Term
| What are some of the cellular structures/systems most vulnerable to disease processes |
|
Definition
aerobic respiration
cell membrane integrity
metabolic processes
genetic apparatus |
|
|
Term
| What are the 3 basic tissue types of the body? |
|
Definition
epithelium
connective tissue
hemolymphatic tisue |
|
|
Term
| What happens when the adaptive capacity of the cell is exceeded? |
|
Definition
| cell injury develops, with potential for cell death |
|
|
Term
True or False
All disease processes are due to sick/malfunctioning cells |
|
Definition
|
|
Term
| Why is light microscopy limiting when identifying cell abnormalities? |
|
Definition
-may appear normal despite biochemical abnormalities
-cell may die with no evidence of structural changes |
|
|
Term
| What are the 3 mechanisms of cell injury? |
|
Definition
-response to injury depends on the type of injury, duration & severity
-consequences of the injurious stimulus depend on the type/status/adaptability/genetic makeup of the cell
-cell injury results from functional or biochemical changes in at least one of the essential cellular components |
|
|
Term
| What are some of the most important targets of cell injury? |
|
Definition
mitochondria (ATP synthesis)
cell membranes (regulate influx/outflow)
protein synthesis
cytoskeleton
genetic apparatus of the cell |
|
|
Term
True or False
Nonlethal cell injury can progress to cell death |
|
Definition
True
If the injury persists |
|
|
Term
| What are indications of a nonlethal injury to a cell? |
|
Definition
-abnormal biochemical function
-recognizable structural change |
|
|
Term
| What is a compensated state? |
|
Definition
| -cell/tissue/organ has degenerated but reached a static condition where they function at a sub-optimal level but can still maintain life of the body |
|
|
Term
| Lethal injury to the cells or tissues or an organism is termed... |
|
Definition
|
|
Term
True or False
Necrosis is irriversible |
|
Definition
|
|
Term
| What is the difference between local cell death & somatic cell death? |
|
Definition
somatic death = whole body
local cell death = necrosis of some cells/tissues |
|
|
Term
| What is the most efficient energy source for a normal cell? |
|
Definition
| phosphate bonds of ATP, requires oxidative phosphorylation! |
|
|
Term
| What are the causes of impaired energy production in a cell? (4) |
|
Definition
Hypoxia
(reduced O2 intake, impaired ability of blood to carry oxygen, failure of blood to flow to tissue)
hypoglycemia
enzyme inhibition
oxidative uncoupling |
|
|
Term
| What are some of the effects of impaired energy production in cells? |
|
Definition
-intracellular accumulation of water & electrolytes (especially sodium)
-swelling of organelles
-switch to anaerobic metabolism |
|
|
Term
True or False
If a cell switches to anaerobic metabolism, pH is likely to decrease |
|
Definition
true
-lactic acid production = more acidic environment |
|
|
Term
|
Definition
| granular cytoplasm, particularily due to influx of water & electrolytes & swollen mitochondria |
|
|
Term
| What causes cell membrane damage? (3) |
|
Definition
free radicals
activation of the complement system (products are damaging)
direct lysis of the membrane (enzymes, viruses, heat/cold, chemical solvents) |
|
|
Term
| What 3 reactions are relevant to cell injury mediated by free radicals? Explain each |
|
Definition
Lipid peroxidation of membranes
-double bonds of mmb lipids are very vulerable to FR, produce peroxides which are unstable = chain reaction
Cross Linking of Proteins
-FR promote x-linking, increasing degradation, decreasing enzyme activity, fragmenting polypeptides
DNA fragmentation
-FR react with thymine in DNA, breaking into single strands = cell death/aging/transformation |
|
|
Term
| How do reactive oxygen species cause cell injury? |
|
Definition
| failure of ROS scavengers to remove them leads to lipid perodixdation, autocatalytic reactions, oxidative stress. Cell membrane damage! |
|
|
Term
| What enzymes are particularly likely to damage cell membranes? |
|
Definition
|
|
Term
