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1. Essential Medical Science > Cell Injury > Flashcards

Cell Injury Flashcards

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1
Q

What is necrosis?

A

Severe cell swelling and rupture. Death of tissue following bioenergy failure and loss of plasma membrane integrity
Includes inflammation and repair

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2
Q

What is apoptosis?

A

Internally controlled cell death, Individual cell deletion in physiological growth control and in disease
Activated or prevented by many stimuli
Increased apoptosis results in excessive cell loss e.g, atrophy

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3
Q

What is oncosis?

A

Pre lethal changes preceding cell death

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4
Q

What can causes cell injury

A

Hypoxia, Physical agents, Temperature, trauma, radiation, Chemical agents, (Drugs etc), Immunologic reactions, Infectious agents, Genetic derangements, Nutritional imbalances

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5
Q

How can trauma cause cell injury?

A

Mechanical disruption of tissue

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6
Q

How can Carbon Monoxide inhalation cause cell injury?

A

Prevents oxygen transport

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7
Q

How can contact with strong acid cause cell injury?

A

Coagulates tissue protein

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8
Q

How can Paracetamol Overdose cause cell injury?

A

Metabolites bind to liver cell protein and lipoproteins

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9
Q

How can Bacterial infections cause cell injury?

A

Toxins and enzymes

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10
Q

How can ionising radiations cause cell injury?

A

Damage to DNA

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11
Q

General Biochemical Mechanisms of cell injury (5)

A

ATP depletions, Oxygen and oxygen derived free radicals, Loss of intercellular calcium homeostasis, Defects in membrane permeability, Irreversible mitochondrial damage

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12
Q

What is reversible cell injury?

A

Cell swelling, pallor, hydropic change, vacuolar degeneration
Decreased ATP = Decreased Na/K pump activity= Inc Na in cell= Inc water in cell (osmosis)= cellular swelling
loss of cell membrane integrity, defects in protein synthesis and DNA damage.

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13
Q

What is irreversible cell injury?

A

Mitochondrial swelling, lysosomes swells, damage to membrane, leakages of enzymes
Membrane damage to lysosomes= leakage of lysosomal enzymes into cytosol=enzymatic cell degradation
Membrane damage to cell membrane= Inc Ca in cell= activates caspaces =(apoptosis )/ activates proteases and other enzymes= enzymatic cell degradation
Membrane damage to mitochondria= Cyt C leakage= activates caspaces= apoptosis

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14
Q

What is Ischaemic/Reperfusion injury

cell injury?

A

New damage on reperfusion mediated by free oxygen radicals

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15
Q

Cellular swelling- necrosis/apoptosis

A

Necrosis

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16
Q

cellular shrinkage necrosis/apoptosis

A

Apoptosis

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17
Q

many cells affected -necrosis/apoptosis

A

Necrosis

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18
Q

once cell affected- necrosis/apoptosis

A

Apoptosis

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19
Q

cell content injected by macrophages necrosis/apoptosis

A

Necrosis

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20
Q

cell contents injected by neighbouring cells necrosis/apoptosis

A

Apoptosis

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21
Q

Inflammation -necrosis/apoptosis

A

Necrosis

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22
Q

No inflammation - necrosis/apoptosis

A

Apoptosis

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23
Q

Loss of membrane integrity- necrosis/apoptosis

A

Necrosis

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24
Q

Apoptotic body formation- necrosis/apoptosis

A

Apoptosis

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25
Q

Cell lysis- necrosis/apoptosis

A

Necrosis

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26
Q

Membrane blebbing but integrity maintained- necrosis/apoptosis

A

Apoptosis

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27
Q

Random degradation of DNA- necrosis/apoptosis

A

Necrosis

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28
Q

chromatin condensation and non-random DNA degradation- necrosis/apoptosis

A

Apoptosis

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29
Q

Mitochondria release pro-apoptotic proteins- necrosis/apoptosis

A

Apoptosis

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30
Q

Organelle swelling and lysosomal leakage- necrosis/apoptosis

A

Necrosis

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31
Q

Caspaces activation- necrosis/apoptosis

A

Apoptosis

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32
Q

What is autophagy?

