer

A

Ex. Serous Atrophy of Fat
- Due to starvation/malnutrition
- Animal mobilizes fat to compensate no stores left
- Heart, Bone marrow, perirenal
- fat turns to fluid/shiny

Question 19

Q

ATROPHY
hypoplasia v atrophy
explain

Answer

A

never achieved full size
v
decreased size due to decrease in cell number

Question 20

Q

Hypoplasia

Answer

A

From slide
*incomplete development or underdevelopment of an organ or tissue, it is less severe in degree that aplasia. It is a congenital condition.

Question 21

Q

Aplasia

Answer

A

from slide
*lack of development of an organ or tissue

Question 22

Q

Hypotrophy =abiotrophy

Answer

A

from slide
*progressive loss of viatilty of certain tissues (you have something written here, but I cant read it..see slide 5) or organs, leading to disorders or loss of function; applied especially to degenerative hereditary diseases of late onset.

Question 23

Q

HYPERTROPHY

Answer

A

Increase in cell size leading to increase in size of the tissue or organ

Question 24

Q

HYPERTROPHY
What cells commonly undergo hypertrophy?
examples?

Answer

A

CELLS WITH LITTLE REPLICATION
- Neurons, cardiac and skeletal muscle, bone, cartilage and smooth muscle

Question 25

Q

HYPERTROPHY
Why wouldn’t we see this in cells that repliate often?

Answer

A

They can just increase in numbers (hyperplasia) if they are dividing all the
time!

Question 26

Q

HYPERTROPHY
Physiologic Hypertrophy

Answer

A

exercise, pregnancy
*bigger cells!

Question 27

Q

HYPERTROPHY
Pathologic Hypertrophy

Answer

A

Pathologic Hypertrophy: cardiac hypertrophy associated with CHF
- Disturbance in aortic outflow (any other pathology)
- Left ventricle compensates through hypertrophy to increase muscle to help
get blood out

Question 28

Q

Hypertrophy: Mechanisms

*this is a graph see answer.

Question 29

Q

HYPERTROPHY
Concentric
what is it?
what happens to the ventricle/ventricle chamber?
what is Hydrotropic cardiomyopathy (HCM) and what animal?

Answer

A

**Concentric: **Thickening of wall
and smaller chamber
- Hypertrophic growth of
ventricle
- Decrease amount of volume of
ventricle chamber
- Dysfunction of diastolic filling

Hypertrophic
cardiomyopathy (HCM) seen
frequently in cats

Question 30

Q

HYPERTROPHY
Eccentric
what is it?
what happens to the ventricles/systolic function?
what is dilated cardiomyopathy DCM and what animal?

Answer

A

**Eccentric: **Thinning of
wall and larger chamber
- Dilation of ventricle
without thickening of the
ventricles
- Decreased systolic
function

Dilated
Cardiomyopathy
(DCM) in Dogs

Question 31

Q

Hypertrophy
explain example of how adaptation to stress can progress to functionally significant cell injury if the stress is not relieved?

Answer

A

Cardiac hypertrophy (different causes/mechanisms)
* limit beyond which enlargement of muscle mass is no longer
able to cope with the increased burden →several regressive
changes occur in the myocardial fibers ( e.g. lysis and loss of
myofibrillar contractile elements)

extreme cases →myocyte death

Question 32

Q

Hypertrophy
Physiological causes of hypertrophy
(2)

Answer

A

-increased workload, e.g. the bodybuilder’s skeletal muscle.
-ormone stimulation, e.g. the pregnant uterus (smooth muscle hypertrophy)

Question 33

Q

Hypertrophy
pathological causes of hypertrophy
(2)

Answer

A

-increased resistance e.g.cardiac muscle hypertrophy as a result of working against an increaded peripheral resistance in hypertention (high blood pressure)
-physical obstruction, e.g. bladder smooth muscle hypertrophy in outflow obstruction caused by an enlarged prostate gland.

Question 34

Q

These are images of 2 turkey poult hearts taken at post mortem. left is normal. what is happening on the right?

