Unit 2 - 2.1-2.4, 2.7 Flashcards
1
Q
A retrogressive process in which cells deteriorate and show a corresponding and variable degree of functional inhibition, chemical alteration, and morphologic change
A
cellular injury
2
Q
What is the sequence of events for cellular injury?
A
- biochemical alteration
- functional abnormality
- morphological change
3
Q
What occurs within the cell to a point where the cell with either recuperate or die?
A
degeneration
4
Q
What is it called when an injury occurs that the cells can recover from?
A
subnecrotic or sublethal damage
5
Q
What happens if necrosis occurs within a small enough area?
A
the viable neighboring cells will replace the dead ones via proliferation
6
Q
What happens if the area of necrosis is too large for the cells surrounding it to adapt?
A
the gap will be replaced with fibrous CT
7
Q
negative response of the cell to injury
A
degeneration
8
Q
Cells have a very limited:
A
number of responses to injury
9
Q
4 injury classifications:
A
- deficiency of a critical material
- lack of cellular energy production
- accumulation of abnormal substances
- physical injury
10
Q
visible changes
A
morphologic changes
11
Q
Why might it be difficult to see morphologic changes?
A
the cell has to live long enough after the injury for the morphologic change to develop
12
Q
What system kicks in when the Krebs cycle isn’t working?
A
anaerobic glycolysis
13
Q
What is the end product of glycolysis?
A
lactic acid
14
Q
Why is a build up of lactic acid bad?
A
lowers cellular pH and eventually blood pH
15
Q
How much ATP is yielded from the Kreb’s cycle?
A
36
16
Q
How much ATP is yielded from glycolysis?
A
2
17
Q
normal blood pH:
A
7.4
18
Q
What can occur when the blood pH goes down to 7.0 (acidosis)?
A
cardiac arrhythmias, CNS dysfunction
19
Q
What can occur when the blood pH goes up (alkalosis)?
A
neuromuscular excitability, decreased myocardial contractility, arrhythmias
20
Q
Why do cells that do a lot of synthesizing have blue staining cytoplasm?
A
because they have a lot of endoplasmic reticulum
21
Q
What enzyme is necessary to transport glucose across the cell membrane of hepatocytes, muscle cells, and adipose cells?
A
insulin
22
Q
When is insulin not required for glucose transport?
A
into the brain
23
Q
characterized by accumulation of lipid within non-adipose cells
A
fatty change
24
Q
Where is fatty change most commonly seen? Less commonly?
A
- liver
- heart and kidney
25
Gross appearance of fatty change?
tissue is lighter in color (yellow to white); may have a prominent lobular pattern; swollen and friable
26
List the three reasons fatty acids enter hepatocytes:
1. beta-oxidation to produce energy (ATP)
2. synthesis of lipoproteins and cholesterol
3. synthesis and export of triglycerides (requires phospholipids and proteins)
27
List the three factors that will lead to the appearance of fat in a cell:
1. more fat arrives in the hepatocytes than the hepatocyte can process
2. decreased beta-oxidation of fatty acids
3. impaired synthesis or release of lipoproteins
28
What are three ways that can increase the amount of fat entering the hepatocyte past the point that the hepatocyte can process?
1. high fat diets
2. fat mobilization (anorexia, pregnancy, lactation)
3. endocrine issues (esp. diabetes)
29
What three methods can lead to decreased beta-oxidation of fatty acids?
1. hypoxia from anemia or passive congestion
2. vitamin deficiencies (niacin, riboflavin)
3. toxins that impair mitochrondrial function
30
What two ways can synthesis or release of lipoproteins be impaired?
1. toxins (damage membranes, inhibit protein synthesis)
| 2. viral infection
31
generally without physiologic effect unless more severe changes also accompany it
fatty change
32
List four diseases in which fatty liver is prominent and can be fatal:
1. ketosis
2. pregnancy toxemia
3. hepatic lipidosis and hypoglycemia (toy breed puppies)
4. hepatic lipidosis syndrome (cats, ponies, donkeys, and miniature horses)
33
What is the major source of fat for the liver?
GI tract
34
What three main tissues use lipids for energy?
heart, skeletal muscle, liver
35
the process by which fatty acids are broken down in mitochondria to generate Acetyl-CoA:
beta-oxidation
36
fatty acids cannot be converted into _____________ in animals
glucose
37
What activates the adipocytes to activate hormone sensitive lipase when blood sugar is low?
glucagon
38
What happens once hormone sensitive lipase is activated and what does this accomplish?
converts triglycerides into free fatty acids;
the low solubility of free fatty acids allows them to bind to serum albumin and can be transported to muscle and liver for oxidation
39
What inhibits hormone sensitive lipase?
insulin
40
What, other than glucagon, can activate hormone sensitive lipase?
stress
41
metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates
gluconeogensis
42
What do triglycerides get broken down into once they enter the hepatocytes from the blood?
