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SMUSPG-PHY1 > Cell INjury > Flashcards

Cell INjury Flashcards

1
Q

What are a cell’s option when injured?

A

adapt -Reaction to change mediated through housekeeping genes

stay injured- irreversible cell death resulting in necrosis or apoptosis

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2
Q

Describe how cells may adapt to increased work dermands

A

1] Size (atrophy and hypertrophy),
2] Number (hyperplasia),
3] Form (metaplasia)

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3
Q

Is celluar adaptation reversible?

A

YEs, once the stress has been removed;

Some may proceed to malignancy

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4
Q

Is Metaplasia normal?

A

NO
replacement of adult cells change in cell TYPE
MAY first step toward neoplasia.
Respects boundaries of tissue types.

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5
Q

What is abnormal proliferation changes in cell size, shape, and loss of cellular organization,

A

Dysplasia

reversible process if the irritant is removed

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6
Q

What metaplasia and hyperplasia of keratinocytes ?

A

Actinic Keratosis
scaly, patchy skin.
increase in proliferation of keratinocytes
infiltration of inflammatory cells in dermis

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7
Q

Describe cerebral atrophy associated with Alzheimer disease

A

gyri are narrowed and the sulci widened

frontal lobe region.

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8
Q

What causes atrophy?

A

1] Disuse- cast, bed bound
2] “deinnervation”- loss motor neuron, no regeneration
3] Loss of stimulation (endocrine)-testes
4] Malnutrition, 5] Ischemia

Evoluntionary goal- DEC in cell size/activity reduces energy requirements
cell more efficient
Elderly- thin skin less energy there, dispersed other vital organs

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9
Q

Describe atrophy due to loss of stimulation hormone (endocrine)

A

a woman after menopause. Ovaries will shrink.
hormones-provide a trophic effect.

adrenal glands

endogenous steroids.

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10
Q

What causes hypertrophy?

A

Muscle unable to adapt with mitotic division, so gets bigger.
NO adding cells.
physiologic, pathologic or compensatory

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11
Q

How a patient with uncontrolled systemic hypertension can cause hypertrophy of the left ventricle

A

narrow vessel and less BV/BF= INC BP
LV adapts by muscle grows
CO dec, less efficient- less BV from heart
pathologic condition

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12
Q

Describe the process of hyperplasia

A

Epithelia/glands,- capable of mitosis d/t stimulation needs, etc.
Nerve or muscle DO NOT ADD MORE CELLS-NO MITOSIS
Hormonal and compensatory causes activation of genes for cell division

EX-BPH number of prostatic glands, as well as the stroma, increased. NORMAL 3-4CM

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13
Q

How does trauma of smoke affect Metaplasia of laryngeal respiratory epithelium?

A

chronic irritation L/T exchange More resilient squamous epithelium instead of normal pseudostratified ciliated columnar epithelium

Cilia prevents mucus build up and pathogen

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14
Q

What is Barrett’s esophagus?

A

normal esophageal squamous mucosa exchanged to gastric type columnar mucosa.
GERD- L/Tmalignant transformation.
reverse if GERD is managed,

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15
Q

Which is further down the road to cancer? Metaplasia or Dysplasia?

A

Dysplasia

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16
Q

Give examples of endogenous material accumulation

A

Fatty acids in liver in DM-production exceeds removal, genetic enzyme deficiencies

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17
Q

Give examples of Abnormal products material accumulation

A

Tay Sachs – abnormal lipids accumulate in tissues, enzymatic problem L/T lack of cascade so this will accumulate in the cell
Autosomal recessive

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18
Q

Give examples of Exogenous material accumulation

A

Lead, coal dust, Smokers
particles w/in macrophages in their lungs.
not digestible= will accumulate

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19
Q

List the 7 causes of cellular injury

A

1] hypoxia, 2] Infections, 3] Immunologic reactions, 4] Congenital disorders, 5] Chemical injury, 6] Physical injury (mechanical, temperature, radiation), 7] Nutritional imbalance

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20
Q

What is the most common cause of celluar injury?