Question 35

Q

This image shows the brain from 2 kittens. which on is abnormal, and what is the vell process?

Question 36

Q

HYPERPLASIA

what is it what happens?

Answer

A

An increase in number of cells in an organ or tissue

Seen in cells that divide frequently

Question 37

Q

HYPERPLASIA
Physiologic
explain
example

Answer

A

Physiologic: mammary glands, bone marrow (only normal in
young animals)
Ex. mammary glands get bigger during pregnancy for
breastfeeding, after hepatectomy (liver removal), hepatocytes can
replicate to form new liver tissue

Question 38

Q

HYPERPLASIA
Pathologic
explain
example

Answer

A

Pathologic: excessive hormones or growth factors
Ex. gingival hyperplasia, epidermal thickening (repeated
irritation)

*thyroid gland

Question 39

Q

Hyperplasia

labile cells
what are they?
where are they?
do they become hyperplastic?

Answer

A

Those that routinely proliferate in normal circumstances, such as those of the epidermis, intestinal epitheliem and bone marrow cells.
readily become Hyperplastic +++

Question 40

Q

Hyperplasia
Permanent cells
what are they?
do they become hyperplasic?

Answer

A

such as neurons and cardiac and skeletal muscle, myocytes, have very little capacity to regenerate or become hyperplastic in most situations +

Question 41

Q

Hyperplasia
Stable cells
what are they?
examples?
do they become hyperplastic?

Answer

A

such as bone, cartilage and smooth musle, are intermediate in their ability to become hyperplastic ++

Question 42

Q

what is Myostatin?
what relevance in whippets and your dogs bella and bleue? lol

Answer

A

Myostatin : protein produced my myocytes that inhibits myocyte growth

differentiation
and growth

Whippets can have a mutation of the myostatin gene which involves a
two-base-pair deletion, and results in a truncated, inactive, myostatin protein

Question 43

Q

METAPLASIA
what is it?
what causes it?
what result?
what might it increase?
where should you look for it?

Answer

A

Change in phenotype of an already differentiated
cell (*what a cell looks like)
- due to chronic irritation (stress)
- may decrease function
- increases chance of transforming into
malignant/neoplastic cells
- look for this on histology!!!

Question 44

Q

METAPLASIA
is it reversible?
if so, when?
examples

Answer

A

Reversible if the cause of irritation is removed
- Ex. Irritation to the lungs from smoking
- Ex. **Vitamin A **deficiency in chickens

Question 45

Q

What is this?
tissue?
process?
morphologial description?
Aetiology?

Answer

A

Tissue : Chicken Oesophagus
Process: metaplasia
Morphological Description: severe
multifocal mucous gland squamous
metaplasia

Aetiology : Vit A deficiency

Question 46

Q

DYSPLASIA

what is it?
what happens?
what is it associated with?

Answer

A

Abnormal development (cell had not
differentiated yet)

Change in cell **shape, size and
organization **- becomes disorganized

Commonly affecting epithelial cells and
associated with neoplastic process

Question 47

Q

what type of cell adaption is present?

dog, liver

Question 48

Q

OTHER IMPORTANT TERMS TO KNOW
Hypoplasia
what is it?
why?
examples?

Answer

A

**Hypoplasia: **incomplete development or underdevelopment of a
tissue/organ
- Cells never fully developed/always have been small
Ex. Cerebellar Hypoplasia Ǖ Feline Panleukopenia Virus

Question 49

Q

OTHER IMPORTANT TERMS TO KNOW

Aplasia
what is it?

Answer

A

Aplasia: lack of the development of an organ or tissue literally just didn’t show up to the party

Question 50

Q

OTHER IMPORTANT TERMS TO KNOW

Hypotrophy

what is it?

Answer

A

Hypotrophy: progressive loss of function of tissue

Question 51

Q

what type of cell adaption is present?

Question 52

Q

This image shows the thyroid and patathyroid of a chicken. what is the cell adaption occurring?

