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1.2.5. Pathological Processes > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What can cause cell injury?

A 
Hypoxia. 
Toxins. 
Physical agents: trauma, temp, pressure, electricity. 
Radiation. 
Microorganisms. 
Immune. 
Deficiencies.
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2
Q

What is the difference between hypoxia and ischemia?

A

Hypoxia = decreased oxygen.

Ischemia = decreased blood supply

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3
Q

Outline the 4 types of hypoxia

A

Hypoxaemia hypoxia = O2 arterial content low.

Anaemic hypoxia = decreased Hb ability to carry O2.

Ischaemic hypoxia = interrupted blood supply.

Histiocytic hypoxia = inability to utilise O2 due to disabled oxidative phosphorylation enzymes

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4
Q

Explain how the immune system can damage body cells?

A

Hypersensitivity = secondary injury to vigorous immune reaction.

Autoimmune reaction = fail to distinguish self

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5
Q

Which cell components are most susceptible to injury?

A

Cell membranes nucleus,
proteins,
mitochondria

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6
Q

What happens at a molecular level during hypoxia

A

Lower O2 = lower oxidative phosphorylation = lower ATP

1) failure of Na K ATPase pump = ion gradient lost = ions pour in = cell swelling.
2) raised glycolysis = lower pH.
3) lower protein synthesis = lipid deposition

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7
Q

Outline what occurs in prolonged hypoxia

A

Irreversible = massive influx of Ca2+ = activation of phospholipase, proteases, endonucleases

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8
Q

Explain what free radicals are and how they cause damage

A

Single unpaired electron in an outer orbit = unstable configuration that will react with other molecules

mutagenic = carcinogenic, lipid peroxidation, autocatalytic chain reaction

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9
Q

Name the 3 free radicals that are of particular biological significance in cells

A

OH (hydroxyl),

O2- (superoxide),

H2O2 (hydrogen peroxide)

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10
Q

How are radicals produced?

A

Oxidative phosphorylation, inflam, radiation, contact with unbound metals, drugs/chemicals

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11
Q

How does the body control free radicals

A

A, C, E vits donate electrons, metal carrier/storage proteins sequester iron/copper, enzymes neutralise

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12
Q

What are heat shock proteins?

A

Aim to mend mis-folded proteins

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13
Q

Describe the 3 ways injured/dying cells look like under a microscope

A

Pyknosis = irreversible condensation of nucleus chromatin

karyorrhexis = fragmentation of nucleus with chromatin distributed irregularly throughout cytoplasm.

karyolysis = dissolution of a cell nucleus

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14
Q

Describe what injured/dying cells look like under an electron microscope

A

Can now visualise organelles: irreversible =

myelin figures (damaged cell membrane collection of fat), 
lysis of ER, 
mitochondrial swelling, 
rupture of lysosomes, 
nucleus pyknosis, 
karyolysis or karyorrhexis
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15
Q

How can we diagnose cell death?

A

Testing cell function with uptake of dye, if alive = no dye due to impermeable cell membrane

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16
Q

Define apoptosis, necrosis and oncosis

A

Apoptosis = controlled cell death non-random DNA cleavage.

Necrosis = morphologic changes that occur after a cell has been dead for a period of time.

Oncosis = cell death with swelling, DNA cleaved in random lengths

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17
Q

What are the types of necrosis?

A

Coagulative: solid organs, protein denaturation.

Liquefactive: loose tissue, enzyme release = liquefaction of tissue.

Caseous: infections, structureless debris (cheese look).

fat necrosis: action upon fat by digestive enzymes, appear as white chalky deposits

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18
Q

Define gangrene

A

Necrosis visible to the naked eye

19
Q

Define infarction

A

Necrosis caused by reduction in arterial blood flow

20
Q

Define infarct

A

Area of necrotic tissue as a result of low arterial blood supply

21
Q

What is the difference between wet and dry necrosis?

A

Dry = necrosis modified by exposure to air (coagulative necrosis).

Wet = necrosis by infection (liquefactive necrosis) (can be wet gas gangrene: presence of anaerobic bacteria that prod gas)

22
Q

What are the causes of an infraction?

