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MoD > Lesson 1 > Flashcards

Lesson 1 Flashcards

1
Q

What are causes of cell injury?

A 
Hypoxia
Chemical agents and drugs
Infections 
Immune-mediated process
Nutritional imbalance
Genetic derangement 
Physical agents
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2
Q

What are four main types of hypoxia?

A

Hypoxaemic
Anaemic
Ischaemic
Histiocytic

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3
Q

What is hypoxaemic hypoxia?

A

Low arterial O2 content t e.g. cardiorespiratory failure or in reduced inspired O2 at high altitudes

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4
Q

What is anaemic hypoxia?

A

Decreased O2 carrying capacity in blood e.g. anaemia or CO poisoning

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5
Q

What is ischaemic hypoxia?

A

Interruption to blood supply e.g. blocked vessel or heart failure

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6
Q

What is histiocytic hypoxia?

A

unable to use O2 due to disabled oxidative phosphorylation enzymes e.g. cyanide or paracetamol poisoning

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7
Q

What are some chemical agents and/or drugs that can cause cell injury?

A

Oxygen in high/low conc.
Glucose and salt in hypertonic concentrations
Trace amounts of poisons: cyanide and arsenic
Daily exposures: air and environmental pollutants, insecticides and asbestos
Drugs: recreational (alcohol) and therapeutic drugs

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8
Q

What are some immune mediated processes that can cause cell injury?

A
  • Reaction to endogenous self antigens (autoimmune disease)

- Hypersensitivity reaction as a result of vigorous immune reaction results in host tissue damage (utricaria and hives)

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9
Q

What are some nutritional imbalances that can cause cell injury?

A 
•Dietary insufficiency
	‒Malnourished states in deprived populations
	-self imposed insufficiency (anorexia nervosa)
•Dietary excess 
	‒Obesity
	‒Diabetes 
	‒Atherosclerosis 
	‒Cancer
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10
Q

What are some physical agents that can cause cell injury?

A
  • Mechanical trauma
  • Extremes of temperature (burns and deep cold) •Sudden change in atmospheric pressure
  • Radiation
  • Electric shock
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11
Q

What are examples of free radicals (that are of biological significance)?

A

• OH• (hydroxyl ions) -the most dangerous
• O2- (superoxide anion radical)
• H2O2 (hydrogen peroxide)
• Reactive oxygen species (ROS)
• Nitric oxide (NO) made by microphages, endothelia, and
neurones

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12
Q

What is the purpose of biological free radicals (in low conc. in normal state)?

A

Required for; killing bacteria, cell signaling, attack lipids in cell membranes, damages proteins, carbohydrates and nucleic acids

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13
Q

What are some causes of free radical production?

A
  • Chemical and radiation injury
  • Ischaemia – reperfusion injury
  • Cellular ageing
  • High oxygen concentrations
  • Killing of pathogens by phagocytes (ROS)
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14
Q

What are some ultra structural changes that are responsible for morphological changes?

A
  • Cell Membranes – plasma membrane and organelle membranes
  • Nucleus - DNA
  • Proteins – structural (enzymes)
  • Mitochondria – oxidative phosphorylation
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15
Q

How is ATP produced?

A
  • produced in mitochondria via oxidative phosphorylation
  • produced by glycolysis pathway in absence of oxygen from glucose in body fluids or as a result of hydrolysis of glycogen
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16
Q

How can free radicals be produced?

A
  • Chemical and radiation injury
  • Ischaemia – reperfusion injury
  • Cellular ageing
  • High oxygen concentrations
  • Killing of pathogens by phagocytes (ROS)
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17
Q

How do heat proteins (HSP) protect against cell injury?

A
  • heat shock response aims to ‘mend’ misfolded proteins/maintain cell viability.
  • Many HSP’s are Chaperonins – provide optimal conditions for denatured protein folding, preventing protein aggregation, label misfolded proteins for degradation.
  • e.g ubiquitin
18
Q

What are the two main processes seen in necrosis?

A
  1. Desaturation of intracellular proteins
  2. Enzymatic digestion by lysosomes inherent to the dying cell and lysosomes of leukocytes that are part of inflammatory reaction
19
Q

What is an approximate time necrosis may be developing?

A

4-12hr after necrosis onset

20
Q

What are types of necrosis?

A
  1. Coagulative necrosis - protein denaturation
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Fat necrosis
  5. Fibrinoid necrosis
21
Q

Provide information on coagulative necrosis?