Question 53

Q

This is an image of a kidney from a dog. What is the morphological diagnosis?

Question 54

Q

This is an image of a goats hear. What is the cell adaption occurring?

Question 55

Q

This is an image of a bovine abomasum. what is the cell adaption occuring?

Question 56

Q

This is an image of a cats stomach. Wha tis the process?

Question 57

Q

WHAT IS CELL INJURY?
(yes this is a repeat, but with more info)
what is it?
is it reversible?
what are the many causes (9)
what are the 3 most common causes?

Answer

A

Disruption of homeostasis stress or stimulus was too intense to adapt
Reversible or Irreversible

Many Causes:
Bacteria, fungi, viruses (infectious)
Hypoxia or anoxia
Immune-mediated diseases
Genetics
Aging
Toxicity

Most common:
oxygen deficiency
infectious agents common/important
immunological dysfunction

Question 58

Q

Oxygen Deficiency

what is hypoxia?

Answer

A

Hypoxia: partial reduction in
O2 (oxygen) delivery to
a tissue

Question 59

Q

Oxygen Deficiency
what is Anoxia

Answer

A

no
O2 (oxygen)delivery to

a tissue

Question 60

Q

Oxygen Deficiency

what 4 things cause hypoxia/anoxia?

Answer

A

1 inadequate oxygenation of blood
2 reduced transport of O2 in blood
3 reduction in blood supply=ischema
4 blockage of the cell respiratory enzymes

Question 61

Q

Oxygen Deficiency

what 4 things cause hypoxia/anoxia?
1- inadequate oxygenation of blood
what happens?

Answer

A

heart failure
respiratory failure

Question 62

Q

Oxygen Deficiency

what 4 things cause hypoxia/anoxia?
2- reduced transport of O2 in blood
what happens?

Answer

A

Anemia
carbon monoxide toxicosis

Question 63

Q

Oxygen Deficiency

what 4 things cause hypoxia/anoxia?
3 reduction in blood supply=ischema
what happens?

Answer

A

Thrombosis

Question 64

Q

Oxygen Deficiency

what 4 things cause hypoxia/anoxia?
4 blockage of the cell respiratory enzymes
what happens?

Answer

A

cyanide toxicosis

Answer 53

A

anoxic damage to muscles of the hind limbs

Answer 54

A

Viruses
bacteria
fungal (mycosis)
protozoan
metazoan parasites

Answer 55

A

‒ Obligate intracellular “parasites”use host cell
enzyme systems
‒ Cell survival depends on method viruses leave the
cell

Answer 56

A

‒ Toxins
‒ Overwhelming and uncontrolled replication

Answer 57

A

Progressive, chronic inflammatory disease

Answer 58

A

‒ Replicate in specific host cells –>cell destruction

Answer 59

A

‒ Inflammation, tissue distortion, utilization of host
nutrients

Answer 60

A

Immune system fails to respond
or
Immune system over-responds or aberrant reaction

Answer 61

A

Congenital defects: Severe Combined Immunodeficiency
(SCIDS, Arabian foals) antigen receptors(lymphocytes)
Acquired defects
May be transient (but not always)

: Results from damage to lymphoid tissue
: Viral infections, Chemicals, Drugs

Answer 62

A

Immune system over-responds or aberrant reaction
- Autoimmune diseases
- Hypersensitivity reactions

: anaphylaxis, Flea allergy dermatitis, Feline asthma

Answer 63

A

Depletion of ATP
Mitochondrial change
Loss of calcium homeostasis
Oxidative stress
Membrane permeability
DNA and protein damage
*** Lots of these mechanisms overlap do not get too caught up in the nitty gritty
details!