A

Cell death: increased quantity of autophagosomes- allow recycling of cellular components, Atg-Autophagy related gene protein involved. No inflammatory response created.

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33
Q

What Is Coagulative Necrosis?

A

Commonest form, Occurs in most organs, Cells retain their outlines, Protein coagulate and no proteolysis occurs. Architecture preserved, loss of proteins and enzymes so metabolic activity ceases. Seen in Mi

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34
Q

What Is Liquefactive Necrosis?

A

Seen in brain, Due to lack of substantial supporting stroma, Neural tissue may totally liquify. Seen in Bacterial or fungal infection, CNS hypoxia

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35
Q

What Is Gangrenous Necrosis?

A

Putrefaction of the tissue, Cause is mostly infectious/ bacteria., Appear black. i.e. Limb ischaemia
Types: Wet gangrene, (associated with infection) Dry gangrene, Gas gangrene

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36
Q

What Is Fat Necrosis?

A

Causes: Enzymes,Trauma

Loss of architecture and lots of vacuoles are formed.

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37
Q

What Is Fibrinoid Necrosis?

A

Seen in Two conditions: Malignant hypertension (wall of artery are bright pick and with dark neutrophils) and Autoimmune diseases

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38
Q

What Is Caseous Necrosis?

A

Tuberculosis is main cause results in Structureless dead tissue, Amorphous pink material in centre with necrotic debris

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39
Q

What is the Commonest cause of medical admission in under 40s’?

A

Paracetamol/Acetaminophen overdose

48% of all poisoning /10,000 medical adms / year. It is the leading cause of acute liver failure.

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40
Q

Whats the size of the liver?

A

Largest organ in the body (1.2-1.5 kg

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41
Q

Whats the livers blood supply?

A

Dual blood supply from hepatic artery and portal vein –

Therefore much less susceptible to ischaemic injury than most organs

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42
Q

What are Idiosyncratic Hepatotoxins?

A

are rare and unpredictable drug reactions

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43
Q

What areIntrinsic hepatotoxins?

A

Drugs like Paracetamol in high doses cause liver injury in everyone

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44
Q

What are the major and minor routes of paracetamol metabolism?

A

Major safe pathways: Glucuronide/sulphate conjugation then renal excretion
Minor pathway: Via CYP2E1 and CYP1A2 = toxic metabolite NAQPI in safe doses this can conjugate then really be excreted so is safe however if toxic doses of paracetamol>4mg are taken then glutathione is depleted so NAPQI binds to cellular proteins= hepatic necrosisDrug metabolising enzymes are in liver cells
further away from portal tracts – they die by necrosis
therefore liver cells by the portal tract survive.

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45
Q

When does acute liver failure occur?

A

severe hepatocyte necrosis resulting in death of over 50% of liver cells

46
Q

What does liver necrosis result in (5)

A 
Lab tests show inc AST and ALT enzymes
Failure of bilirubin metabolism=jaundice
Failure to synthesise Factors 2,7,9,10=bleeding tendency
Shock=low GFR=hepatorenal syndrome-renal failure
Hepatic encephalopathy(coma) due to failure to detoxify nitrogenous compounds and circulation of excitatory AAs
47
Q

What is the management of Paracetamol overdose?

A 
Activated charcoal (<1hr 150mg/kg), N Acetyl cysteine. 
if severe liver failure only treatment is transplant Continue N Acetyl cysteine, Intubated, sedated, ventilated, Filtration to support kidneys, Only correct clotting if bleeding/insertion of lines, Feeding, Antibiotics and Antifungals, work up for liver transplantation
48
Q

Symptoms of ALD

A

Abdominal pain
Severe: Developing coma, Extreme clotting disturbance, Acidotic, Renal failure , Liver tests markedly disturbed, ALT - (normal < 35 ) - 14,800

49
Q

What is fibrous repair?