A

Thrombosis, embolism, blood supply twisting: sigmoid colon or spermatic cord

23
Q

What is the difference between a thrombus and an embolism?

A

Thrombus: formation of a solid mass of blood within the circulatory system

Embolism: blockage of a blood vessel by solid, liquid or gas at a site distant from its origin

24
Q

How and why does infarcted tissue look different?

A

Can be white = occlusion of end artery in solid tissue.

Red = dual blood supply in loose tissue.

25
Q

Outline ischaemia-reperfusion injury

A

Damage can be worse if blood flow returns to a damaged but not yet necrotic tissue = prod of oxygen radicals, increased neutrophils so increased inflam, delivery of complement proteins

26
Q

When does apoptosis occur physiologically and pathologically?

A

Maintain a steady state, embryogenesis, cytotoxic T cells killing virus infected/neoplastic cells, damaged cells, GvsH disease

27
Q

Name the 3 stages of apoptosis

A

Initiation: activate caspases,

execution,

degradation and phagocytosis

28
Q

How is the intrinsic and extrinsic pathway resulting in apoptosis activated?

A

Intrinsic = p53, cytochrome C (released from mitochondria = activation of caspases).

Extrinsic = TNFα (secreted by T killer cells)

29
Q

What can accumulate in a cell?

A 
Water, 
electrolytes, 
lipids, 
carbs, 
proteins, 
pigments
30
Q

When do lipids accumulate?

A

= steatosis

Alcohol, DM, obesity, toxins, when cholesterol cannot be eliminated by the liver

31
Q

In what conditions do proteins accumulate in cells?

A

Alcoholic liver disease,

alpha1-antitrypsin def = accum in ER, not folded correctly

32
Q

When do pigments accum in cells?

A

Exogenous = Urban air pollutant and tattooing - phagocytosed by macrophages.

Endogenous = haemosiderin, bilirubin

33
Q

Name an example of an accumulation of endogenous pigments?

A

Hereditary haemochromatosis: genetically inherited, increased absorption = accum of iron, often associated with liver/pancreas scarring

34
Q

What is accumulating in jaundice?

A

Bilirubin – breakdown prod of haem

35
Q

Outline the mechanisms of intracellular accumulation

A

Abnormal met, alteration in protein folding/transport, enzyme def, inability to degrade phagocytosed particles

36
Q

What are 2 the classification of calcified tissue?

A

Dystrophic: localised (abnormal Ca met/conc).

Metastatic: generalised (hypercalcaemia secondary to disturbances in Ca met)

37
Q

What causes hypercalcaemia?

A

Increase PTH: primary = parathyroid hyperplasia/tumour, secondary = renal failure, ectopic = secretion of PTH-related protein by malignant tumours.

Destruction of bone tissue: tumours, paget’s diseases (increased bone turnover), immobilisation

38
Q

What are the effects and lab diagnosis of excessive alcohol intake?

A

effects = liver cirrhosis, failure

lab = AST, ALT, CRP, GGTP

39
Q

What is the presentation and lab diagnosis of Hep B?

A

pres = jaundice, fatigue, abdo pain, nausea/vomiting

lab = serology, AST, ALT, LDH

40
Q

What is the lab diagnosis of acute pancreatitis

A

lipase, amylase

41
Q

Outline hereditary haemochromotosis

A

genetically inherited, increased absorption = accum of iron, often associated with liver/pancreas scarring

pres = Fatigue, malaise, joint and bone pain, liver cirrhosis

complications = organ damage

treat = bloodletting, desferrioxamine: iron-chelating compound

42
Q

What is alpha-1 antitrypsin def?

A

pathophysiology = liver prod incorrectly folded alpha-1 antitrypsin = accum in ER

pres = shortness of breath, wheezing, chackles

complications = proteases in lung go unchecked = emphysema

43
Q

What is coal-workers pneumoconiosis?

A

Inhaled coal dust builds up, cannot be removed by the body = inflammation, fibrosis, necrosis

pres = cough, dyspnea, lung function impairment

complications = fibrosis, emphysema

1.2.5. Pathological Processes (11 decks)

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