Answer 64

A

Cells need ATP as their form of energy to carry out their functions
What happens if ATP is lost?
- 5-10% loss ĺ VERY BAD
Failure of the Na+/K+ Pump
Cell membrane damage ĺ loss of gradients
(influx of Ca2+, H2O and Na+, Efflux of K+)
Swelling of ER
Altered Cell metabolism
Consistently in a state of anaerobic glycolysis
Build-up of lactic acid
Depletion of glycogen stores
Detachment of Ribosomes
Decreased protein synthesis

Answer 65

A

Damage to the mitochondria will lead to the formation of
the mitochondrial permeability transition pore
(MPTP)
What happens when the pore opens?
Membrane potential is lost
- ATP depletion from failure of oxidative phosphorylation
Increased Reactive Oxygen Species (ROS)
Released from the mitochondria into the cytoplasm
Activation of Apoptosis
Apoptotic activating proteins leak out and cause
programmed cell death

Answer 66

A

Calcium is an ion found in higher concentrations
extracellularly
If too much calcium builds up intracellularly, different
signaling cascades may occur

Answer 67

A

How can calcium accumulate?
Release from the ER or the mitochondria
Damage from outside of the cell

Answer 68

A

What happens when calcium accumulates inside the
cytoplasm?
Activation of enzymes ĺ phospholipases, proteases,
endonucleases and ATPases* (EUHDNVGRZQ$73«OLN(breaks down ATP…like girl c’mon seriously?)
Opening of the MPTP leading to even more decreased ATP!

Answer 69

A

Can be physiologic or pathologic

Answer 70

A

Physiologic Ǖ A byproduct produced by the mitochondria during cellular
respiration
Pathological Ǖ released by activated WBCs during inflammatory responses

Answer 71

A

ROS are normally removed by scavenging mechanisms
- Ex. Antioxidants like Vitamins A and E help remove ROS

Answer 72

A

**ROS are normally removed by scavenging mechanisms
- Ex. Antioxidants like Vitamins A and E help remove ROS

Answer 73

A

Increased production causes oxidative stress and decreased scavenging

Answer 74

A

radiation, toxins, inflammation, aging, degenerative diseases, etc.

Answer 75

A

Membrane damage, oxidative modification of proteins, DNA damage

Answer 76

A

Inflammation (lecs to come)
Transition metals (ie. Iron, Copper)
Nitric oxide (NO)
Absorption of radiant energy

Answer 77

A

Inflammation (lecs to come)
Rapid bursts of ROS produced by activated
WBCs (esp. neutrophils)
generatessuperoxide anion (O2
*-
)

Answer 78

A

Transition metals (ie. Iron, Copper)
Frequently donate or accept free electrons
Catalyze free radical formation

Answer 79

A

Nitric oxide (NO)
Important chemical mediator
Generated by endothelial cells,
macrophages, neurons, and others
Can act as a free radical
Can be converted into peroxynitrite anion
ONOO-

, or NO2, or NO3

Answer 80

A

H2O + **ionizing radiation ***OH + H

Answer 81

A

Spontaneous decay: O2
* + H2O O2 + H2O2
Enzymes
Storage and transport proteins
Antioxidants - Vitamin E, Vitamin A, glutathione

Answer 82

A

O2 + H2O O2 + H2O2

Answer 83

A

Enzymes: catalase,superoxide dismutase, glutathione
peroxidase
‒ Break down H2O2 and O2

‒ Located near sites where oxidants are formed

Answer 84

A

Storage and transport proteins - transferrin, ferritin,
ceruloplasmin
‒ Bind reactive metals: Fe, Cu

Answer 85

A

Antioxidants - Vitamin E, Vitamin A, glutathione
‒ Block initiation
‒ Inactivate (scavenge)

Answer 86

A

lipid peroxidation in membranes
oxidative modification of proteins
lesions to DNA

Answer 87

A

extensive membrane damage

Answer 88

A

damage active sites, change conformation, enhance degradation
-generated by monamine oxidase (MOA) in outer nmitochondrial membrane

Answer 89

A

cell aging, malignant transformation
-MOA: single or double stranded breaks, cross-linking of DNA strands, formation of adducts

Answer 90

A

All membranes ĺ plasma membrane, mitochondrial membrane and lysosomal

Answer 91

A

ROS
Decreased synthesis of phospholipids
Decreased production of ATP
Increased breakdown of phospholipids ĺ Phospholipases!
cytoskeletal abnormalities

