1-Cell Responses to Bad Things Flashcards
(129 cards)
1
Q
Give me a definition of pathology.
A
the study of disease and the structural, biochemical, and functional changes in cells, tissues, and organs that underlie disease
2
Q
What does general pathology study?
A
The study where CELLS and TISSUES react to abnormal stimuli, which are the cause of disease
3
Q
What does Systemic pathology study?
A
Studies alterations in specialized ORGANS and tissues that are responsible for disorders
4
Q
What are the 2 etiologies for disease?
A
Genetic or acquired
5
Q
What is the pathogenesis of disease? (generally)
A
The sequence of events in the response of cells or tissues to a harmful agent
6
Q
What does diagnostic pathology study?
A
morphological changes in tissues to identify the nature and progression of disease
7
Q
What is adaptation?
A
The ability to adjust and come with change.
8
Q
What happens if the cell stress exceedes adaptive capabilities?
A
Cell injury
9
Q
Name 4 different cell adaptations to stress/injury
A
Hypertrophy (increase size), Hyperplasia (increase #), Atrophy (decrease size and fxn) and Metaplasia (change phenotype)
10
Q
What types of injuries are reversible?
A
mild or transient, no damaging or long term effects. (like hypoxia)
11
Q
What types of injuries are irreversible?
A
If it’s long and progressive, causing necrosis or apoptosis
12
Q
What occurs during hypertrophy?
A
increase in SIZE of cells, not #’s.
13
Q
What happens to an organ when it’s cells undergo hypertrophy?
A
It gets bigger and heavier, like cardiac or skeletal muscle in athletes.
14
Q
What types of molecules signal a cell to undergo hypertrophy?
A
Growth factors and vasoactive agents
15
Q
Which signaling pathway does a cell use for physiological hypertrophy?
A
P3K/Akt pathway
16
Q
Which signaling pathway does a cell use for pathological hypertrophy?
A
G-proteins
17
Q
What kind of drugs make the smooth ER selectively hypertrophic?
A
Barbituates
18
Q
What occurs during hyperplasia?
A
Increase in the NUMBER of cells in an organ
19
Q
What signals cells to undergo hyperplasia?
A
Growth factors
20
Q
When do cells undergo physiological hormonal hyperplasia?
A
when the tissue needs an increase in functional capacity
21
Q
What are some examples of hormonal hyperplasia?
A
proliferation of the glandular epithelium of the boob (puberty and pregnancy)
22
Q
When do cells undergo physiological compensatory hyperplasia?
A
After damage. It increases the tissue mass.
23
Q
What is the famous example of compensatory hyperplasia?
A
Liver resection causes partial re-growth of the liver by compensatory hyperplasia (look up myth of prometheus)
24
Q
When does pathological hyperplasia occur?
A
When there is excess hormones or growth factors
25
What are some examples of pathological hyperplasia?
endometrial hyperplasia (menstration), benign prostatic hyperplasia (BPH)
26
What occurs during atrophy?
The organ/tissue is reduced in size from a decrease in cell size and number
27
What are some examples of physiological (normal) atrophy?
Embryonic structures (notocord), and uterus (postpartum)
28
What are some causes of pathological atrophy?
Decreased workload, denervation, low blood supply, and bad nutrition
29
What decreases in the cell to cause atrophy?
Protein synthesis
30
What happens in autophagy?
The cell eats its own components to survive.
31
What occurs in metaplasia?
It's a reversible change, where 1 differentiated cell type is replaced with another cell type.
32
How does metaplasia and GERD relate?
When stomach acid irritates the esophagus for a long time, it undergoes metaplasia from squamous to columnar
33
How does metaplasia and smoking relate?
Chronic irritation of the respiratory tract causes metaplasia from columnar to squamous (thereby losing it's cilia and ability to transport phlem *cough cough*)
34
What occurs in connective tissue metaplasia?
When tissues undergo trauma, cartilage, bone or adipose tissue can form in the tissues that do not contain these elements. Whaaaaaaaaaaaaaaaaaaaa
35
Does metaplasia change the phenotype of an already differentiated cell?
No. It reprograms the STEM cells to differentiate into a new cell type.
36
Why does hypoxia injure cells?
No oxphos --> no ATP --> bad things.
37
What are some morpholgical signs of reversible injury?
cell swelling, blebbing of membrane, detachment of ribosomes, and clumping of nuclear chromatin.
38
Why does cell swelling occur in reversible injury?
Loss of ATP production --> failure of Na/K ATPases on plasma membrane --> more Na in cell --> cell swells
39
When the injurious stimulus isn't removed, and the cell injury becomes irreversible, what is the sequence of morphological events that occurs?
(BULG). Biochemical alterations --> Ultrastructural changes --> Light microscopy changes --> Gross morphological changes.