| What is acute pancreatitis? |
|
Definition
| release of pancreatic lipase which damages nearby cells |
|
|
Term
| What are the effects of cell membrane damage? (3) |
|
Definition
loss of structural integrity
loss of function
deposition of lipfuscin pigment |
|
|
Term
| Why does a deposition of lipofuscin pigment occur after a cell has suffered membrane damage? What is it? |
|
Definition
-granular brown pigment deposited in cytoplasm
-phospholipids & proteins (cell mmb remnants)
-due to organelle mmb damaged due to a lack of antioxidants resulting in lipid peroxidation |
|
|
Term
| What effect does lipofuscin pigment deposition have on a cell? |
|
Definition
| -has no effect on the cell and is a normal change in aging |
|
|
Term
| What is a fatty degeneration? Is it specific or nonspecific? |
|
Definition
accumulation of TGs in the cytoplasm of parenchymal cells in organs such as the liver
-nonspecific response |
|
|
Term
| How are free fatty acids metabolized under normal circumstances |
|
Definition
-free FAs carried in portal blood from intestine to liver
-processed into TGs, PLPs & cholesterol esters
-form apoprotein complexes, secreted into plasma as lipoproteins |
|
|
Term
| What is the initial cause of fatty liver syndrome in cats? Explain the basic concept of the disease |
|
Definition
considerable reduction in food intake (anorexia / diet) forcing the cat to mobilize fat stores as a source of energy
-transport mechanisms become saturated so TGs accumulate in hepatocyes |
|
|
Term
True or False
In fatty liver syndrome in cats, the ability of the liver to esterify fatty acids mobilized from adipose tissue is normal |
|
Definition
|
|
Term
| How would you treat fatty liver syndrome in cats? |
|
Definition
-reduce the need to mobilize fat
-a feeding tube (PEG tube) is often surgically inserted into the stomach to provide calories since the cat often has a poor appetite |
|
|
Term
| What might cause an accumulation of TGs in liver cells, and what causes are associated with each? |
|
Definition
-increased mobilization of adipose tissue (starvation / diabetes)
-overactivity of enzymes which convert FAs to TGs (alcohol consumption)
-reduced oxidation of TGs to other forms (anemia & hypoxia)
-decreased synthesis of apoproteins (protein malnutrition) |
|
|
Term
| Describe the appearance of a liver with significant accumulation of fat |
|
Definition
-pale & enlarged
-friable (fragile) greasy texture
-potential to rupture & bleed into abdominal cavity |
|
|
Term
| What are the typical intracellular accumulations seen resulting from cellular ingury? |
|
Definition
Fatty degeneration
Iron deposition
Bilirubin accumulation
Other (proteins, cholesterol, glycogen, melanin, carbon) |
|
|
Term
| What causes local accumulation of iron? |
|
Definition
the breakdown of hemoglobin at the sides of hemorrhage
-iron deposited in local macrophages or in connective tissue as hemosiderin |
|
|
Term
| Where is hemosiderin generally deposited when iron is present in excess? |
|
Definition
| -in macrophages especially in bone barrow, spleen & liver |
|
|
Term
True or False
hemosiderin cannot be seen via microscope |
|
Definition
|
|
Term
| What is hemochroomatosis? |
|
Definition
-inherited defect
-accumulation of free ferric iron which is reduce to produce toxic free radicals
-damage to heart, liver & pancreas |
|
|
Term
| Describe the normal metabolism of bilirubin |
|
Definition
1. Old RBCs broken down & recycled
2. Hemoglobin molecule broken down into individual components
3. Porphyrin ring is catabolized to form bilirubin
4. Bilirubin is bound to albumin, carried in plasma to the liver
5. Bilirubin is conjugated in liver to glucuronide (now water soluble)
6. Glucuronide-bilirubin complex is excreted into bile, goes to intestine, out in feces or to kidney & out in urine |
|
|
Term
True or False
Jaundice is a sign of disease, but not a disease itself |
|
Definition
|
|
Term
| What is jaundice? What are the 3 general mechanisms causing it? |
|
Definition
An increase in serum bilirubin due to:
-hemolytic jaundice