Answer 92

A

decreased phospholipid synthesis: secondary to defetive mitochondrial function and/or hpoxia
decreased production of ATP–> decreaded phospholirid synthesis

Answer 93

A

increased phospholipid breakdown:
activation of calcium dependent phospholipases
accumulation of lipid breadksown products

Answer 94

A

-increased cytosolic calcium
–>activation of proteases–>damage to cytoskeleton

Answer 95

A

Plasma Membrane:
loss of cellular contents
ion and fluid (osmotic) imbalance

Answer 96

A

Mitochondrial Membrane:
MPTP opening leads to the leakage of pro-apoptotic proteins

Answer 97

A

Lysosomal Membrane
enzyme leakage leading to digestion of proteins and nucleic acids

Answer 98

A

Accumulation of misfolded proteins
‒ Genetic mutations
‒ Free radical damage
Cells have repair mechanisms for
misfolded proteins
When overwhelmed proteins
accumulated in the ER
→“ER stress” initiates
apoptosis

Answer 99

A

Radiation, cytotoxic anticancer
drugs, hypoxia
‒ Direct damage
‒ Free radical damage
Cells have repair mechanisms
When overwhelmed initiates
apoptosis

Answer 100

A

Reversible
Cell swelling (Hydropic Degeneration)
Lipidosis (fatty change)
Catch it early or its GAME OVER

Answer 101

A

Irreversible
Necrosis
Apoptosis

Answer 102

A

cells have a limited repertoure of responses to injury, depending on the celltype and the nature of teh injury
1-adaption (increase efficiency or productivity)
2-degeneration (diminished functinal capacity)
3-death

Answer 103

A

Ballooning Degeneration
Swinepox Virus
reversible

Answer 104

A

Can be called “hydropic degeneration” or ballooning
degeneration (specifically in epidermis)
Increase in the size and volume of the cell
**“bulging”

Answer 105

A

How does this happen?
Loss of ionic and fluid homeostasis
Influx of fluid into the cell leading to cell swelling

Answer 106

A

Causes:
Hypoxia - how does this cause it? (lack of oxygen which means lack of ATP)
Toxins

Answer 107

A

Which cells are commonly affected?
- Cardiomyocytes
- Hepatocytes
- Proximal Tubule epithelium
- Neurons

Answer 108

A

Pale in color (pallor)
Wet
Swollen with smooth edges find

Answer 109

A

1.Plasma membrane alterations
2.Mitochondrial changes
3.Dilation of the ER
4. Nuclear alterations

Answer 110

A

1.Plasma membrane alterations,such as
blebbing, blunting, and loss of microvilli

Answer 111

A

2.Mitochondrial changes, including
swelling and the appearance of small
amorphous densities

Answer 112

A

3.Dilation of the ER, with detachment of
polysomes; intracytoplasmic myelin figures
may be present (see later)

Answer 113

A

Nuclear alterations, with disaggregation
of granular and fibrillar elements

Answer 114

A

release of Ca from the endoplasmic reticulum

Answer 115

A

-presence of inrracytoplasmic fally vacculation
-can be seen with cell swelling

Answer 116

A

Etiology: hypoxia, toxicity or metabolic disorders
Abnormalities in the synthesis, utilization and/or
mobilization of fat

Answer 117

A

Pathogenesis: impaired metabolism of Fatty Acids leads to the
accumulation of lipids - formation of fat vacuoles

Answer 118

A

Which cell are more susceptible?
Cardiac and skeletal muscle, liver (hepatic lipidosis), kidneys
Liver is most central organ to lipid metabolism
- all these cells need a ton of energy: use fats for energy

Answer 119

A

How does lipidosis occur?

** Excessive delivery of FFAs** from fat stores or diet
Decreased oxidation of FFAs (not being oxidized into
ketone bodies to be used!)

