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2 - PP > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Define hypoxia

A

Decreased oxygen supply to cells or tissues

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2
Q

Define ischaemia

A

Decreased oxygen supply to cells or tissues due to decreased blood supply

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3
Q

Explain ischaemia reperfusion injury

A

If blood flow is returned to a damaged but not yet necrotic tissue, damage sustained can be worse than if blood flow had not been returned
Caused by increased production of oxygen free radicals with reoxygenation
Increased number of neutrophils resulting in more inflammation and increased tissue injury
Delivery of complement proteins and activation of the complement pathway

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4
Q

State the causes of hypoxia

A

Hypoxaemic hypoxia - arterial content of oxygen is low
Anaemia hypoxia - decreased ability of haemoglobin to carry oxygen
Ischaemic hypoxia - interruption to blood supply (blockage of vessel or heart failure)
Histotoxic hypoxia - inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes

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5
Q

Discuss the causes of cell injury and cell death

A

Hypoxia
Physical agents, e.g., trauma, heat, cold, radiation, changes in pressure, electric currents
Chemical agents and drugs, e.g., poisons, alcohol, therapeutic drugs, toxins
Microorganisms
Immune mechanisms
Hypersensitivity reactions - host tissue is injured secondary to an overly vigorous immune reaction
Latex glove allergy
Autoimmune reactions - immune system fails to distinguish self from non-self
Dietary insufficiency and dietary excess
Genetic abnormalities, e.g., inborn errors of metabolism

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6
Q

What cell components are most susceptible to injury

A

Cell membranes - plasma membrane, organellar membranes
Nucleus - DNA
Proteins - structural, enzymes
Mitochondria - oxidative phosphorylation

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7
Q

What is reversible hypoxic injury

A

Low levels of ATP means the sodium potassium pump stops working
Leads to build up of sodium and water into the cell, leading to cell swelling
Calcium also begins to enter the cytoplasm from outside and ER
Cell relies on anaerobic respiration/glycolysis which decreases pH
Ribosomes fall off of ER so protein synthesis decreases leading to lipid deposition

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8
Q

What is irreversible hypoxic injury

A

In prolonged hypoxia, large increases in calcium in cell activates many pathways include ATPase and phospholipases which attack cell membrane, attack protease which activates destructive enzymes to the cytoskeleton

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9
Q

What are free radicals and state common examples

A

Reactive oxygen species
Single unpaired electron in an outer orbit - unstable configuration hence react with other molecules, often producing further free radicals
OH• (hydroxyl), O2- (superoxide) , H2O2

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10
Q

How are free radicals produced

A

Produced in normal metabolic reactions eg. Oxidative phosphorylation
Kept in mitochondria and locked away
Inflammation - oxidative burst of neutrophils
Radiation - H2O -> OH•
Contact with unbound metals within the body - iron and copper
Free radicals damage occurs in haemachromatosis and Wilson’s disease
Drugs and chemicals - in the liver during metabolism of paracetamol or carbon tetrachloride by P450 system

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11
Q

How are free radicals controlled

A

Anti-oxidant system - donate electrons to the free radical - vitamins A,C and E
Metal carrier and storage proteins sequeste iron and copper
Enzymes that neutralise free radicals

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12
Q

Explain how free radicals can cause cell injury

A

Free radicals injure cells if number of free radicals overwhelm the antioxidant system = oxidative imbalance
Primarily damage lipids in cell membranes
Lipid peroxidation - takes an electron from other molecules and so on, leading to a chain reaction producing further free radicals
Oxidise proteins, carbohydrates and DNA
These molecules become bent, broken or cross-linked
Mutagenic and therefore carcinogenic

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13
Q

Discuss heat shock proteins

A

Heat shock proteins - in cell injury, heat shock response aims to mend misfolded proteins and maintain cell viability
Unfoldases or chaperonins
Eg. Ubiquitin

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14
Q

Discuss the appearance of dead cells under a microscope

A

In hypoxia, cells begin to look pale as they swell when injured
When cells are dead - become pink as proteins become denatured and strongly pick up eosin stain
Under a light microscope - cytoplasmic, nuclear changes, abnormal intracellular accumulations
Under an electron microscope - blebs seen as cell membrane lose strength and become leaky
Eventually, lysosomes and enzymes will rupture and may leave cell (irreversible)

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15
Q

Define oncosis

A

Cell death with swelling, the spectrum of changes that occur in injured cells prior to death

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16
Q

Define necrosis

A

In a living organism the morphologic changes that occur after a cell has been dead some time

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17
Q

Discuss the differences between the four types of necrosis

A

Coagulative - lots of protein denaturation leading to pink clumping of cells
Organ or tissue with lots of solid support - lots of connective tissue
Denaturation of proteins dominates over release of active proteases
Cellular architecture somewhat preserved, creating a ‘ghost outline’ of cells
Liquefactive - enzyme release results in liquid like cells
Organ or tissue with loose tissues - eg. Brain
Or presence of many neutrophils - lots of inflammation
Enzyme degradation is substantially greater than denaturation
Leads to enzymatic digestion of tissue
Caseous necrosis - contains structureless debris but no ghost outline like in coagulation necrosis
Associated with infections, especially tuberculosis
Fat necrosis - pancreatitis - enzymes leak out into abdominal cavity and breakdown triglycerides in cell membrane into fatty acids
Areas of calcification in fat necrosis
Test for serum amylase, lipase and proteases are also released by pancreas