A

Hypoxia
Lack of oxygen → lack of ATP -> lactic acid buildup

ACIDOSIS- L/T protein/receptors/enzymes degrades

Na/K pump failure= swelling___water follow salt into cell

cell rupture= lysosomal enzyme leaks= enter ECS__to blood vessel…spread, damage metabolic changes

1] ischemia MCC: loss of blood supply D/T arteriosclerosis, thrombus
2] Cardiopulmonary failure,
3] Decreased oxygen carrying capacity-Anemia

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21
Q

What happens with inflammed unbroken skin?

A

Decubitus Ulcer
long term mechanical trauma to skin-reversibility.
Skin broken__extends___undermin___bone__RBC

22
Q

What are the cause cellular injury

A

Hypoxia
Infection
Chemical injury
Physical

immunological reactions- Hypersensitivity or Autoimmune disease

congenital disorders- Defect Enzyme or structural protein,

nutritional imbalanceInadequate calorie/protein/vitamin or Excess calorie

23
Q

What are the 3 mechanisms of cell injury?

A 
1]Peroxidation caused by oxygen-derived free radical, 
Superoxide anion (O2˙-), 
Hydroxyl radical (OH˙)
Hydrogen peroxide (H2O2)- NO WOUND CARE

2] Mitochondrial dysfunction- depleted ATP

3] Increased cell membrane permeability-
1- 2nd messenger calcium influx into cell
2. L/2 enzymatic up-regulation-
proteases ,ATPases, Phospholipases, endonucleases -all break down cellular components

24
Q

What are protective factors against free radicals?

A

gobble up excess electrons
1]Antioxidants- ACE

2] Superoxide dismutase- breaks down superoxide that L/T hydrogen peroxide (H2O2)