-hepatocellular jaundice
-obstructive jaundice |
|
|
Term
| What is hemolytic jaundice |
|
Definition
RBCs broken down in large numbers increasing production of bilirubin
-liver cannot keep up with conjugation so it accumulates in the serum |
|
|
Term
| What is hepatocellular jaundice |
|
Definition
| injury to the liver reducing efficiency in uptake, conjugation & excretion of bilirubin |
|
|
Term
| In hepatocellular jaundice, which will increase, the level of conjugated or unconjugated bilirubin? |
|
Definition
|
|
Term
| What is obstructive jaundice |
|
Definition
-blocked biliary tract preventing excretion of bile
-conjugated bilirubin backflows into the plasma |
|
|
Term
| In hemolytic jaundice, which will increase, the level of conjugated or unconjugated bilirubin? |
|
Definition
|
|
Term
| In obstructive jaundice, which will increase, the level of conjugated or unconjugated bilirubin? |
|
Definition
|
|
Term
| Why is bilirubin not excreted in the urine in hemolytic jaundice? |
|
Definition
| it is bound to albumin (lipid-soluble not water soluble) |
|
|
Term
| What typically causes the accumulation of unconjugated bilirubin? |
|
Definition
|
|
Term
| What typically causes the accumulation of conjugated bilirubin? |
|
Definition
| hepatitis or obstruction of bile flow |
|
|
Term
| What is the functional significance of bilirubin accumulation? |
|
Definition
-deposition of bilirubin in connective tissue of skin, sclera & internal organs
-affects colour but not function
-deposition in parenchymal cells can cause cellular injury
e.g. in liver cells = liver toxicity |
|
|
Term
| What other substance are likely to accumulate intracellularly? |
|
Definition
cholesterol & cholesterol esters
proteins
glycogen
pigments |
|
|
Term
| Which types of cell are affected in a somatic mutation? |
|
Definition
| cells of tissues (not eggs or sperm) |
|
|
Term
| What are the cellular effects of abnormalities in DNA? |
|
Definition
-interference with mitosis
-failure to synthesize structural proteins
-failure of growth-regulating proteins
-failure of enzyme synthesis |
|
|
Term
| What would be the effect of damage to the DNA that encodes RBC precursors? |
|
Definition
|
|
Term
| What are the ultrastructural changes of reversible cell injury? |
|
Definition
-plasma membrane blebbing
-loss of microvilli
-ER dilation
-eosinophilia
-cellular swelling
-fatty change |
|
|
Term
| How long in the necrotic process does it take for changes to become visible by light microscopy? |
|
Definition
|
|
Term
| What are the 3 types of morphologic evidence of necrosis? |
|
Definition
-gross evidence
-cytoplasmc evidence
-nuclear evidence |
|
|
Term
| What are the 4 types of gross evidence of necrosis |
|
Definition
Coagulation
Liquefaction
Caseous
Fat |
|
|
Term
| Describe the cause, appearance, and examples of occurrence of coagulation necrosis |
|
Definition
Cause
-ischemia (lack of blood supply)
Appearance
-denatured proteins
-loss of nuclei
-pale, dry tissue
Occurrence
-injection sites, infarcts |
|
|
Term
| Describe the cause, appearance, and examples of occurrence of liquefaction necrosis |
|
Definition
CAUSE
leukocyte enzymatic digestion of tissue, often due to bacterial/fungal infections
APPEARANCE
-viscous mass of digested tissue, yellow pus if initiated by acute inflammation
OCCURRENCE
-bacterial/fungal infections, hypoxic death of cells in CNS |
|
|
Term
| Describe the cause, appearance, and examples of occurrence of caseous necrosis |
|
Definition
Cause
-tuberculosis infection
Appearance
-loss of cell architecture, cheese-like debris, distinct inflammatory border
Occurence
-tuberculosis |
|
|
Term
| Describe the cause, appearance, and examples of occurrence of fat necrosis |
|
Definition
Cause
-fat destruction due to lipase activity
Appearance
-chalky white areas (Ca2+) = fat saponification
-necrotic fat cell with calcium deposits
Occurence
-acute pancreatitis |
|
|
Term
| Discuss the two types of fat necrosis |
|
Definition
Enzymatic
-pancreatic injuries/acute pancreatitis
-enzymes released into adjacent tissue
