chapter 2 Flashcards
(41 cards)
Cell injury =
how can they die?
EX:
anything that disrupts cell structures/ deprives cell of o2 and nutrients..
reverses
irrevereses if this cells die
ex: ischemia-hypoxia, during MI lack of 02 injures myocard cells
Cell adaption =
reversible structural/ functional response to physiologic (normal) and pathologic (adverse) conditions. and still remain in a steady state.
Cell injury/ adaption are the same how?
Both are reversible.
Atrophy is?
physiologic(normal) happens?
Pathologic(adverse) happens?
3 FUCKING EXAMPLES
= decrease in size/ work = happens w. EARLY development. (THYMUS PUBERTY) = happens w. DECREASE in workload. (- UBIQUIT BY MALNUTRITION - PROTEIN DEGEN IN PROTEASOMS - PROTEIN SYN DECREASE
Hypertrophy is?
Physiologic(normal) happens?EX?
Pathologic(adverse) happens?EX?
= increase in size/ work demand or hormones.
= strength training (PREG HORMONE INDUCED UTERINE, MECH: STRENGTH, TROPIC: GROWTH, VASOACTIVE)
= hemodynamic overloads (HYPERTENSION = HEART DYSFUNCTIONS)
Hyperplasia is?
```
Physiologic(normal) happens?(2
EX:(2))
Pathologic(adverse) happens?
(1)
(EX(1))
~~~
= increase in cell #
= 1. Compensatory: allows organs to regenerate normal process.
(EX: LIVER REMOVAL, HYPERPLSIA OF LIVER COMPENSATES FOR LOSS.
- WOUND HEALING INFLAM. PROCESS)
2. Hormonal: replaces lost tissue/ supports new growth.
EX:ENDOMETRIUM;INCREASE ESTRO VS PROGESTRO
= Excessive hormonal/ growth factor stimulation. Produces an abnormal proliferation of normal cells.
Dysplasia is?
PRECURER OF? UNLESS?
- abnormal changes in size, shape, organization of cells
it’s not a true cell adaptation. - AKA atypical hyperplasia (atypical increase in cell number)
PRECURCES OF CANCER, UNLESS EFFECTS BASEMENT THEN CANCER(NEOPLASM).
Metaplasia is? Involved in? EX: (2) 1. 2. SOMETHING DAMAGES SOMETHING
- reversible replacement of 1 mature cell type by another less differentiated mature cell.
involved in: tissue repair, damage, regenerating.
EX:
SMOKING; CILLIATED COLUMNAR -> SQUAMOUS.
GASTRIC REFLUX DAMAGES SQUAMOUS
The conditions that allow cellular adaption to occur?
- ?
- 4 types?
- The adaptation may be physiologic (normal) or pathologic (abnormal).
- Four types:
atrophy, hypertrophy, hyperplasia, metaplasia.
Ischemia-hypoxia =
Def?
Ex?
- when you have ischemic aka lack of bld flow you have hypoxia aka lack of O2.
- EX: Ischemia aka low blood flow; atherosclerosis(plaque build up in arteries) and thrombosis(attacks plaque in artery in heat) AKA clot formation, no blood flow aka ischemia
ischemia-reperfusion=
- Def:
- ischemia-reperfusion Injury Due To?
- More?
- what causes damage where?
- overload of what?
- opens what?
- whats escaping?
- whats activating?
- Blood flow and o2 restores.
- More oxidative stress
- (ROS) that cause membrane damage and mitochondrial Ca+ overload.
- Opens mitochondrial permeability transition pore with ATP escaping and apoptosis activating,
ischemia-reperfusion is impt but come with?
their own injuries.
Ischemia-reperfusion types of injury in?
6
- myocardial,
- hepatic,
- intestinal,
- cerebral,
- renal,
- stroke
Free radicals are?
SINGLE unpaired electron outer orbits,
making it capable of inducing injury,
initiating chain rxn.
ROS are?
chemically reactive molecules formed are :natural oxidant species in enzymes/organelle
ROS largest source is?
mitochondrial oxidative phosphorylation..(MITO IS THE LARGEST SOURSE
Explain in detail how ROS’s largest source
Mito oxidative phosphorylation:
-o2 reduced to water in oxidative phosphorylation.
- So because of electron leakage.
- o2 creates REGENERATIVE ROS like hydrogen peroxide.
so a bunch of ROS in just regular ass mito.
Perioxisomes generate ROS how?
- metabolizes long fatty acids
- ER stressed
- lots proteins produced
- lots of protein folds
- leads to ROS
Enzyme systems that can generate ROS:
- cyclooxygenase system
- cytochrome P450,
- nitric oxide synthase systems.
Enzyme systems that can generate ROS:
nitric oxide synthase EXPLAINED??
Catalyzes the synthesis of nitric oxide FROM l-arginine
-Its a powerful vasodilator increasing blood flow to organs in process called flow-mediated vasodilation
Main Roles of ROS in Cell Injury?
- CAN produce in that reperfusion injury.
- Free radicals can be removed
- accumulate in cells either because of insufficient removal or excess production and lead to cellular injuries
Identify Cellular accumulations of cellular injury?( things that can go wrong in cell that can cause cell injury)
(8) list and describe
- water accum =
Loss of ATP production/ Na+/K+ pump = swell.
2. Lipid accum = fatty liver (alcoholism, obesity, type2 diabetic)
- Glycogen (carbs)accum =
a lot of vacuoles form in cytoplasm/ Glycogen storage diseases (RARE) - Proteins accum = renal convoluted tubule of the nephron and in the antibody-forming-> B lymphocytes.
- Pigments: Melanin, hemoproteins (iron overload), bilirubin (jaundice)
- Ca+: calcium salts clump/ harden, interfering with normal cell structure/ function
- Urate: too much uric acid = gout.
Identify SYSTEMIC accumulations of cellular injury?( how injuries effect systems)
(8)
- Fatigue/ malaise
- Fever
- Loss of well-being
- Appetite changes
- Increase heart rate
- increase wbc
- Pain
- Cell enzymes in extracellular fluid:
LDH, CK, others elevated in blood = biochem markers of cellular injury.
Coagulative necrosis
in?
does?
stuc change =
- In: kidneys, heart, adrenal glands.
- Does: Protein denaturation they’re unfolding losing 3d shape losing function.
(So Changes protein albumin from gelatinous and transparent to firm and opaque) - Structural change = functional change.