A

If the damaged cells cannot regrow or local damage is very severe so the architecture of the tissue is destroyed, healing takes place by the formation of scar tissue (sometimes called fibrous repair).

50
Q

What is the function of acute inflammation?

A

Acute inflammation is the body’s initial response to injury .its main roles are: to clear away the dead tissue, protect against local infection and allow the immune system into the damaged area.

51
Q

What are the two most important factors in determining the outcome of injury?

A

the ability of the cells to replicate, the ability to rebuild complex architectural structures

52
Q

What are Labile cell populations?

A

High normal turnover, Active stem cell population, Excellent regenerative capacity eg Epithelia

53
Q

What are Stable (quiescent) cell populations?

A

Low physiological turnover, Turnover can massively increase if needed, Good regenerative capacity eg liver, renal tubules

54
Q

What are Permanent cell populations?

A

No physiological turnover, Long life cells. No regenerative capacity eg neurons, striated muscle cells

55
Q

What are Stem cells populations?

A

Cells lost through injury or end of normal lifespan of cell are replaced from the stem cell pool present in many labile and stable cell populations. When stem cells undergo mitotic division one of the daughter cells retains stem cell characteristics. The other cell progresses along a differentiation pathway e.g. epidermis. Prolonged self-renewal, Asymmetric replication. Reservoirs present in many adult tissues (‘Adult’ stem cell ‘niches’)
Stem cell pool present in many labile and stable cell populations
Located in specific areas e.g. basal layers of epidermis, bottom of intestinal crypts
Survival of stem cells crucial to regeneration e.g. vulnerable to radiation injury

56
Q

What is healing by regeneration?

A

Restitution of specialised function

57
Q

What is healing by repair?

A

Fibrosis and scarring= Loss of specialised
function. Normal structure cannot be replaced
Healing by non-specialised fibrous tissue (‘Scar’)

58
Q

Architectural considerations for healing

A

Rebuilding of complex architectures limited- eg Glomeruli, lung
Survival of connective tissue framework essential eg cirrhosis

59
Q

What is Complete Restitution?

A

Loss of labile cell population can be completely restored e.g minor skin abrasion
Cells at edge of defect multiply to cover defect. Once these cells cover defect, proliferation stops – contact inhibition. Epidermis is built from base upwards

60
Q

What controls regeneration?

A

Proliferation of stem cell / amplifying cell compartments
Covering of defect, Contact inhibition, Complex control by growth factors, cell-cell and cell-matrix interactions
These mechanisms are lost in neoplasia

61
Q

What happens after a minor skin abrasion?

A

Limited loss of epidermis. Cells at margins proliferate and spread out as a thin sheet across the dermis. Once defect is covered the stimulus for them to proliferate and move is switched off – contact inhibition. Epidermis then grows from base upwards

62
Q

What is organisation?

A

The repair of specialised tissue by formation of a fibrous scar, Basic stereotyped pathological process
Production of granulation tissue (often on scaffold of fibrin) and removal of dead tissue by phagocytosis
Granulation tissue contracts and accumulates collagen, forming a scar
Organisation is a common consequence of pneumonia and infarction Organised area – firm and puckered

63
Q

What does Granulation tissue contain?

A

New capillary loops, Phagocytic cells (Neutrophils +Macrophages), (Myo)fibroblasts

64
Q

What is granulation tissue?

A

Endothelial cell proliferation, Buds, Canalisation, New vessels then PhagocytesRemove dead / Damaged tissue then Proliferation and migration of myofibroblasts, Synthesise collagen and ECM, Acquire myofibrils and
contractile ability resulting in Wound contraction which is important for reducing volume of tissue for repair – can reduce it by 80%

65
Q

What happens during Maturation of granulation tissue?