Impaired synthesis of Apoprotein
Impaired combination of protein and triglycerides to
form lipoproteins (need to be in this form to be transported)

** Impaired release of lipoproteins** from hepatocytes

main causes: hypoxia, toxicity, metabolic disorders

Answer 120

A

Can be yellow/pale
Rounded edges
Greasy texture
Soft

Answer 121

A

Looks like fat!

Large cytoplasmic vacuoles

DISPLACES THE NUCLEUS TO THE PERIPHERY

Answer 122

A

Seen frequently in mini horses
Also seen in ruminants and cats

Answer 123

A

Physiologic in Ruminants: Undergo small amounts of hepatic
lipidosis to form ketone bodies to keep up with their energy
requirements
** Pregnancy toxemia and early lactation** -very high energy requirements

Answer 124

A

Pathological: obesity (fat accumulation), starvation causing
mobilization of fat (liver gets overwhelmed processing all the fat and it
can accumulate in the liver) and diabetes also causes mobilizationof
triglycerides

Answer 125

A

Can be fatal:
Death of hepatocytes is irreversible - liver dysfunction

Answer 126

A

Necrosis: cell death from irreversible injury by hypoxia, ischemia and direct
cell membrane injury

Answer 127

A

Plasma membrane damage does not stay intact
Swelling of the mitochondria and lysosomes as well as cell

USUALLY ACCOMPANIED BY INFLAMMATION UNLIKE
APOPTOSIS **cell shrink/membrane intact

If you can see inflammation (redness/swelling) you can assume its
necrosis!!

Answer 128

A

Biochemical alterations occur first!
Ultrastructural changes - occur in <6 hours
Histological Changes - 6-12 hours
Gross changes - 1-2 days
Loss of Cell Nuclei

Karyolysis: nuclear fading 3
Pyknosis: nucleus shrinks 1
Karyorhexis: nuclear 2 fragmentation

you have gotten skinn/shrink. I can pick you up

Know the attached chart!

Answer 129

A

Pale
Soft
Visible zone of
inflammation
MDx: hepatitis, multifocal coalescing,
Inflammation yes

Etiology: histomonas meleagridis
Disease Name:”blackhead”

Answer 130

A

Losing basophilia, binding of eosin to denatured proteins
turns pick
**Enzyme digested organelles **- Vacuolation and moth-eaten
appearance
**Calcification **may occur

Answer 131

A

Mainly seen in liver, heart, kidney, skeletal
muscle Why?
Response to hypoxia or ischemia
Can be a response to toxic injury

Always think of INFARCTS: local areas of
coagulative necrosis

Answer 132

A

Histology:
Necrotic cells are surrounded by phagocytic
WBCs - neutrophils and macrophages

Answer 133

A

Unique to** CNS** due to high presence of lipids in the brain
- Dead cells digested and are transformed into a mass of liquid
(PUS!!!)
Leukoencephalomalacia:
Leukomyelomalacia:
Polioencephalomalacia:
Poliomyelomalacia:
All of these can overlap!

Answer 134

A

Leukoencephalomalacia: necrosis of **white **matter of the brain

Answer 135

A

Leukomyelomalacia: necrosis of white matter of the spinal cord

Answer 136

A

Polioencephalomalacia: necrosis of grey matter of the** brain**

Answer 137

A

Poliomyelomalacia: necrosis of **grey **matter of the spinal cord

Answer 138

A

Etiology?
Thiamine
(B1) deficiency

Lead poisoning

Polioencephalomalacia

Answer 139

A

Etiology?

Ingestion of Moldy corn
containing Fusarium
verticilioide

Leukoencephalomalacia

Answer 140

A

Etiology?

