Cell Injury & Adaptive Response Flashcards
1
Q
symptoms
A
patient’s subjective observations, usually not quantifiable
2
Q
signs
A
abnormalities on physical exam, usually quantifiable
3
Q
findings
A
x-rays or results
4
Q
syndrome
A
cluster of related symptoms and or signs typically due to a single cause in an individual patient
5
Q
etiology
A
the cause of a disease
overly simplistic to think of a disease having a single cause
6
Q
pathogenesis
A
sequence of events by which the disease develops
7
Q
pathognomonic
A
a particular abnormality is found only in one condition
8
Q
forme fruste
A
very mild variant of a more serious disease
9
Q
incidence
A
number of new cases per unit time (usually a year)
10
Q
how is incidence expressed?
A
“new cases per 100,000 people per year”
11
Q
prevalence
A
number of cases at any one time
12
Q
how is prevalence expressed?
A
“cases per 100,000 people”
13
Q
risk
A
how much your particular situation increases your chance of getting a disease compared with everyone else
14
Q
diagnosis
A
name given to the particular disease once identified
15
Q
prognosis
A
expected outcome for a particular case of a disease
16
Q
what influences prognosis?
A
influenced by diagnosis, the age & general health of the patient, available treatments
17
Q
what hurts cells?
A
hypoxia
poor nutrition-cells respond in different ways
infectious agents-several mechanisms depending on agent
immune injury-4-5 types, antibody or t-cell mediated
chemical agents-noxious stuff or too much good stuff
physical agents-trauma, radiation, etc.
18
Q
what is the prototype for cell injury?
A
hypoxia
19
Q
mechanisms of hypoxia
A
- ischemia
- hypoxemia
- failure of oxidative phosphorylation
20
Q
ischemia
A
ischemic hypoxia
lack of arterial blood flow (arterial occlusion, venous occlusion)
pump failure
21
Q
hypoxemia
A
hypoxic hypoxia
failure to ventilate or perfuse the lungs
failure of lungs to oxygenate blood
inadequate RBC mass
inability of hemoglobin to carry or release oxygen
22
Q
failure of oxidative phosphorylation
A
histotoxic hypoxia
cyanide, carbon monoxide, dinitrophenol
23
Q
how do different cells tolerate hypoxia?
A
differently
brain can last 3 minutes without oxygen while leg can last 6 hours
24
Q
which types of hypoxia can be treated?
A
ischemia
hypoxemia
we can supply oxygen ut we cannot make cells use it
25
hypoxic injury
1. lack of O2 stops oxidative phosphorylation/ETC
- Na/K ATPase fails
2. Na and H2O enter cell-acute cellular edema
- early sign of cell injury
3. anaerobic metabolism leads to lactic acid accumulation and pH drop
- denatures proteins
4. Ca ATPase fails
- Ca enters cytoplasm from ECF and ER
- Transition from reversible to irreversible injury
5. Ca entry is key step leading to cell death
6. rigor mortis due to Ca-induced sarcomere shortening
26
Ca entry steps leading to cell death
activates phospholipases that damage membranes
activates proteases that destroy proteins
activates endonucleases that destroy DNA
opens pores in outer mitochondrial membrane
-shuts down oxidative phosphorylation
-mitochondria release free radicals
-mitochondria release capsases that induce apoptosis
27
free radical injury mechanisms
common mechanism of cell injury
| -radiation, poisons, normal metabolism
28
free radical injury cause
unpaired electron in outer (valence) orbital, typicall O2 derivatives
-superoxide (O2), hydroxyl (OH), hydrogen peroxide (H2O2)
29
free radical injury effects
damage cell membranes
cause DNA mutations
aging
30
how to combat limited ability to dispose of free radicals
superoxide dismutase and catalase
| antioxidants-vitamin e, vitamin c
31
chemical injury mechanism
depends on nature of poison
- acids/alkalis destroy membranes
- formalehyde crosslinks proteins and DNA
32
other poison examples
```
cyanide-blocks ETC
mushrooms (toadstools)-destroy ribosomes
chemotherapy-damages DNA
strychnine-motor neuron synapses
carbon monoxide-replaces O2 on hemoglobin, blocks ETC
```
33
cellular accumulations/deposits
can indicate cellular injury or systemic disease
- triglycerides (fatty change, steatosis)
- glycogen
- complex lipids or carbohydrates
- pigments
- calcium
34
what organs do fatty changes involve?
liver
| heart
35
what do fatty changes indicate?
not injurious to cells but marker for injury
36
what are fatty changes linked to?