glycerol and fatty acids
43
What does beta-oxidation depend on?
oxygen
44
What is the main source of energy for hepatocytes?
oxidation of fatty acids
45
What are most fatty acids metabolized to?
phospholipids
46
Which tissue type synthesizes more triglyceride than the liver?
adipose
47
What are the two most common causes of hypoxia and thus, decreased beta oxidation of fatty acids?
anemia and central passive congestion
48
When doing a cross-section of a liver, what is a common way to tell if its morpholigic changed is indicative of fatty liver?
grease/fats left on the knife
49
What happens if a liver is extremely fatty?
it will float in formalin or water
50
How would the consistency of a fatty liver feel?
friable; break easily between fingers
51
What are the bright red areas you can see in yellow livers with very distinct lobular patterns?
blood in the central veins of the hepatic lobules
52
Where does blood flow to in the liver?
from the portal triad to the central vein
53
Why are the centrilobular regions of the liver the most vulnerable to hypoxia?
it's the lowest of any part of the lobule; last in line to receive oxygen
54
What is the major significance of fatty change
it tells us that we must look for the cause
55
a condition in which there are excessive ketones (acetoacetic acid and beta-hydroxybutyric acid) in the blood
ketosis
56
When can ketosis occur in cows?
at peak lactation
57
When can ketosis occur in sheep and goats?
in late gestation
58
Why can ketosis occur in pregnant or nursing animals?
high energy expenditure (inadequate quality/intake of food)
59
How does acetyl-CoA have to enter the Krebs Cycle?
bound to oxaloacetate
60
What does the liver do to oxaloacetate when carbohydrates are inadequate?
converts it to glucose (via gluconeogenesis)
61
If all of the oxaloacetate is being converted to glucose, what happens to the acetyl-CoA?
converts it to ketones (which build up in the blood)
62
Why can't fat be visualized on a normal histological slide?
tissue gets soaked in xylene which dissolves the fat
63
How can you visualize fat on a slide?
freeze tissue, then stain with Oil-red-O
64
What type of dog breed commonly gets hepatic lipidosis?
toy breed dog puppies
65
Puppies with hepatic lipidosis typically present with what 2 major clinical signs?
neurological signs (due to brain swelling) and cerebral neuronal necrosis (secondary to hypoglycemia)
66
microvesicular type hepatic lipidosis looks like:
vacuolation consisting of many small vacuoles (as opposed to a few large ones)
67
a fairly common idiopathic disease that occurs mostly in obese cats following a period of anorexia
hepatic lipidosis
68
Why is hepatic lipidosis a major problem in cats compared to other animals?
their hepatocytes become dysfunctional when filled with fat
69
a condition in which the liver fails to remove certain chemicals (especially ammonia and mercaptans) from the portal blood
hepatic encephalopathy
70
Can cross the blood-brain barrier and is toxic to astrocytes, causing them to swell:
ammonia
71
thought to act as false neurotransmitters
mercaptans
72
a purely descriptive term referring to a waxy, homogenous, amorphous, solid, translucent appearance
hyaline degeneration
73
seen as a hyalinization of collagen - grossly it has a smooth, white, glossy appearance
connective tissue hyaline
74
describe the microscopic appearance of extracellular hyaline
hyalinized area containing no or relatively few nuclei and stains intensely pink with H&E
75
What is the effect of connective tissue hyaline in scars?
no effect
76
What is the effect of connective tissue hyaline in vessel walls?
inelasticity - high blood pressure
77
What is the effect of depositional hyaline?
interferes with fluid exchange
78
hyaline materials deposited around cells:
depositional hyaline
79
What is the significance of tubular casts?
an indication of severe damage to the renal glomerulus, usually due to glomerular amyloidosis or glomerulonephritis
80
The deposition of a protein especially in the spleen, kidney, and liver. Lymph node and adrenal may be involved:
amyloid extracellular hyaline
81
What stain placed on the cut surface of an organ with amyloidosis will generally impart a red-brown color?
Lugol's iodine
82
Seen especially in kidney tubular epithelium and adrenal cortical cells as small cytoplasmic hyaline droplets
hyaline droplet degeneration
83
Seen as bright-pink staining globules in the cytoplasm of plasma cells. Seen in chronic diseases or those associated with a hyperammaglobulinemiaL
Russell bodies
84
may be intranuclear or intracytoplasmic, single or multiple and basophilic or eosinophilic
viral inclusion bodies
85
seen as a rhomboid, red staining crystal in the nucleus of liver and kidney epithelium of the dog and cat (cause and significance unknown)
crystalline inclusion bodies
86
Purplish staining, homogenous or concentrically laminated bodies which may occur in the alveoli of the prostate, mammary gland or lung
corpora amylacea
87
What is the significance of corpora amylacea intracellular hyaline?
may indicate a past inflammatory process
88
keratin of squamous epithelium that may accumulate excessively in conditions of chronic irritation or altered metabolism
keratohyaline
89
Where are cytoplasmic inclusions more common?
epithelial cells of the respiratory tract, urinary bladder mucosa, and stomach
90
What is the name of the inclusion body that is a hallmark for rabies?