A

Vascularity and Cellularity decrease whilst Collagen, ECM, wound strength increases over approx 3mths

66
Q

What is Healing by first intention?

A

Requires a Clean, uninfected surgical wound, Good haemostasis, Edges apposed eg with sutures or staples

67
Q

What are the stages of healing by first intention?

A

If little or no skin lost the edges of the incision are joined by a thin layer of fibrin (red) and this is eventually replaced by a collagen covered by surface epidermis. Coagulated blood forms the scab. Fibrin join should not be disrupted – sticking plaster or sutures help. Epidermis grows over defect. If the wound is gaping, epidermal cells can grow down into defect. These usually stop growing and become reabsorbed but can remain and grow to form a keratin filed cyst – implantation dermoid. The only residual defect is the inability to reconstruct the elastic network within the dermis

68
Q

What is Healing by second intention?

A

Wound edges not apposed, Not a fundamentally different process, More florid granulation tissue reaction (“leaving a wound to granulate”) More extensive scarring

69
Q

What are the stages of healing by second intention?

A

Healing by secondary intention tissue defect is larger. Becomes replaced by granulation tissue which eventually contracts leaving a scar

70
Q

What does Wound strength look like over time?

A

70-80% of original strength by week 12 (when sutures are taken out at day 7 approx 10%)

71
Q

What are local factors inhibiting healing?

A

Infection, Haematoma, Blood supply, Foreign bodies, Mechanical stress

72
Q

What are systemic factors inhibiting healing?

A

Age (Children heal better than adults. elderly usually have co-existant diseases i.e ischemia), Drugs (eg Steroids: immunosuppressive actions, and interfere with formation of granulation tissue), Anaemia, Diabetes
Malnutrition (Protein malnutrition (dietary deficiency or loss) impairs wound healing), Catabolic states
Vitamin C deficiency (Vitamen c involved in collagen synthesis- scurvy leads to problems with wound healing), Trace metal deficiency

73
Q

What is a keloid?

A

Dermal injury is sometimes followed by excessive fibroblast proliferation and collagen production.This is genetically determined – Keloid.

74
Q

What are the stages of a Fracture healing?

A

Haemorrhage around and within the bone - haematoma as bone surrounded by BVs, Haematoma is organised (provides framework/scaffold for repair) , Removal of necrotic fragments, Osteoblasts lay down disorganised woven bone (callus), Remodelling according to mechanical stress, Replacement by more orderly lamellar bone

75
Q

Why does Non-union of fractures occur?

A

Misalignment – slows healing, prevent good functionalr result – increasing risk of degenerative disease in adjacent joints – oesteoarthrisits
Movement – pain and xs callus – preventing or slowing healing
Infection delays healing –risk of chronic oesteomyelitis. More likely in compound fractures when skin is broken
Pathological fractures – primary disease of bone or secondary involement eg metastases. Treatment of underlying pathological conditon may be required before bone will heal

76
Q

What are the stages of healing in the brain?

A

Neurons are terminally differentiated, Supporting tissue is glial cells rather than collagen and fibroblasts etc – these can proliferate, Hence damaged tissue is removed, often leaving cyst Gliosis rather than scarring

77
Q

What Controls healing?

A

Healing is tightly controlled by complex networks of cytokines etc. e.g: EGF and salivary GFs in epidermis, Demis: IGF1/2 and somatomedins, MMPs from Bvs. BVs: PDGF and TGF-B

78
Q

Were does Epidermal growth factor a come from? What is its function?

A

From: Platelets, macrophages, saliva, plasma
Function: Mitogenic for keratinocytes and fibroblasts. Stimulates granulation tissue formation

79
Q

Were does Transforming growth factor b (TGFb) come from? What is its function?