-TGs broken down into glycerol + FAs, complex with Ca2+ forming chalky white appearance
Nonenzymatic
-breasts & subctaneous fat
-usually following trauma
-inflammatory response induced (granulomatous inflammation) |
|
|
Term
| Nonenzymatic fat necrosis is also known as .... and is typically seen in which tissues? |
|
Definition
traumatic fat necrosis
-breasts & subcutaneous fat |
|
|
Term
| What are the 4 cytoplasmic signs of necrosis? Explain each |
|
Definition
More homogenous & deeply staining
-denaturation of proteins & loss of ribosomes
Vacuolated/bubbly Appearance
-loss of Na+ pump function due to loss of energy production = inflow of Na & water = swollen mitochondria
Autolysis
-lysosomal enzymes released resulting in self-digestion
Calcification of dead ceals |
|
|
Term
| What is the most definitive indicator of necrosis, cytoplasmic or nuclear evidence? |
|
Definition
|
|
Term
| What is the nuclear evidence of necrosis? (4 points) |
|
Definition
-clumping of nuclear chromatin
-shrunken, dark nucleus (pyknotic)
-fragmented nucleus (karrhyorhexis)
-lysed nucleus (karrhyolysis) |
|
|
Term
| abnormal deposition of calcium alts in dead/dying tissues is known as.... |
|
Definition
|
|
Term
| What types of problems are associated with tissue necrosis? |
|
Definition
1. Altered function
e.g. blood supply loss = stroke or heart attack
2. Loss of tissue
-loss of blood flow with potential 2ndary infection
3. Secondary infection
-no blood flow = no inflammatory cells or immune system access
-necrosis of skin = loss of the first protective barrier against infection
4. Systemic effects
-fever, more WBC
5. Local effects
-e.g. bleeding ulcurs after necrosis of stomach lining, abdominal pain
6. Release of enzymes from necrotic cells
-necrotic cells release cytoplasmic enzymes into blood (can use serum tests to ID tissue type) |
|
|
Term
True or False
Inflammation is commonly seen in almost all necrotic tissue |
|
Definition
False
No blood flow = no inflammatory cells |
|
|
Term
| Why is fever associated with necrosis? |
|
Definition
| necrotic cells release pyrogens (fever-inducing agents) |
|
|
Term
What post-mortem changes occur in the body following death? (4)
Explain each a little |
|
Definition
Rigor mortis
-reduction of ATP in muscles
Post mortem lividity
-settling of blood in lower regions, breakdown of hemoglobin = green colour
Post-mortem blood clotting
-especially in heart chambers
Putrefaction
-fermentation by bacteria produces gas
-stomach may rupture, liver appear foamy due to gas bubbles |
|
|
Term
| What might cause a cell to follow apoptosis in normal situations? (4) |
|
Definition
1. Programmed cell death during embryogenesis
2. Hormone-driven regression of tissues
3. Cell death in tissues with normal rapid turnover
4. Elimination of potentially harmful lymphocytes during maturation |
|
|
Term
| What pathological circumstances might induce apoptosis? (4) |
|
Definition
Damage to DNA
Accumulation of misfolded proteins
Viral infections
Atrophy of organs |
|
|
Term
| What cells of the immune system are capable of inducing cell death in neighbouring through apoptosis? |
|
Definition
|
|
Term
True or False
Apoptosis requires energy |
|
Definition
|
|
Term
| Which induces greater secondary inflammation, necrosis or apoptosis? |
|
Definition
|
|
Term
| What mediates the signalling for apoptosis? |
|
Definition
-external signals (adjacent cells, circulating factors)
internal signals (mitochondria) |
|
|
Term
| What enzymes mediate apoptosis? |
|
Definition
|
|
Term
| What is necessary for a cell to produce a tumour rather than undergo apoptosis? |
|
Definition
-must avoid endogenous suicide signals
-must avoid recognition & response from cytotoxic T cells |
|
|
Term
| Which is more traumatic, apoptosis or necrosis? |
|
Definition
|
|
Term
| What causes lysosomal enzyme release from necrotic cells? |
|
Definition
| -lack of oxygen = anaerobic metabobolism = lower pH = damage to lysosomal membranes |
|
|
Term
True or False
Lysosomal enzyme release is a cause of cell death |
|
Definition
False
It is a result of cell death |
|
|