40
What is the first sign of cell injury?
Cell swelling
41
What part of the cell is injured for a cell to undergo necrosis?
Membrane.
42
What part of the cell is injured for a cell to undergo apoptosis?
DNA
43
Generally, what is the pathogenesis of necrosis?
membrane injured --> cell swells --> cell components leak out of cell --> inflammation of tissue
44
Is necrosis pathological, physiological, or both?
ALWAYS Pathological
45
What is the general pathogenesis of apoptosis?
DNA injured --> cell signals itself to die --> shrinks --> fragments into nucleosome-sized fragments --> cell membrane remains intact --> apoptotic bodies are eaten
46
Is apoptosis pathological, physiological, or both?
Both
47
Coagulative necrosis- cause
ischemia
48
Coagulative necrosis- clinical presentation
firm, eosinophilic, anucleate cells
49
Liquefactive necrosis- cause
focal bacterial infections
50
Liquefactive necrosis- clinical presentation
creamy yellow (pudding) discharge in CNS, hypoxic death of cells in CNS
51
What type of necrosis is gangrene?
Nothing specific- used in clinical practice to say it's a combo of coagulative and liquefactive necrosis
52
Caseous necrosis- cause
TB infections
53
Caseous necrosis- clinical presentation
"Cheese"-like consistency of tissue, form granulomas
54
Why is the pattern of fat necrosis weird?
Because it's not specific- just used clinically
55
Fat necrosis- cause
release of pancreatic lipases into the pancreas and peritoneal cavity
56
Fat necrosis- clinical presentation
Focal areas of fat destruction, usually asympomatic
57
Fibrinoid necrosis- cause
complexes of antigens and antibodies deposit into the walls of arteries
58
Fibrinoid necrosis- clinical presentation
bright pink fibrinoid on histological cross section
59
What % of ATP depletion is needed before problems occur?
Only 5-10% depletion
60
Why is ATP bad for Ca homeostasis?
Ca++ ATPase pump fails --> influx of Ca++
61
What 3 things injure mitochondria?
Ca++, ROS, and low O2
62
What is the function of the high-conductance pore when mitochondria are injured?
loss of mitochondrial membrane potential --> failure of oxphos --> NECROSIS
63
What are the function of the caspases and cytochrome c on the mitochrondrial membrane?
they're enzymes that can be bound when DNA is damaged --> these leak into the cytosol --> death by APOPTOSIS
64
Is cytosolic free Calcium high or low in the cell?
Very very very low.
65
Where is Ca++ stored?
mitochondria and ER
66
Increased Ca++ activates which enzymes?
(PEA's). Phospholipases, Endonucleases, ATPases
67
Which 2 metals causes ROS formation?
Cu and Fe
68
What do ROS's do to lipids in membranes?
It peroxidizes them, attacking the double bonds.
69
What is the effects of ROS's on proteins?
They oxidize proteins, changing the morphology.
70
What is the effects of ROS's on DNA?
ROS's can cause single and double strand breaks as well cross linking of the strands.
71
If a tissue is hypoxic, what energy-producing pathway can still occur?
Anaerobic glycolysis
72
What is hypoxia?
When there is a reduced O2 availability from various causes
73
Which is worse: hypoxia or ischemia? Why?
Ischemia. It's worse because O2 and nutrients are decreased, therefore over time even glycolysis can't occur.
74
What is ischemia-reperfusion injury?
Reperfused tissues may lose more cells at the end of ischemia.
75
What is the mechanism behing ischemia-reperfusion injury?
Either from cell antioxidant defense mechanisms are down and/or Ca may enter reperfused cells.
76
What is the most affected organ by adverse reactions of drugs?
The liver. Most of drug metabolism happens there.
77
What is direct chemical cell injury?
Where chemicals bind directly to critical molecular components on cells.
78
What is indirect chemical cell injury?
Chemicals are converted to a reactive toxic metabolite and then can cause membrane damage by making ROS's
79
Does apoptosis elicit an inflammatory reaction in the cell?
No. The apoptotic bodies are rapidly eaten b4 cell contents leak out.
80
Why is apoptosis a normal physiological process?
It maintains homeostasis by regulating cell populations and harmful cell populations.
81
In apoptosis, do cells grow or shrink?
Shrink
82
What is the most characteristic feature of apoptosis?
Chromatin condensation.
83
What eats apoptotic bodies?
Macrophages
84
The intrinsic pathway of apoptosis is a result of what dysfunction?
increased mitochondrial permeability
85
The intrinsic pathway of apoptosis leads to the activation of what initiating caspase?
Caspase 9
86
The extrinsic pathway of apoptosis is a result of what dysfunction?
Binding of plasma membrane death receptors (TNF's)
87
The extrinsic pathway of apoptosis leads to the activation of what initiating caspases?
