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Cellular Response To Injury Flashcards

1
Q

What is apoptosis? Describe features and functions of apoptosis.

A
  1. Apoptosis is
    - Programmed cell death to remove unwanted cells
    - Tightly regulated process
    - Occurs with minimal disturbance to surrounding cells
    - Does not elicit inflammatory response
  2. Functions
    - Can be triggered by physiologic or pathological causes
    - Remove degraded and un-needed cells
    - Remove damaged cells
    - Stop excess growth
  3. Features
    - Cell shrinkage
    - Chromatin condensation
    - Intact plasma membrane
    - Apoptotic bodies
    - Phagocytosis of apoptotic bodies
    - Activated caspases
    - No inflammation
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2
Q

What are the causes of apoptosis? List some important stimuli for apoptosis

A
  1. Physiological causes/stimuli
    - Absence of stimulating hormone -> Endometrium during menstruation, prostate
    - Developmental atrophy -> Embryogenesis
    - Cell death post-completion of function -> Neutrophils post-inflammatory response
    - Deletion to maintain constant numbers -> Intestinal epithelium
    - Elimination of potentially harmful self-destructive lymphocytes
  2. Pathological causes/stimuli
    - Accumulation of misfolded proteins -> Neurodegenerative disease
    - Irreparable DNA damage due to radiation, cytotoxic, hypoxia, aging-> Triggered by p53 to avoid malignant transformation
    - Infection -> Hepatitis
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3
Q

Describe the mechanisms that results in apoptosis.

A
  1. Extrinsic/Death-receptor pathway
    - TNF family receptors are activated
    - Cause activation of caspases
  2. Intrinsic/Mitochondrial pathway
    - Tip of balance to favour pro-apoptotic bodies over anti-apoptotic bodies
    - Causes increased mitochondrial permeability
    - Leakage of pro-apoptotic bodies into cytoplasm
    - Activates caspases
  3. Execution phase
    - Intrinsic and extrinsic pathway converges in this phase
    - Activated caspases causes cleavage of cytoskeleton and matrix protein
    - Cleavage of DNA in nuclei
  4. Phagocytosis
    - Apoptotic bodies are phagocytosed prior to inflammation
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4
Q

What is atrophy? What are the causes of atrophy?

A
  1. Atrophy is
    - Decrease in cell size and number leading to
    - Decrease in size of organ or tissue
  2. Causes of atrophy
    A. Physiological
    - Embryogenic -> Thyroglossal duct
    - Reduced hormonal stimulation -> Endometrium post-menopausal
    B. Pathological
    - Decreased workload -> Muscle atrophy after immobilisation in plaster or bed-bound
    - Denervation -> Motor neurone disease
    - Decrease blood supply -> Senile atrophy of brain
    - Decrease nutrition -> Cachexia from malnutrition
    - Pressure -> Tissue compression by tumours
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5
Q

What are the mechanisms of atrophy?

A
  • Decrease protein synthesis due to decrease metabolic activity
  • Increase protein degradation via ubiquitin-proteasome pathway
  • Increase autophagy with increase autophagic vacuoles
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6
Q

Describe the 2 different forms of pathological calcification and give an example of each.

A
  1. Dystrophic calcification
    - Occurs in abnormal/diseased tissue
    - Normal serum Ca levels
    - Eg. Atherosclerosis, sclerotic aortic stenosis, TB calcified nodes
  2. Metastatic calcification
    - Occurs in normal/viable tissue
    - Raised serum Ca levels
    - Eg. Nephrocalcinosis, pulmonary calcinosis, gastric mucosal
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7
Q

Describe the different principal pathological causes of hypercalcemia and give some clinical examples. What are the causes of metastatic calcification?

A
  1. Increased PTH levels
    - Hyperparathyroidism, paraneoplastic syndrome
    - Increased Ca reabsorption from kidneys and absorption from gut
  2. Increased bony destruction
    - Multiple myeloma, skeletal metastasis, Paget’s disease
    - Increase bone breakdown causing increase Ca levels
  3. Vitamin D abnormalities
    - Hypervitaminosis D
  4. Renal failure
    - Secondary hyperparathyroidism due to increase phosphate levels
  5. Idiopathic hypercalcemia
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8
Q

What happens inside cells when they are injured? What are the mechanisms/biochemical features of cell injury?

A
  1. ATP depletion
    - Increased anaerobic glycolysis and lactate production
  2. Mitochondrial damage
    - Increase mitochondrial permeability
  3. Influx of Ca
  4. Accumulation of free radicals
  5. Plasma membrane damage
    - Increase membrane permeability
  6. DNA/protein damage
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9
Q

What is a free radical? What are the pathologic effects of free radicals?

A
  1. Free radicals are
    - Single, unpaired electron
    - Partly reduced, highly unstable, highly reactive species
  2. Pathological effects
    - Overall necrosis or apoptosis of cells by
    - Lipid peroxidation
    - Oxidation of proteins
    - DNA lesions/Breakage of DNA
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10
Q

What is hyperplasia? What are the different type of hyperplasia with examples?

A
  1. Hyperplasia is
    - Increase in number of cells
    - Causing increase in mass or volume of organ or tissue
  2. Types of hyperplasia
    A. Physiological
    - Hormonal -> Breast in puberty and pregnancy
    - Compensatory -> Post-partial hepatectomy, skeletal muscle with increased workload
    B. Pathological
    - Hormonal -> BPH, Endometrium hyperplasia
    - Infection -> Papillomavirus (skin warts)
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11
Q

What are the cellular mechanism of physiological hyperplasia?

