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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
Q

What are the two patterns of REVERSIBLE cell injury?

A

Cellular swelling - failed Na+/K+ pump

fatty change- cell accumulation of fat. Impair oxygenation 1. DEC ATP impairs pump -> severe swelling

26
Q

List the causes of reversible cell injury

A

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
Q

List different causes of irreversible cell injury

A

1] Severe membrane injury,

2] Marked mitochondrial dysfunction,

3] Rupture of the lysosomes,

4] Nuclear changes

28
Q

List the different nuclear changes

A

1] Pyknosis-degeneration and condensation of nucleus shrunken and dark

2] Karyorrhexis-nuclear fragmentation

3] Karyolysis-dissolution of the nucleus
Eukaryote- normal nucleaus

29
Q

How can loss of cell membrane be quantified?

A

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
Q

What enzymes indicate hepatitis?

A

transaminases (AST/ALT) tests for liver damage, enzymes that remove a nitrogen group (amines) from proteins to other molecules

31
Q

What enzymes indicate Pancreatitis?

A

Lipase-KEY*** Pancreas makes this only

amylase- mouth Parotid gland

32
Q

What enzymes indicate biliary tract obstruction and bone

A

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
Q

Why does necrosis trigger an immune response but apoptosis does not

A

Necrosis- destroy cellular components, loss of cell integrity, release of substances

Apoptosis-no mass spilling of cellular contents, in nucleus

34
Q

What is the most common form of necrosis and where does it commonly occur?

A

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
Q

What is the difference between ischemia and infarction

A

1st- ischemia lack of blood supply

2nd- infarction tissue death

36
Q

Describe liquefaction necrosis

A

cells spill enzymes that hydrolyze proteins
tissue has a liquid center.
cavitiies in tissue

EX-abscess, brain infarct, lung, liver and pancreatic necrosis

37
Q

Why is draining an abscess painful?

A

liquid stuff is very acidic- liquid in the abscess will destroy whatever ‘cain’ is used

38
Q

What disease is caseous necrosis a characteristic feature of?

A

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
Q

What affect fatty tissue necroseis?

A

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
Q

What occurs with obstruction/injury of pancreatic acini?

A

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
Q

Are fibrinoid in arterioles, capillaries, or venules?

A

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
Q

What is dead tissue caused by thrombosis or lack of blood flow and subsequent contamination with bacteria?

A

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
Q

What is example of dry gangrene?

A

Frostbite- dry gangrene: is coagulative necrosis;

Microscopic pattern of wet gangrene: is liquefactive necrosis and bacterial infection

44
Q

What enzyme is apart of the cascade event for apoptosis?

A

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
Q

What virus can cause apoptosis?

A

hepatitis

46
Q

What are the stimuli for apoptosis

A

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
Q

WHAT ARE physiological examples of apoptosis in embryogenesis

A

organogenesis and development,
webbing of fingers -INACCURATE APOPTOSIS
formation of heart

48
Q

WHAT ARE physiological examples of apoptosis in menstrual cycle

A

hormone dependent

Glandular layer of the endometrium-degenerate and slough off

49
Q

WHAT ARE physiological examples of apoptosis in thymus

A

selective death of lymphocytes
Thymus performs negative selection of T cells.
If T0cells attack your own cells- Apoptosis

50
Q

WHAT ARE how apoptosis is associated with neurodegenerative disease

A

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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