```
heavy drinking
obesity and metabolic syndrome
-non-alcoholic steatohepatitis (NASH)
malnutrition/hyperalimentation
outdated tetracycline
ileal bypass for weight reduction
```
37
hyperalimentation
feeding by vein
38
fatty change mechanisms
too much free fat coming to the liver
too much fatty acid synthesis by the liver
impaired fatty acid oxidation by liver
excess esterification of fatty acid to triglycerides by liver
too little apoprotein synthesis by liver
failure of lipoprotein secretion by liver
39
glycogen/other lipids or polysaccharides storage diseases
infusions of glucose (dextrose)
inborn errors of metabolism
cannot be broken down, builds back up
40
pigments-carbon
smoke and soot
engulfed by macrophages
lungs-anthracosis
inert, ugly
41
pigments-lipofuscin
```
remnants of intracellular membranes damaged by free radicals
indicator of oxidative stress
wear and tear pigment
inert
seen in hard working organs-liver, heart
```
42
pigments-melanin
present in melanocytes and their tumors (melanomas)
43
eumelanin
protects from UV light
44
pheomelanin
generates free radicals on UV exposure
| redheads
45
albinos
do not produce melanin
46
hyperpigmentation
increased ACTH-increased production of melanin
47
hemochromatosis
do not break down melanin adequately
48
pigments-bilirubin
```
yellow-orange
product of hemoglobin breakdown
conjugated by live and excreted by bile
elevated levels produce jaundice-check nailbeds and sclera
multiple causes
```
49
pigments-jaundice
too many red cells being broken down
-hemolytic processes (sickle cell, thalassemias, pernicious anemia)
liver can't conjugate bilirubin fast enough
50
example conditions that cause jaundice
liver cannot conjugate bilirubin fast enough:
liver disease
newborn "physiologic jaundice of the newborn"
breast feeding (first few weeks)
hereditary defects (Gilbert's non-disease, Crigler-Najjar)
biliary obstruction:
gallstones, pancreatic cancer
51
pigments-calcium
calcium phosphate, calcium hydroxide buildup
52
dystrophic calcification
occurs with normal calcium metabolism
53
examples of normal dystrophic calcification
pineal gland, airway cartilages, mitral valve annulus, aortic valve sinuses-can lead to aortic stenosis
54
examples of abnormal dystrophic calcification
breast cancers, caseous necrosis of TB, surgical scars, pancreatic necrosis-intractable pain, retained abortions-"lithopedion"
55
results of abnormal calcium metabolism
metastatic calcification
- occurs with high calcium and/or phosphate levels
- indicators of disease causing increased ca/phos
56
calcium precipitation-pH gradients
sites of pH gradients make precipitation of ca and phos more likely to occur
small airway walls, gastric fundus epithelium, renal tubular walls
57
necrosis
gross and microscopic changes that indicate cell death
58
types of necrosis
coagulation
liquefactive
caseous
apoptosis
59
coagulation necrosis
usually due to ischemic hypoxia or free radical injury
| death of groups of cells
60
gross characteristics of coagulation necrosis
soft, pale
61
micro characteristics of coagulation necrosis
loss of nuclei but cytoplasm intact
62
coagulation necrosis response
dead cells product acute inflammatory response
| may be replaced by scar, destroyed, walled-off, infected, or even heal
63
liquefaction necrosis
usually due to bacterial infections or poisons or ischemic hypoxia in CNS
death of groups of cells
64
what causes liquefaction necrosis?
hydrolysis via lysosomal or WBC enzymes "pus"
65
gross characteristics of liquefaction necrosis
gelatinous mass or nothing there
66
caseous necrosis
aka saponification (soap formation)
usually due to immune injury in response to certain infections (TB, fungus)
deaths of groups of cells
midpoint between coagulation and liquefaction
67
gross characteristics of caseous necrosis
crumbled, friable devris
| pale, cheesy
68
terms for apoptosis
programmed cell death
cell suicide
physiologic way for cell to die
69
two triggers for apoptosis
mitochondrial damage-leak enzymes called caspases (Ca2 entry can cause this)
death receptor-Fas (CD95) or TNF receptors bind their ligands
70
examples of apoptosis
```
embryologic remodeling of hands
breast shrinkage after lactation period
cells in outer layers of epidermis
neurons that don't synapse
killing of virally-infected cells
```
71
what causes apoptosis?