Caspase 8 and 10
88
The extrinsic and intrinsic apoptotic pathways lead to the activation of what 2 executing caspases?
Caspase 3 and 6
89
Apoptosis is triggered mainly by DNA damage, but what other 2 mechanisms can trigger apoptosis?
growth factor deprivation and protein misfolding.
90
How can there be intracellular accumulations if a substance's rate of metabolism is altered?
If the production is normal but the rate of metabolism to remove it is inadequate, then it can accumulate in cells.
91
How can a substance accumulate in cells if the transport is altered?
Defects in protein folding and transport can accumulate the substance, and is part of a lot of degenerative disorders in the CNS
92
How can a substance accumulate in cells if a substances enzymes are altered?
If the enzymes are altered, the metabolism is altered for the substance and can cause storage disorders.
93
What happens if a cell can't metabolize or transport a substance?
It accumulates, like carbon particles.
94
What is steatosis?
Abnormal accumulations of triglycerides in parenchymal cells (liver, heart, muscle, kidney)
95
What types of things cause steatosis?
toxins, protein malnutrition, diabeeeetus, obesity, alcoholism and anoxia
96
What is the main mechanism behind triglyceride accumulations in the liver?
Either there is WAYYY to much coming in or it's export mechanism is defective.
97
Why does alcoholism cause fatty accumulations in the liver?
Because it causes a reduced breakdown and an increased synthesis of fats in the liver.
98
What is the histological appearance of fatty accumulations?
Clear vacuoles
99
What types of staining could you use to identify fatty accumulations on a histological specimen?
Sudan IV or Oil Red-O (shows up orange-red)
100
What is the gross examination of a liver with fatty accumulations?
Yellow, heavy, greasy (like a McDonalds hamburger patty)
101
Atherosclerotic plaques are an accumulation of what substance?
Cholesterol
102
What is the histological appearance of atherosclerotic plaques?
Foamy
103
What are Xanthomas?
clusters of foamy cells in the subepithelial connective tissue, showing up as yellow wart-type things on the skin
104
An accumulation of what substance in macrophages causes xanthomas?
Cholesterol
105
What is cholesterolosis?
focal accumulations of cholesterol-laden macrophages in the gallbladder
106
Neimann-Pick disease is a defect in what cellular organelle?
Lysosomes
107
Neimann-Pick disease involves accumulations of what substance?
Cholesterol
108
What is the histological appearance of intracellular protein accumulations?
Rounded, eosinophilic droplets, vacuoles or aggregates in the cytoplasm.
109
Protein accumulations are best seen in which organ?
Kidney (renal tubules)
110
If there is a defect in the protein α1-antitrypsin, what clinical manifestation might occur?
Emphysema
111
Accumulations of the cytoskeletal proteins keratin intermediate filaments in the liver is indicative of what chronic condition?
Alcoholism
112
Accumulations of the cytoskeletal proteins cause neurofibrillary tangles in the CNS, which is indicative of what chronic condition?
Alzheimers
113
What is the histological appearance of hyaline accumulations?
homogenous, glassy, pink
114
What is the histological appearance of glycogen accumulations?
Clear vacuoles in the cytoplasm
115
Tattoing causes pigment accumulation in what dermal cells?
Macrophages
116
What endogenous pigment is the "wear-and-tear" pigment, and is the tell tale sign of ROS injury?
Lipofuscin
117
What is the histological appearance of lipofuscin?
Yellow-brown, finely granular, often perinuclear
118
How is melanin synthesized in melanocytes?
Tyrosine ----Tyrosinase---> DHPhe
119
Hemosiderin serves to store which substance?
Fe
120
What is the histological appearance of hemosiderin?
Yellow-to-brown, granular
121
What 3 conditions can cause hemosiderin accumulations?
(Basically anything that increases Fe). 1. eating more Fe, 2. hemolytic anemia, 3. repeated blood transfusions
122
What is the histological appearance of Fe pigments?
coarse, blue granular pigments in the cytoplasm (under Prussian blue histological stain)
123
When does dystrophic calcification occur?
When tissues are dying. Remember dy- for dy-
124
In distrophic calcification, are serum levels of Ca increased, decreased, or normal?
Normal. There is no problem with Ca metabolism, just that local tissues are necrosing.
125
When does metastatic calcification occur?
When there is an issue with Ca metabolism, and there is Ca deposition in otherwise normal tissues.
126
In metastatic calcification, are serum levels of Ca increased, decreased, or normal?
Increased
127
Increased secretion of what hormone can cause metastatic calcification?
PTH
128
What is the morphological appearance of calcium salt accumulations?
basophilic, amorphous granular, clumped, either extra- or intracellular
129
What 2 effects lead to cellular aging?
Genetic abnormalities and/or cellular damage.