A

From:Platelets, T lymphocytes, macrophages, endothelial cells, keratinocytes, smooth muscle cells, fibroblasts
Function:Chemotactic for PMNs, macrophages, lymphocytes, fibroblasts, and smooth muscle cells; stimulates TIMP synthesis, angiogenesis, and fibroplasia; inhibits production of MMPs and keratinocyte proliferation

80
Q

Were does Platelet-derived growth factor (PDGF) come from? What is its function?

A

From: Platelets, macrophages, endothelial cells, keratinocytes, smooth muscle cells
Function: Chemotactic for PMNs, macrophages, fibroblasts, and smooth muscle cells; activates PMNs, macrophages, and fibroblasts; mitogenic for fibroblasts, endothelial cells, and smooth muscle cells; stimulates production of MMPs, fibronectin, and HA; stimulates angiogenesis

81
Q

Were does Keratinocyte growth factor (KGF) come from? What is its function?

A

From: Fibroblasts
Function:Stimulates keratinocyte migration, proliferation, and differentiation

82
Q

Were does Tumor necrosis factor (TNF) come from? What is its function?

A

From: Macrophages, mast cells, T lymphocytes
Function: Activates macrophages; regulates other cytokines; multiple functions

83
Q

Were does Vascular endothelial cell growth factor (VEGF) come from? What is its function?

A

From: Many types of cells
Function: Increases vascular permeability; mitogenic for endothelial cells

84
Q

Were does Transforming growth factor a (TGFa) come from? What is its function?

A

From: Macrophages, T lymphocytes, keratinocytes, and many tissues
Function: Similar to EGF; stimulates replication of hepatocytes and most epithelial cells

85
Q

What is an ulcer?

A

It is a local defect, or excavation of the surface of an organ or tissue that is produced by sloughing of inflammatory necrotic tissue. loss of area of epidermis and dermis to produce a defect, even down to fat, muscle, tendons and bone

86
Q

What is an erosion?

A

loss of area of epidermis

87
Q

What are the causes of ulcers?

A

Vascular 90% (Venous 70%, Arterial 10%, Mixed 10%)

Others 10%

88
Q

What are rare causes of ulcers?

A

Inflammatory – pyoderma gangrenosum, panniculitis
Neuropathic – peripheral neuropathy
Malignant – SCC, BCC, lymphoma
Vascular – vasculitis, occlusive disease
Iatrogenic – pressure sores, drugs (hydroxyurea, warfarin necrosis)
Infection – bacterial, fungal
Metabolic – diabetes mellitus, calcinosis cutis
Traumatic(accidental/self induced), Burns (chemical,electrical,thermal,radiation)

89
Q

Venous leg ulcers- Epidemiology

A

Middle aged to elderly women, 5% of population

70% recurrent

90
Q

Venous leg ulcers- Risk factors

A

valvular incompetence, previous damage to venous system eg DVT, obesity,immobility

91
Q

How does venous hypertension occur?

A

Fibrosis = decreased ankle movement = decreased m pump= venous hypertension = inc tissue perfusion=inc oedema= fibrosis cycle .
Venous hypertension also affects the capillaries leading to skin hypoxia. (can also occur due to arteriole fibrosis which can also lead to polypoid hypertrophy due to lymph obstruction)

92
Q

What type of things would you expect to see in a history of those with venous leg ulcers?

A

Varicose veins , History of leg swelling , History of blood clots in deep veins, i.e. deep vein thrombosis (DVT) causing post-thrombotic syndrome (in 5% of cases) , Sitting or standing for long periods , End of day throbbing and aching in the calf muscles , High blood pressure , Multiple pregnancies , Previous surgery, Fractures or injuries , Obesity , Increasing age and immobility

93
Q

What would an examination of those with venous leg ulcers?

A

Medial gaiter area, Relatively painless, Superficial
Associated signs of chronic venous hypertension
Venous duplex scan to diagnose- may need to treat with compression stockings.