usually due to immune response or in response of cellular damage
72
what happens with apoptosis?
death of single cell
cell membrane remains intact-no leakage of cell contents
no inflammatory response
remains phagocytized by microphages
73
gangrene
advanced and grossly visible necrosis
74
mostly coagulation gangrene
"dry" gangrene
| usually no infection
75
mostly liquefactive gangrene
"wet" gangrene
foul-smelling
infected
76
types of bacterial gangrene
clostridial "gas" gangrene
trench mouth
fournier's gangrene
77
clostridial gangrene
flesh eating bacteria that produce cell membrane disrupting toxin
78
trench mouth
bacterial gangrene caused by malnutrition
79
fournier's gangrene
scrotal necrosis
80
living cell adaptations
changes in response to stress or injury or lack of normal stimulation
81
what happens if cells are effective with adaptations?
mitigate injurious agent
82
what happens if cells are ineffective with adaptations?
cell death
83
what triggers cell adaptations?
reversible alterations in gene activity
84
atrophy
decrease in cell size may result in decreased organ size
reversible, usually
fewer organelles and decreased function, some may die
85
causes of atrophy
```
loss of motor innervation
decreased blood supply
loss of hormonal stimulation
malnutrition
aging
```
86
examples of atrophy
loss of breast tissue after menopause
loss of muscle mass inside a cast
shrinkage of kidney with arterial disease
87
misnomers of atrophy
not cell loss, but decrease in cell size
88
hypertrophy
increase in cell size, may result in increased organ size
| cells have increased protein synthesis, increased organelles
89
causes of hypertrophy
increased workload
| increased hormonal stimulation
90
examples of hypertrophy
skeletal muscle of strength athlete
heart of obese person
heart of hypertensive person
smooth muscle of uterus in pregnancy
91
misnomers of hypertrophy
BPH
| calluses
92
heart hypertrophy can be _______or ______
physiologic
| pathologic
93
hyperplasia
increase in cell number, may result in increased organ size
generally reversible with stimulatory agent
genetic mutations will not reverse
94
hyperplasia may be _________ or ________
physiologic
| pathologic
95
causes of hyperplasia
compensatory-"growing back"
hormonal stimulation
genetic mutations-risk for cancer
96
examples of hyperplasia
```
female breast at puberty
endometrium during menstrual cycle
lymph nodes close to infection
adrenal cortex under "stress"
bone marrow after blood donation
gingival tissue in people on phenytoin (Dilantin)
```
97
metaplasia
adaptive substitution of one cell type for another
theoretically reversible
often involves epithelium in response to a stimulus
certain metaplasias due to gene mutations-they won't reverse
98
examples of metaplasia
columnar to stratified squamous epithelium in gallbladder with stones
columnar to stratified squamous epithelium in cervix of women with HPV
stratified squamous to columnar epithelium in esophagus of people with chronic reflux (Barrett's)
is it really adaptive?
99
dysplasia
bad growth, atypia, atypical hyperplasia
used in reference to epithelium
loss of cell uniformity and orientation
100
is dysplasia cancer?
no, they resemble cancer cells but are not invasive
101
what causes dysplasia?
genetic mutations that create a growth advantage
102
anaplasia
nuclear changes
103
what promotes dysplastic process?
ongoing epithelial injury promotes dysplastic process
bronchi of smokers
cervix of HPV-infected women
reflux of acid into esophagus
104
what is really ugly anaplasia
carcinoma in situ
105
what happens with bizarre cells obtain blood supply?
form a mass, neoplasia
106
neoplasia
new growth
107
what do anaplasia cells look like and what are they capable of?
ugly cells; can be:
1. dysplasia-confined to an epithelium OR
2. cancer-invading
108
what is dysplasia in terms of types of cells?
precancerous anaplastic cells confined to an epithelium and not invading, not neoplasm
109
what is neoplasm with anaplasia?
malignant (cancer)
| will invade and spread
110
what if neoplasm does not exhibit anaplasia?
it is benign, not cancer
| may compress surrounding structures but will not invade or spread
111
what mediates atrophy, hypertrophy, hyperplasia and metaplasia?
normal growth and differentiation genes
| proto-oncogenes
112
proto-oncogenes
normal gene
113
what mediates dysplasia and cancer?
same growth and differentiation genes that now function abnormally
oncogenes
114
oncogenes
loss of cell regulation