Negri bodies
91
refers to the location of the tumor outside of the bone marrow
extramedullary
92
Occurs when your bone marrow produces abnormal antibodies that can't be broken down; deposited in your tissues as amyloid and cannot be broken down
primary amyloidosis (AL)
93
protein deposits accumulate in one or more organ systems in the body; caused by chronic infection or inflammatory disease
secondary amyloidosis (AA)
94
Primary protein of AL amyloid is:
serum amyloid A (SAA)
95
List the common sites for amyloid to occur (5):
kidney, liver, spleen, lymph nodes, and adrenal
96
What color should normal kidneys be?
mahogany brown
97
Why is albumin the protein that most often leaks into the nephron?
low molecular weight
98
What is a consequence of urinating gram quantities of protein at micturition?
weight loss and muscle wasting
99
combination of generalized edema, ascites, and pleural effusion and hypercholersterolemia secondary to protein losing nephropathy:
nephrotic syndrome
100
What is the primary way that amyloid causes damage?
compression of normal tissue resulting in ischemia (and often organ failure)
101
Why is calcium build up a sequelae of necrosis (known as dystrophic calcification)?
regulation of influx of Ca++ into cytoplasm can no longer be controlled; accumulates in the mitochondria
102
deposition of calcium salts in otherwise normal tissues because of elevated levels of serum calcium
metastatic calcification
103
Occurs in multiple tissues including liver, pancreas and kidney as an accumulation of glycogen in cytoplasmic vacuoles.
Glycogen infiltration
104
Describe the gross appearance of organs with glycogen infiltration:
organs may be lighter in color
105
How does glycogen infiltration appear microscopically?
fuzzy lined vacuoles, single or multiple, in cytoplasm
106
Where can you see glycogen infiltration in well fed animals?
liver
107
What does glycogen infiltration affect in poorly controlled DM?
B cells of islets of Langerhands, duct epithelium of the pancreas, renal tubular epithelium
108
Which two types of tumors often have heavy glycogen infiltration?
seminoma and renal carcinoma
109
Treating dogs with what drug will increase liver glycogen? What is this called?
corticosteroids; steroid hepatopathy
110
What disease of horses can cause glycogen infiltration?
polysaccharide storage myopathy
111
What is the effect of glycogen infiltration?
not harmful but indicates a fault in the metabolism of the cell
112
What is the form in which glucose is normally stored within hepatocytes in the liver?
glycogen
113
What is a major metabolic disease affecting glucose metabolism that all of you are familiar with?
DM
114
What color does PAS stain glycogen?
magenta
115
Glucocorticoids are often induced by:
stress
116
reduction in mass of a tissue or organ
atrophy
117
increase in the size of cells, resulting in enlargement or rogans
hypertrophy
118
increased number of cells in an organ or tissue
hyperplasia
119
transformation or replacement of one adult cell type with another
metaplasia
120
any change that results in loss of the ability to maintain the normal or adapted homeostatic state
cell injury
121
Hallmarks of Cell Degeneration:
cell swelling, fatty change, glycogen accumulation, lipofuscin, hyaline changes, amyloid, calcification, gout
122
A complex protein that accumulates within cells; homogeneous pink materal
amyloid
123
more common in birds and reptiles, but can occur in other species (assoc. with renal dz due to decreased excretion of urates)
gout
124
accumulation of lipid (TG) within vacuoles within cells
fatty change
125
the oxidized products from membrane lipids (yellow to brown)
lipofuscin
126
dense, homogenous, glossy, translucent; many causes (protein leak most common)
hyaline changes
127
no nuclear displacement with:
glycogen accumulation
128
What are the three pathogeneses for fatty change?
overload, injury to cells, deficiencies
129
What are the three pathogenic mechanisms for glycogen accumulation?
1. severe hyperglycemia
2. high glucocorticoids
3. lysosomal storage disease
130
cytoplasm contains rounded, eosinophilic droplets, vacuoles, or aggregates
hyaline droplets
131
protein casts within renal tubules
hyaline casts
132
compacted collagen, scar tissue
CT hyaline
133
Describe the gross appearance of calcification:
chalky, white tissue; hard, gritty on cut surface
134
Describe the gross appearance of amyloid:
enlarged, pale, waxy, translucent
135
Has dark blue staining material, along BM, stippled throughout cell, large clumps. What is this the microscopic appearance of?
calcification
136
Widespread excessive calcification:
calcinosis
137
What is the term used for calcification in the cavities or lumina?
calculi/calculus
138
Accumulation or urate crystals
gout
139
White, firm, crystal depsoits on gross appearance:
gout
140
Granulomas with radiating crystalline material on microscopic appearance:
gout
141
What is the most common action for toxins?
free radicals