94
Q

What are associated signs of chronic venous hypertension? (5)

A

Venous flare, Lipodermatosclerosis, Varicose veins, Varicose eczema, Atrophie blanche.

95
Q

Arterial leg ulcers- Risk factors

A

Diabetes , Smoking, High blood lipids, High blood pressure, History of heart disease, cerebrovascular disease or peripheral vascular disease, Renal failure, Obesity, Rheumatoid arthritis, Clotting and circulation disorders

96
Q

Arterial leg ulcers-History

A

Intermittent claudication, Rest pain or paraesthesia, Pain at ulcer site, Other symptoms of vascular disease e.g angina

97
Q

Arterial leg ulcers- examination

A

Punched out painful ulcer Lower leg/foot, Loss of hair appendages, Dry skin, Nail thickening, Pale or cyanotic(dusky) or pre-gangrenous toes, Cool peripheries, Position dependent ischaemia (pallor if leg raised = Buerger’s sign), Reduction in proximal and or peripheral pulses +/- bruit

98
Q

What are Neuropathic ulcers?

A

Due to distal polyneuropathy (motor/sensory/autonomic), Under metatarsal heads / heel, Painless but warm with pulses

99
Q

What are causes of Neuropathic ulcers?

A

Diabetes. Other causes of polyneuropathy: Alcohol,B1/B12 deficiency, RA,PAN,Charcot Marie Tooth

100
Q

What are Diabetic skin conditions ?

A

Necrobiosis lipoidica, Granuloma annulare, Diabetic dermopathy, Acanthosis nigricans

101
Q

Rare causes of ulcer can result in?

A

Initial pustule, Rapidly breaks down into a very painful rapidly spreading ulcer, Profuse sero-purulent discharge
Base of the ulcer : dark red or dusky in colour.
Margins: Overhanging (undermined) and bluish

102
Q

What is Pyoderma gangrenosum?

A

Vasculitic ulcer, Solitary 50% - no cause identified

Associated with: IBD, RA, Monoclonal gammopathy

103
Q

What are malignancy ulcers?

A

Malignant - rolled edges, Rare, Can occur as a primary malignant lesion or can occur 2° to chronic ulcer
Needs biopsy + excision

104
Q

What are Indications for a biopsy?

A

Clinically atypical ulcer to to exclude or diagnose malignancy

105
Q

Is ulcer healing by primary or second intention?

A

Wounds with tissue loss or wounds with margins not apposed e.g. Ulcer

106
Q

What are the steps of Healing by second intention?

A

Phagocytosis to remove debris, Granulation tissue to fill in defects and repair specialised tissues lost, Organisation, Epithelial regeneration and early fibrous scar, Scar contraction

107
Q

What controls the mechanism of healing and repair?

A

Complex interplay of various cytokines e.g. PDGF, EGF, KGF, VEGF. The same cell produces many cytokines and most cytokines have many functions.

108
Q

What is Ankle brachial pressure indices used for? what values indicate disease?

A

Assess suitability to apply compression. ABPI is defined as: Ratio of systolic blood pressure to occlude dorsalis pedis/posterior tibial pulsation on doppler compared to the systolic pressure of the ipsilateral upper arm
<0.5 significant arterial disease 0.5-0.9 suggest claudication >1.0 non significant arterial disease

109
Q

Management of ulcers:

A

Treat the underlying cause of the ulcer, Treat the ulcer
Treat any associated infections, Avoid trauma to lower legs, Stop smoking, Moderate regular exercise, Avoid obesity, Elevate legs, Treat lower limb oedema & prevent chronic venous hypertension (supportive hosiery
Encourage healing: Dressing choice, Topical treatments

110
Q

How do you Debride necrotic material?

A

Remove slough/dead tissue: Chemical debridement/ Manual debridement/ Surgical debridement/ Larvae (Maggots!) treatment

1. Essential Medical Science (8 decks)

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