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18
Q

Define apoptosis

A

Cell death with shrinkage, induced by a regulated intracellular program where a cell activates enzymes that degrade its own nuclear DNA and proteins
Programmed cell death

19
Q

Explain when apoptosis occurs physiologically and pathologically

A

Occurs physiologically when in order to maintain a steady state - maintain the size of tissue
Hormone controlled involution
Embryogenesis - when the webbing cells between digits are destroyed (sculpting)
Metamorphosis
Occurs pathologically when virus or tumour cells that are a danger to the body
Occurs when DNA is damaged
Graft versus host disease - own white blood cells are cancerous
Inject bone marrow from donor but may be recognised as foreign

20
Q

Explain the intrinsic and extrinsic pathway of apoptosis

A

Both result in activation of caspases - enzymes that control and mediate apoptosis
Caspase 3 most important in apoptosis
Cause cleavage of DNA and proteins of the cytoskeleton
Chromatin within nucleus begins to breakdown and clumps
Intrinsic - signal from within cell triggers when damage to DNA that cannot be repaired or withdrawal of growth factors needed for survival
P53 protein becomes activated and makes outer mitochondrial membrane leaky
Cytochrome C is released from mitochondria and causes activation of caspases
Extrinsic - initiated by extracellular signals and triggers when cells are a danger eg tumour cells, virus infected cells
One of the signals is TNFα
Secreted by T killer cells
Binds to cell membrane receptors (death receptor)
Results in activation of caspases

21
Q

Discuss the stages of apoptosis

A

Normal cell
Condensation
Fragmentation
Apoptic bodies -
Apoptotic bodies are then phagocytosed
Both intrinsic and extrinsic pathways caused cells to fragment and bud off into apoptotic bodies
Apoptotic bodies express proteins on their surface which are recognized by phagocytes

22
Q

Discuss the differences between apoptosis and necrosis

A

Necrosis occurs for groups of cell, apoptosis targets individual cells
Necrosis leads to swelling, apoptosis leads to shrinking
Necrosis disrupts plasma membrane, apoptosis doesnt
Necrosis causes cellular contents to leak out, apoptosis doesnt
Necrosis causes inflammation, apoptosis doesnt

23
Q

Define gangrene

A

Necrosis visible to the naked eye

24
Q

Distinguish between the 3 types of gangrene

A

Dry gangrene - necrosis modified by exposure to air (coagulative necrosis) eg. Frostbite
Wet gangrene - necrosis modified by infection (liquefactive necrosis)
Gas gangrene - wet gangrene where the infection is with anaerobic bacteria that produce gas

25
Q

Define infarction

A

Necrosis caused by reduction in arterial blood flow

26
Q

Define infarct

A

An area of necrotic tissue caused by reduction in arterial blood supply

27
Q

Distinguish between the two types of infarct

A

White infarcts - solid organs, occlusion of an end artery (sole arterial support for an organ segment)
Eg. heart, kidney, spleen etc
Red infarcts - loose tissue, dual blood supply (lungs), leak from vessels and bleed into area, collateral blood supply (bowel), prior congestion, reperfusion

28
Q

What are examples of molecules leaking out in cell injury

A

Potassium mainly leaks out - burns means potassium moves into tissues and cause cardiac arrest
Enzymes leak out - troponin, CK in myocardial infarction
Myoglobin leaks out and causes renal failure
Happens in massive trauma or dehydration

29
Q

What can accumulate within cells after cell injury

A

Water and electrolytes, lipids, carbohydrates, proteins, pigments

30
Q

When does water accumulate in cells

A

Hydropic swelling
Occurs when energy supplies are cut off
Indicates sever cellular distress
Particular problem in the brain - no where to enlarge meaning key parts of the brain are compressed leading to vessels being narrowed

31
Q

What is steatosis

A

Often seen in liver (hepatic steatosis)
If mild - asymptomatic
Causes - alcohol, diabetes, obesity, toxins
No ATP, ribosomes dislodged
Entire organ swells up and becomes a yellow colour - grease on knife if cut
Becomes heavier

32
Q

Why does cholesterol accumulate in the liver

A

Cannot be broken down and is insoluble
Can only be eliminated through the liver
Excess stored in cell in vesicles
Accumulates in smooth muscle cells and macrophages in atherosclerotic plaques
Present in macrophages in skin and tendons of people with hereditary hyperlipidaemias = xanthomas

33
Q

In what conditions does protein accumulation occur

A

Seen as eosinophilia droplets or aggregations in the cytoplasm
Alcoholic liver disease - Mallory’s hyaline (damaged keratin filaments)
α1-antitrypsin deficiency
Liver produces incorrectly folded α1 antitrypsin protein
Cannot be packaged by ER, accumulates within ER and is not secreted
Systemic deficiency - proteases in lung act unchecked resulting in emphysema

