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GenPath > Cell Injury + Cell Death > Flashcards

Cell Injury + Cell Death Flashcards

1
Q

Examples of physiological hypertrophy

A

Skeletal, cardiac muscle (increased workload)
Uterine smooth muscle (increased estrogenic activity)

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2
Q

Examples of pathological hypertrophy

A

Cardiac muscle hypertrophy due to pressure overload
Arterial smooth muscle hypertrophy due to hypertension
Bowel smooth muscle hypertrophy due to colon obstruction

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3
Q

Examples of hyperplasia

A

Glandular proliferation in breast at puberty
Benign prostatic hyperplasia
Liver regeneration

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4
Q

Hypertrophy is?

A

Increase in cell size

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5
Q

Hyperplasia is?

A

Increase in cell number

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6
Q

Examples of physiological atrophy

A

Thymus involution (shrinking of thymus with age)
Closure of ductus arteriosus and foramen ovale
Brain, muscle atrophy with age

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7
Q

Causes of pathological atrophy

A

Disease
Ischemia
Malnutrition

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8
Q

Examples of pathological atrophy

A

Poliomyelitis causing musclular atrophy
Renal artery stenosis causing affected kidney atrophy due to decreased workload

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9
Q

Types of metaplasia (3)

A

Columnar to Squamous
Squamous to Columnar
Connective tissue metaplasia

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10
Q

Examples of columnar to squamous

A

Smoking, ductal stones

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11
Q

Example of squamous to columnar

A

Barrett esophagus
Esophagus normally lined with nonkeratinising squamous epithlium suited to handle friction from food bolus. Acid reflux from the stomach causes metaplasia to nonciliated, mucin-producing columnar cells, better able to handle the cellular stress of gastric acid.

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12
Q

Connective tissue metaplasia

A

Formation of bone, cartilage or adipose in tissue that does not normally contain them (e.g. myositis ossificans - calcium deposition in muscle during bruise healing causes hard bone like structure within the muscle)

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13
Q

Other examples of metaplasia

A

Squamous metaplasia is common in the transformation zone between ectocervix and endocervix - it can be either physiological: metaplasia as cervix becomes more everted during puberty OR pathological: Cervical Intraepithelial Neoplasia (CIN), and development of cancer

Intestinal metaplasia due to increased gastric acidity (could be due to gastrinoma), H. pylori or bile reflux from small intestine

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14
Q

Causes of cell injury (7)

A

Oxygen deprivation, physical agents, chemical agents, infectious agents, immunlogic reactions, genetic derangements, nutritional imbalances

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15
Q

Mechanisms of cell injury (4)

A

Cell membrane damage
Mitochondrial damage (leading to insufficient aerobic respiration)
Ribosomal damage (leading to altered protein synthesis)
Nuclear damage

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16
Q

Cell membrane damage caused by

A

Complement-mediated lysis by MAC (membrane attack complex)
Bacterial toxins
Free radicals

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17
Q

Mitochondrial damage caused by

A

Hypoxia
Cyanide poisoning

18
Q

Ribosomal damage caused by

A

Alcohol in liver
Antibiotics in bacteria (protein synthesis inhibitors like macrolides/aminoglycosides LOL)

19
Q

Nuclear damage caused by

A

Viruses
Radiation
Free radicals

20
Q

Early changes caused by cell injury

A

*Reversible
Cytoplasmic swelling
Mitochondrial & ER swelling
Chromatin clumping

21
Q

Late changes caused by cell injury

A

*Irreversible
Change in densities of mitochondrial matrix t
Cell membrane disruption
Nuclear shrinking (pyknosis)
Nuclear dissolution (karyolysis)
Nuclear fragmentation (karyorrhexis)
Lysosome rupture

22
Q

Subcellular responses to cell injury

A

Unfolded protein response
Autophagy

23
Q

What is unfolded protein response? And what is the side effect?

A

Increased expression of protective (cell stress/heat shock) proteins including:
Small proteins (molecular chaperones) that protect proteins from further damage
Ubiquitin (cofactor in proteolysis) which tags damaged proteins for removal via proteosome

BUT this may lead to aggregates of ubiquitin and damaged proteins presenting as inclusion bodies such as:
Mallory hyaline bodies in hepatocytes due to alcoholic liver damage
Lewy bodies in neurons in Parkinson’s disease

24
Q

What is autophagy?