Equine herpesvirus 1
Rabies (lyssavirus)
West Nile Virus
(Flavivirus)

Poliomyelomalacia

Answer 141

A

Usually begins as coagulative necrosis
- affects distal extremities - Frostbite**

Answer 142

A

Dry gangrene: no bacterial infection- tissue
appears very dry

Wet gangrene: bacterial infection that
makes tissue appear wet
- mastitis goat (wet); Clostridium novyi

Answer 143

A

Caseous = CHEESE
- White necrotic debris

Associated with bacteria that can
replicate in phagosomes Ǖ hard for body
to get rid of!
Ex. Mycobacterium, Cornyebacterium
pseudotuberculosis
Ex. Tuberculosis

Histology:
Eosinophilia of necrotic area with a rim
of inflammatory cells
-** NO NEUTROPHILS**

Answer 144

A

Enzymatic Necrosis
Traumatic Necrosis of Fat
Abdominal Fat Necrosis
Saponification

Answer 145

A

Enzymatic Necrosis
- Pancreas, commonly following repeated pancreatitis
- Lipases become activated and destroy surrounding adipocytes

Answer 146

A

Traumatic Necrosis of Fat:
- Trauma to tissue can lead to necrosis of surrounding fat
Ex. Surgery, Dystocia (difficult birth)

Answer 147

A

idiopathic or possibly related to vitamin E deficiency
seen in the omentum, mesentery and retroperitoneum
may cause intestinal stenosis (narrowing) in extreme cases (lumen of intestines
becomes narrow)

Answer 148

A

Saponification: Fat necrosis where calcium deposits in an injured area

Answer 149

A

Antigen antibody complexes accumulate and
deposit in the walls of arteries following immune
reactions (TYPE III HYPERSENSITIVITY)
- Fibrinoid = Fibrin + Antigen-Antibody
complexes

Looks like fibrin on histology - very strandy!

Answer 150

A

Programmed cell death
- Cells will activate enzymes to degrade their own DNA
and proteins
- apoptotic cells break up into fragments, called
apoptotic bodies, which contain portions of the
cytoplasm and nucleus
- plasma membrane stays intact

Answer 151

A

No inflammation!! - make sure you know this!

Answer 152

A

Physiological: embryogenesis, thymus involution

Pathological: Viral infection, Extensive DNA damage,
accumulation of misfolded proteins

Answer 153

A

Cell shrinkage with increased cytoplasmic
density

** Pyknosis:** chromatin condensation

Formation of cytoplasmic blebs and
apoptotic bodies

Phagocytosis of apoptotic cells by adjacent
healthy cells

Answer 154

A

Intrinsic Pathway
Cytochrome C
Extrinsic Pathway

Answer 155

A

Intrinsic Pathway
-** major mechanism of apoptosis**
- increased mitochondrial permeability and release of pro-apoptotic
molecules (death inducers)

Answer 156

A

Cytochrome C:released into cytoplasm to initiate suicide
“point of no return”–>activation of caspases

Initiators: Caspases 8 and 9
Executioners:Caspases 3 and 6

Answer 157

A

Extrinsic Pathway
- Initiated by death receptors (TNFs) 2 present on every cell!
- some substances bind to these receptors, bind and activate caspases

Answer 158

A

Shrinkage
Plasma membrane remains intact
- Increased density of cytoplasm

Answer 159

A

Edible for phagocytes
Expressed phospholipids in the outer layer of the membrane in
order to be identified by macrophages
May become coated with natural antibodies & proteins of the
complement system

Answer 160

A

secrete substances that recruit phagocytes
some express thrombospondin, which is easily identified by
phagocytes)
macrophages may produce proteins that bind to apoptotic cells for
engulfment

Answer 161

A

Too Little Apoptosis
Mutation in p53 gene(tumor suppresor gene)
Defective apoptosis and increased abnormal
cell survival
Leads to proliferation of neoplastic cells and
thus, neoplasia is a common
consequence

Answer 162

A

Too Much Apoptosis: Neurodegeneration
and ischemia

Answer 163

A

-pathological process
location
distribution(must, duration and severity (optional)

Answer 164

A

-pathologic process
location
cause

Answer 165

A

distribution<–locally, extensive,

process<–necrotizing hepitatis–>organ/location
Edx: Clostridial Hepatitis

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Block 2 Flashcards

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