3] Glutathione peroxide-hydoxyl radical or hydrogen peroxide → water

4] Catalase-hydrogen peroxide → oxygen and water

25
What are the two patterns of REVERSIBLE cell injury?
Cellular swelling - failed Na+/K+ pump fatty change- cell accumulation of fat. Impair oxygenation 1. DEC ATP impairs pump -> severe swelling
26
List the causes of reversible cell injury
1] Dec. ATP by oxidative phosphorylation, 2] Dec. function of Na/K ATPase pumps, 3] Switch to glycolysis: dec. intracellular pH, 4] Detachment of ribosomes from the RER- NO proteins made, no enzymes, no pumps working
27
List different causes of irreversible cell injury
1] Severe membrane injury, 2] Marked mitochondrial dysfunction, 3] Rupture of the lysosomes, 4] Nuclear changes
28
List the different nuclear changes
1] Pyknosis-degeneration and condensation of nucleus shrunken and dark 2] Karyorrhexis-nuclear fragmentation 3] Karyolysis-dissolution of the nucleus Eukaryote- normal nucleaus
29
How can loss of cell membrane be quantified?
means cell death intracellular enzymes leak out -measurable EX MYOCARDIAL INJURY Markers 1] Creatine phophokinase (CPK), 2] MB isoenzyme (CPKMB), 3] Lactate dehydrogenase (LDH) (prostate CA). elevated for wk 4] Troponin***KEY- 4hr post cell death
30
What enzymes indicate hepatitis?
transaminases (AST/ALT) tests for liver damage, enzymes that remove a nitrogen group (amines) from proteins to other molecules
31
What enzymes indicate Pancreatitis?
Lipase-KEY*** Pancreas makes this only | amylase- mouth Parotid gland
32
What enzymes indicate biliary tract obstruction and bone
Alk Phosp- bone and biliary tract. obstructing stone in the biliary tree- alk phos elevated. RUQ pain-***check liver enzymes and alk phos AP- elevated, biliary tree liver normal
33
Why does necrosis trigger an immune response but apoptosis does not
Necrosis- destroy cellular components, loss of cell integrity, release of substances Apoptosis-no mass spilling of cellular contents, in nucleus
34
What is the most common form of necrosis and where does it commonly occur?
Coagulative- Common : heart, liver, adrenal gland, spleen kidney coagulation and denaturing of proteins in cytoplasm vascular with loss of blood supply- vascular distribution. wedge-shaped with a base of organ capsule.
35
What is the difference between ischemia and infarction
1st- ischemia lack of blood supply | 2nd- infarction tissue death
36
Describe liquefaction necrosis
cells spill enzymes that hydrolyze proteins tissue has a liquid center. cavitiies in tissue EX-abscess, brain infarct, lung, liver and pancreatic necrosis
37
Why is draining an abscess painful?
liquid stuff is very acidic- liquid in the abscess will destroy whatever ‘cain’ is used
38
What disease is caseous necrosis a characteristic feature of?
TB-granulomatous inflammation cheesy tan to white granulomas appearance in lung tissue coagulation + liquefaction areas of cavitation-cystic spaces being formed as the necrotic liquefied debris drains out via the bronchi.
39
What affect fatty tissue necroseis?
lipase FAT tissue death= TG released. Lipase breaks TG to fatty acids: negatively charge attract Ca with positive charge to the area = saponification breast, pancreas, omentum, liver
40
What occurs with obstruction/injury of pancreatic acini?
pancreas makes enzymes to everything we ingest. Lipases, proteases, amylase etc. obstruct pancreatic duct- enzymes spill into the pancreas and digest itself damage fat- production of soaps, soft, chalky white areas
41
Are fibrinoid in arterioles, capillaries, or venules?
NO- walls of small or medium-sized muscular blood vessels Cause- Malignant hypertension, polyarteritis nodosa, and temporal arteritis Assoc-immune-complex vasculitis and hypertension. Fibrin deposit in damaged necrotic vessel walls. tissue damage look like bright pink, fibrin-like quality
42
What is dead tissue caused by thrombosis or lack of blood flow and subsequent contamination with bacteria?
Gangrene necrosis Common sites: lower limbs, gallbladder, GI tract, and testes TX- is revascularization. clear the obstruction, saves the tissue, if not, tissue needs to be removed
43
What is example of dry gangrene?
Frostbite- dry gangrene: is coagulative necrosis; Microscopic pattern of wet gangrene: is liquefactive necrosis and bacterial infection
44
What enzyme is apart of the cascade event for apoptosis?
Programmed cell death- orderly process autodigestion of intracellular components- genetic switch in the nucleus ***caspases- Caspases digest nuclear and cytoplasmic proteins, also activate endonucleases 1] bcl-2 gene-inhibit apoptosis. YOUTH. Turned off w/ apoptosis 2] p53 gene- suppressor gene; stops to repair DNA OR allows IF DNA damage great 3] Bax genes-stimulate apoptosis, ACTIVATED BY P53 4] c-myc genes-w/ p53 apoptosis; w/ bcl-2 inhibits apoptosis
45
What virus can cause apoptosis?
hepatitis
46
What are the stimuli for apoptosis
1] Cell and DNA injury, 2] Lack of hormones (trophic factors), cytokines, or growth factors, 3] Receptor-ligand signals - Ligand like: Fas or TNF, 4] Worn out cells-promotes cell turnover, 5] Cells produced in excess , 6] Cells developed improperly, 7] Cells infected by viruses
47
WHAT ARE physiological examples of apoptosis in embryogenesis
organogenesis and development, webbing of fingers -INACCURATE APOPTOSIS formation of heart
48
WHAT ARE physiological examples of apoptosis in menstrual cycle
hormone dependent | Glandular layer of the endometrium-degenerate and slough off
49
WHAT ARE physiological examples of apoptosis in thymus
selective death of lymphocytes Thymus performs negative selection of T cells. If T0cells attack your own cells- Apoptosis
50
WHAT ARE how apoptosis is associated with neurodegenerative disease
brain - immunologically privileged site. NO an inflammatory process W/ CELL DEATH. THEORY apoptosis or not exactly sure.

SMUSPG-PHY1 (15 decks)

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