A

Cell stress > cell eats its own organelles > atrophy
*this forms residual bodies which may accumulate as lipofuscin

Eliminate abnormal toxic molecules
Allows recycling of molecular components > survival mechanism

25
Q

What is autolysis?

A

Death of cell after death of organism/after cell is surgically removed from the organism
Degraded by post-mortem release of digestive enzymes from lysosomes

26
Q

What is apoptosis?

A

Programmed cell death

27
Q

Examples of physiological apoptosis

A

In embryogenesis: apoptosis of limb buds (precursors to limbs) and organ involution
Immature lymphocytes in lymph organs to prevent autoimmunity
Endometrial cells in menses
Crypt regeneration in GIT

28
Q

Examples of pathological apoptosis

A

Viral infection, such as Hepatitis (hepatocytes) and HIV (CD4 T helper cells)
Atrophy in parenchymal organs due to duct obstruction (e.g. pancreas, kidney, parotid)

29
Q

Loss of apoptosis can lead to

A

Neoplastic lymphoid proliferation - follicular lymphoma, low grade: t(14, 18) and BCL2 gene rearrangement

30
Q

Characteristics of necrosis

A

Always pathological, large number of cells in one area. Death of cells in living tissues characterised by breakdown of cell membrane. Digestion and denaturation of proteins caused by hydrolytic enzymes released from damaged lysosomes.

31
Q

Causes of necrosis

A

Organ/tissue lose function, intracellular enzymes released, initiate inflammation

32
Q

Examples of release intracellular enzymes

A

Cardiac muscle cells - troponin T, creatine kinase (CKMB) after acute myocardial infarction
Hepatocytes - ALT, AST
Skeletal muscle cells - creatine kinase (CKMM)
Pancreatitis - release of pancreatic enzymes causing fat necrosis

33
Q

Types of necrosis (7)

A

Coagulative
Liquefactive
Caseous
Haemorrhagic
Suppurative
Fat
Gangrene

34
Q

Coagulative necrosis?

A

Necrotic tissue remains firm
Secondary to hypoxia (ischemia, infarction) EXCEPT brain
Ghost cell - no nuclei, paler region
E.g. AMI, renal infarct
**RED INFARCTION: when blood re-enters a loosely organised tissue

35
Q

Liquefactive necrosis?

A

Necrotic tissue is liquefied
E.g. cerebral infarct, post-stroke

36
Q

Caseous necrosis?

A

Cheesy
Granuloma (enclosed within distinctive inflammatory border with epithelioid cells, lymphocytes, AFB in langerhan giant cells seen in Ziehl-Neelsen stain)
Typical of tuberculosis

37
Q

Haemorrhagic necrosis?

A

Dual blood supply or secondary to venous congestion
E.g. Volvulus of intestine leading to venous occlusion, congestion of intestinal veins
Chronic obstruction of hepatic portal vein (Budd-Chiari syndrome/hepatic vein thrombosis) or vena cava (heart failure)

38
Q

Suppurative necrosis?

A

Seen in abscess formation - collection of neutrophils and pus
E.g. Occurs in entamoeba histolytica infection (parasite) - trophozoites or amoebiasis can be seen, resemble large foamy histiocytes but with small single round eccentric nucleus and ingested RBCs

39
Q

Fat necrosis?

A

Appears chalky white due to deposition of calcium in a process called saponification (fatty acids join w calcium)
Acute pancreatitis, pancreatic enzymes digest retroperitoneal fat

40
Q

Gangrenous necrosis?

A

Characteristic of lower limb and GIT ischemia

41
Q

Differences between apoptosis and necrosis

A

Apoptosis: membrane preserved, single cell, non-inflammatory, active process
Necrosis: membrane breached, many cells, inflammatory, passive process

42
Q

What is senescence?

A

In germinal cells, telomerase is present, so the length of the telomeres can be maintained (the cell can replicate endlessly)

However, in somatic cells, telomerase is absent, so telomere is shortened with every round of DNA replication and chromosomes become unstable. As the chromosome becomes more unstable, it eventually reaches senescence, a point where apoptosis occurs.

GenPath (5 decks)

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