A
  1. Increased local production of growth factors
  2. Increased growth factor receptors on cells
  3. Activation of intracellular signalling pathway
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12
Q

What is hypertrophy? What are the types of hypertrophy?

A
  1. Hypertrophy is
    - Increase in cell size leading to
    - Increase in organ or tissue size and synthesis of structural components
    - Triggered by functional demand, growth factors or hormonal stimulation
2. Types of hypertrophy
A. Physiological
- Hormonal -> Uterus in pregnancy
- Functional demand -> Skeletal muscle hypertrophy
B. Pathological
- Cardiomegaly in chronic HTN
- Hormonal -> BPH
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13
Q

What is the difference between hyperplasia and hypertrophy?

A
  1. Hyperplasia
    - Increase in NUMBER of cells
    - Increase in VOLUME or MASS of organ or tissue
    - Occurs if cell is able to synthesize DNA thus permitting mitotic division
  2. Hypertrophy
    - Increase in SIZE of cells
    - Increase in SIZE of organ or tissue
    - Increase in synthesis of structural components
  • Hyperplasia and hypertrophy commonly co-exist
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14
Q

What are the sequence of events that occur in reversible ischaemic cellular injury?

A
  1. Reduce oxidative phosphorylation
    - Reduce ATP production
  2. Failure of Na/K pump
    - Na + H20 influx, K efflux
    - Cell swelling
  3. Ca influx
    - Intracellular release and extracellular influx
  4. Further reduction in ATP production, protein and glycogen synthesis
    - Anaerobic metabolism -> increase lactate and reduce cellular pH
  5. Activation of enzymes
  6. Cytoskeleton changes (Morphology of reversible ischaemic injury)
    - Cell swelling
    - Mitochondrial swelling
    - Blebbing of plasma membrane
    - Chromatin condensation
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15
Q

What are the morphological changes in irreversible cellular injury?

A
  1. Severe mitochondrial swelling
  2. Lysosomal swelling -> Release of lysozymes
  3. Extensive plasma membrane damage -> Myelin figures
  4. Chromatin condensation, fragmentation, dissolution
  5. Cell death by necrosis or apoptosis
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16
Q

Describe reperfusion injury and mechanism causing it

A
  1. Reperfusion injury is
    - Further injury to ischaemic cells after perfusion is restored
  2. Due to
    - Generation of free radicals -> Reactive O2, nitrogen species
    - Activation of inflammatory and complement cascades
17
Q

What is metaplasia and give some examples. What are the possible outcomes of metaplasia?

A
  1. Metaplasia is
    - Reversible change of one differentiated cell type to another
    - Can be adaptive or pathological
  2. Examples
    A. Columnar to squamous cell
    - Respiratory tract -> Chronic smoking irritation, Vitamin A deficiency
    B. Squamous to columnar cell
    - Barrett’s esophagus -> Chronic gastric acid irritation
  3. Outcomes of metaplasia
    - Reversible or resolution
    - Chronic on-going changes
    - Malignant transformation -> Cell losing normal protective function due to persistence of chronic irritation
18
Q

What is the mechanism causing metaplasia?

A
  1. Chronic irritation -> gastric acid, smoking, vitamin A deficiency
  2. Release of cytokines, growth factor and extracellular matrix proteins
  3. Stimulate reprogramming of stem cells
  4. Cause precursor cells to differentiate down new pathway
19
Q

Describe the cellular changes in necrosis.

A
  1. Usually due to irreversible injury
  2. Cell swelling
  3. Chromatin condensation (pyknosis), fragmentation (karyorrhexis), dissolution (karyolysis)
  4. Plasma membrane disrupted
  5. Myelin figures
  6. Leakage of cellular contents
  7. Adjacent inflammation
20
Q

What are the patterns of tissue necrosis?

A
  1. Coagulation necrosis
    - Architecture is preserved
    - Seen in heart (AMI)
  2. Liquefactive necrosis
    - Digestion of tissue -> Liquid viscous mass
    - Seen in brain
  3. Caseous necrosis
    - Friable, cheesy material
    - Seen in tuberculosis
  4. Gangrenous necrosis
    - Coagulative necrosis in limb
  5. Fat necrosis
    - Lipase breakdown of fatty acids
    - Seen in pancreatitis
  6. Fibrinoid necrosis
    - Antibody-antigen immune complex deposition
    - Seen in vascular arteritis
21
Q

What are the morphological and chemical changes associated with early/reversible cell injury?

A
  1. Decreased production of ATP
  2. Cell membrane damage
  3. Mitochondrial damage
  4. Defects in protein synthesis
  5. Cytoskeleton damage
  6. DNA damage
22
Q

What are the phenomena that characterise irreversible cell injury?

A
  1. Severe mitochondrial damage/dysfunction
    - Reduce in oxidative phosphorylation
    - Reduce ATP generation
  2. Extensive membrane damage and function
23
Q

Can you given an example of a protein that leaks across degraded cell membranes.

A
  1. Cardiac muscle leaks
    - Enzyme creatine kinase and troponin
  2. Liver and bile duct epithelium leaks
    - Alkaline phosphatase
  3. Hepatocytes leak
    - Transaminases
  4. Pancreas leaks
    - Lipase and amylase
24
Q

What is steatosis? Which organs are commonly involved in steatosis? What are the causes of hepatic steatosis?

A
  1. Steatosis is the abnormal accumulation of triglycerides in cells
  2. Organs involved
    - Liver
    - Cardiac
    - Kidney
    - Skeletal muscle
  3. Causes of hepatic steatosis
    - Alcohol abuse
    - Toxins or drugs
    - Obesity
    - Diabetes mellitus

Pathology (17 decks)

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