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Path Pro 2023 > Cell Injury And Death 2 > Flashcards

Cell Injury And Death 2 Flashcards

1
Q

Apoptosis charcateristics

A

Programmed cell death
Shrinkage
Regulated intracellular program (activates enzymes that degrade DNA and proteins)
DNA breakdown (cleavage, non random)

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2
Q

Apoptosis steps

A

Condensation
Fragmentation
Apoptic bodies

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3
Q

Physiological apoptosis

A

Maintain steady state
Hormone controlled
Embryogenesis - develop hands structure by cell death in webbed section

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4
Q

Pathological apoptosis

A

Cytotoxic T cell
Virus infected/neoplastic
Damaged with damaged DNA (very pink)

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5
Q

Stages of apoptosis

A

Initiation - intrinsic/extrinsic pathway
Execution - cleave DNA and compartmentalise
Degradation (phagocytosis)
appear eosinphillic

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6
Q

Intrinsic pathway apoptosis

A

Signal comes from within cell
Triggers:
- DNA damage
- Withdrawal of growth factors/hormones
P53 protein activated = leaky Mitochondrial membrane
Cytochrome C released - activates CASPASES

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7
Q

Extrinsic pathway apoptosis

A 
Extracellular signals 
Triggers:
- tumour cells, virus infected cells
TNFa - tumour necrosis factor alpha
- binds to cell membrane (death receptor)
Activates CASPASES
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8
Q

What do intrinsic and extrinsic pathways result in

A

Shrinkage
Formation of apototic bodies
Antigens recognised by phagocytes
Ingested and degraded

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9
Q

Apoptosis vs Necrosis/oncosis

A

Apoptosis

  • single cells
  • Shrinkage
  • nucleus fragmentation into clumps
  • intact plasma membrane & cellular contents
  • no inflammation
  • eliminate unwanted cells

Oncosis/Necrosis

  • groups of cells
  • swelling
  • pyknosis, karryorrhexis, karyolysis of nucleus
  • enzymatic digestion, cell leaks out of cell
  • membrane disrupted
  • INFLAMMATION
  • pathological
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10
Q

Gangrene (wet/gas and dry)

A

Necrosis visible to naked eye

Wet - infection, liquefactive

Dry - exposure to air, coagulative

Gas - infected with anaerobic bacteria (crash/crush injury, bubbles of bacteria)

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11
Q

Infarction

A

Necrosis caused by reduction in arterial blood flow

-can result in gangrene

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12
Q

Infarct

A

Area of necrotic tissue

Loss of arterial blood supply

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13
Q

Causes of infarction and where

A

Reduction of arterial blood supply

  • atherosclerosis
  • occlusion (thrombus/thromboembolism)
  • twisting (testes/bowel)
  • compression

Heart, lungs, brain, kidneys, limbs, GI, testes

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14
Q

Types of infarct

A

White (usually Coagulative) - solid organs

Red (usually Liquefactive) - cerebral

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15
Q

White infarct

A

Solid organs - heart, spleen, kidney
Occlusion of end artery
Wedge shaped
Coagulative

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16
Q

Red infarct

A

Haemorrhagic
Loose tissue - lung/bowel
Dual blood supply
Re-perfusion

17
Q

Complications of infarction

A

None
Death

Depends on:

  • alternative blood supply
  • speed (could another route be made)
  • tissue involved
  • oxygen content of blood (if already anaemic = BAD)
18
Q

Ischaemia-reperfusion injury

A

If blood flow is returned to damaged (not yet necrotic) tissue, damage sustained can be worse

  • production of free radicals
  • lots of neutrophils = more inflammation and more tissue injury
  • complement proteins activate complement pathway
19
Q

Abnormal cellular accumulations examples

A 
caused by: Deranged metabolism
Examples:
Normal cell components 
Abnormal cell components:
- endogenous from dysfunctional metabolism/synthesis 
- exogenous (infections/minerals)
Pigment
20
Q

Why can cellular accumulations occur

A

Abnormal metabolism
Alterations in protein folding and trasnport
Deficient in critical enzymes
Inability to degrade/phagocytoses particles

21
Q

Accumulation of water - oncosis

A

Cellular distress eg hypoxia
Sodium and water enter cell
Droplets
Hydropic swellings

Brain - sulci (grooves) not visible, gyri (raised ridges) enlarged

22
Q

Fatty liver/steatosis

A

Macrovesicular - large lipid droplets

Microvesicular - within hepatocytes

23
Q

Cholesterol accumulation

A

Insoluble
Eliminated via liver
Stored in vesicles
LDL- R abnormality

=

  • atheroslclerosis (LDL oxidised, engulfed by macrophages, foam cells —> plaque)
  • Xanthoma - cholesterol macrophages within tendons
  • Inflammation and necrosis
  • cholesterolosis - cholesterol macrophages in gall badder
24
Q

Accumulation of proteins

A

Eosinophilic in cytoplasm
Extracellular space sometimes (amyloidosis)
Diseases:
- alcoholic liver disease (mallorys hyaline damaged keratin)

  • a1 antitrypsin deficiency
    = liver produces incorrect folded a1 antitrypsin protein (protease inhibitor)
    Cannot be packaged, accumulates within ER
    Proteases in lungs unchecked = emphysema
25
Q

Accumulation of pigment exogenous

A
  • carbon/soot/dust
    Phagocytosed
    Black pigment Within lungs (anthracosis) and surface of lungs
    Drained into lymph nodes
  • tattooing
    Phagocytosis in dermis
    Some pigment reach lymph nodes
26
Q

Accumulation of pigment endogenous

A 
Haemosiderin 
- Iron storage 
- Haemoglobin derived
- yellow/brown 
- local excess = bruise
Hereditary haemochromotatosis/haemolytic anaemia
Billirubin 
- haem broken down
Billiverdin —> billirubin (travels bound to albumin)
Conjugated in liver and excreted in bile
GUT: stercobillingogen = brown faeces
BLOOD STREAM: urobillogen = yellow urine
27
Q

What accumulates as a result of leaky permeable membrane

A

Potassium
Enzymes
Myoglobin
= local inflammation, general toxic effects, aid diagnosis

28
Q

Key enzymes leaked

A

Troponin
AST
CK
Indicate cardiac/liver damage (ALT)

29
Q

Myoglobin leak

A

Dead myocardium and striated muscle
Excessive amounts = rhabdomyolysis
Damages kidneys, blocks renal tubes
Renal failure/injury

30
Q

Pathological accumulation of calcium (localised and generalised)

A

Localised (dystrophic)

  • common
  • not to do with calcium metabolism
  • atherosclerotic plaques, heart valves, ,malignancy)

Generalised (metastatic)

  • due to Hypercalcaemia
  • dysfunction in calcium metabolism
31
Q

Why can metastatic calcification occur

A

Hypercalcaemia
Increased PTH = increase bone resorption
- primary adenoma/tumour (MOST COMMON)
- secondary renal failure
- tertiary ectopic production (squamous cell lung)

Destruction of bone tissue

  • primary tumour of bone marrow
  • skeletal metastases
  • Paget’s disease - accelerated bone turnover
  • Immoblilsation
32
Q

Hypercalcaemia effects

A

BONES, STONES, MOANS, GROANS

  • bone disease
  • renal stones
  • confusion/drowsiness
  • thirst/Polyuria
  • nausea, vomiting, abdominal pain

Path Pro 2023 (21 decks)

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