34
Q

When do exogenous pigments accumulate in cells

A

Carbon/coal dust/soot - urban air pollutant
Inhaled and phagocytosis by alveolar macrophages
Anthracosis (accumulation of carbon dust in lungs) and blackened peribronchial lymph nodes
Usually harmless, unless in large amounts = fibrosis and emphysema = coal workers pneumoconiosis
Tattooing - pigments pricked into skin
Phagocytosed by macrophages in dermis and remains there
Some pigment will reach draining lymph node

35
Q

When do endogenous pigments accumulate in cells

A

Haemosiderin - iron storage molecule
Derived from haemoglobin, yellow/brown
Forms when there is a systemic or local excess of iron eg bruise
With systemic overload of iron, haemosiderin is deposited in many organs = haemosiderosis
Seen in haemolytic anaemia, blood transfusions and hereditary haemocrhomatosis
Hereditary haemochromatosis - body takes in more iron than needed in intestines
Iron deposited in skin, liver, pancreas, heart and endocrine organs - often associated with scarring in liver and pancreas
Symptoms include liver damage, heart dysfunction and multiple endocrine failures, especially of the pancreas
Repeatedly take blood from patients to treat

36
Q

How does jaundice accumulate in cells

A

Accumulation of bilirubin - bright yellow
Breakdown product of heme from red blood cells, stacks of broken porphyria rings
Formed in all cells of body but must be eliminated in bile
Taken from tissue by albumin to liver, conjugated with bilirubin and excreted in bile
If bile flow is obstructed or overwhelmed, bilirubin in blood rises and jaundice results
Yellow sclera

37
Q

Discuss the types of pathological calcification

A

Dystrophic - much more common than metastatic
Occurs in an area of dying tissue, atherosclerotic plaques, ageing or damaged heart valves, in tuberculous lymph nodes
No abnormality in calcium metabolism, or serum calcium phosphate concentrations
Local change/disturbance favours nucleation of hydroxyapatite crystals
Can cause organ dysfunction eg. Atherosclerosis, calcified heart valves
Metastatic - disturbance is body-wide
Due to hypercalcaemia secondary to disturbances in calcium metabolism
Hydroxyapatite crystals are deposited in normal tissues throughout the body
Usually asymptomatic but can be lethal

38
Q

What causes hypercalcaemia

A

Increased secretion of parathyroid hormone resulting in bone resorption
Primary - due to parathyroid hyperplasia or tumour
Secondary - due to renal failure and the retention of phosphate
Ectopic - secretion of PTH-related protein by malignant tumours
Destruction of bone tissue
Primary tumours of bone marrow eg. Leukaemia, multiple myeloma
Diffuse skeletal metastases
Paget’s disease of bone - when accelerated bone turnover occurs
Immobilization

39
Q

Discuss cellular ageing

A

As cells age, they accumulate damage to cellular constituents and DNA
After a certain number of divisions, they reach replicative senescence - related to the length of chromosomes
Ends of chromosomes are called telomeres, with every replication the telomere is shortened
When the telomeres reach a critical length, the cell can no longer divide
Germ cells and stem cells contain telomerase enzyme - maintains the original length of telomeres
Many cancer cells produce telomerase and so have the ability to replicate multiple times

40
Q

Discuss the effects on the liver of chronic excessive alcohol intake

A

Fatty change - steatosis (accumulation of fat)
Acute alcoholic hepatitis - inflammation of liver due to excessive alcohol intake
Cirrhosis - impairment of liver leading to scarring and liver failure

41
Q

What is the lab results of acute pancreatitis

A

Increase in serum amylase and serum lipase (acute pancreatitis only)

42
Q

What is haemochromatosis, presentation, complication and treatment

A

Body takes in more iron than needed in intestines
Iron deposited in skin, liver, pancreas, heart and endocrine organs - often associated with scarring in liver and pancreas
Bronzing of the skin
Symptoms include liver damage, heart dysfunction and multiple endocrine failures, especially of the pancreas
Repeatedly take blood from patients to treat

43
Q

What is alpha-1 antitrypsin, pathophysiology, presentation and complication

A

Liver produces incorrectly folded α1 antitrypsin protein
Cannot be packaged by ER, accumulates within ER and is not secreted
Protein accumulation - alpha-1 antitrypsin deactivates enzymes released from neutrophils during inflammation
Systemic deficiency - proteases in lung act unchecked resulting in emphysema
Presents with coughing and wheezing

44
Q

What is coalworker’s pneumoconiosis, presentation and complication

A

Carbon/coal dust/soot - urban air pollutant
Inhaled and phagocytosis by alveolar macrophages
Anthracosis (accumulation of carbon dust in lungs) and blackened peribronchial lymph nodes
Usually harmless, unless in large amounts = fibrosis and emphysema = coal workers pneumoconiosis

2 - PP (15 decks)

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