A
  • Most common form
  • Occurs in most organs
  • A result of protein denaturation
  • Gross: Firm, pale wedge of tissue, can be soft later on
  • Microscopy – “ Ghost cells”. Neutrophils can infiltrate but NOT a prominent feature
22
Q

Provide information on liquefaction necrosis?

A
  • Usually seen in brain
  • Seen in infections resulting in abscess formation
  • Degradation of tissue by enzymes.
  • Necrotic material - creamy yellow because of dead leukocytes -> pus (NEUTROPHILS)
23
Q

Provide information on caseous necrosis?

A
  • “Cheese like” gross appearance

* Amorphous debris surrounded by histiocytes -> granulomatous inflammation

24
Q

Provide information on fat necrosis?

A
  • Destruction to adipocytes (consequence of trauma) or secondary to release of lipases from damaged pancreatic tissue.
  • Fat necrosis causes fatty acids which react with calcium -> white deposits in fatty tissue
  • Can mimic breast tumour on radiology and is biopsied to exclude cancer.
25
Q

Provide information of fibrinoid necrosis

A
  • Seen in immune reactions involving blood vessels.
  • Deposits of “immune complexes” + fibrin that has leaked out of vessels.
  • Bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists
26
Q

Describe white infarct

A
  • Solid organ- Robust stromal support limits haemorrhage into necrotic area from adjacent capillaries
  • Arterial insufficiency
  • End artery
  • Common site: heart, spleen , kidney
27
Q

Describe red infarct (haemorrhaging infarct)

A
  • Organs with dual blood supply /numerous anastamoses between capillary beds
  • Organs that have loose stromal support
  • Raised venous pressure leading to increased capillary pressure/tissue pressure -> in arterial insufficiency
28
Q

What are three types of gangrene?

A
  • Wet gangrene (necrosis modified by bacteria)
  • Dry gangrene (necrosis modified by air)
  • Gas gangrene (necrosis modified by gas from bacteria)

Clinical term to describe Visible Necrosis

29
Q

Describe apoptosis?

A
  • Energy dependent programmed cell death
  • Characteristic non random internucleosomal cleavage of DNA
  • Distinct morphological features
  • Does not result in an inflammatory response
  • Apoptosis can be physiological or pathological
30
Q

Explain physiological apoptosis

A
  • Embryogenesis and fetal development (loss of webbing as hand develops).
  • Hormone dependent involution e.g. shedding of endometrium at menstruation
  • Cell deletion in proliferating cell populations e.g. regulation of immune system or intestinal crypts
  • Death of cells that have served their function (neutrophils/lymphocytes).
31
Q

Explain pathological apoptosis

A
  • Neoplasia
  • Autoimmune conditions (failure of induction of apoptosis in lymphoid cells directed against host antigens)
  • AIDS - HIV proteins may activate CD4 on uninfected T helper lymphocytes with apoptosis -> immunodepletion
32
Q

What are some ways in which apoptosis can be regulated?

A
  • Genes
  • Inhibitors - growth factors, extracellular cell matrix, sex steroids, some viral proteins
  • Inducers - growth factor withdrawal, loss of extracellular matrix attachment, glucocorticoids, viruses, free radicals, ionising radiation
33
Q

What is the mechanism of apoptosis?

A
  • Activation of a cascade of caspases (cysteine-dependent aspartate-directed proteases)
  • 2 pathways resulting in activated caspase 3 which cleave proteins -> chromatin condensation, nuclear fragmentation, blebbing
  • Extrinsic pathway – external “death receptors” (TNF receptors or Fas receptors) are activated by a ligand
  • Intrinsic pathway – withdrawal of growth factors or hormones causes molecules to be released from mitochondria (e.g. Bcl2, Bax, p53)
  • Apoptotic cell eventually phagocytised by macrophages/histiocytes/neighbouring cells -> no acute inflammation
34
Q

Compare necrosis and apoptosis in relation to their pattern, cell size, nucleus and plasma membrane

A 
Pattern:
	• N - contiguous groups of cells
	• A - single cells
Cell size:
	• N - enlarged (swelling)
	• A - reduced (shrinkage)
Nucleus:
	• N - pyknosis, karyorrhexis, karyolysis
	• A - fragmentation into nucleosome sized fragments 
Plasma membrane:
	• N - disrupted, early lysis 
	• A - intact; altered structure (orientation of lipids)
35
Q

Compare necrosis and apoptosis in relation to their cellular contents, adjacent inflammation and physiologic/pathological role

A

Cellular contents:
• N - enzymatic digestion (may leak out of cell)
• A - intact (may release into apoptotic bodies)
Adjacent inflammation:
• N - frequent
• A - no
Physiologic or pathological role:
• N - invariably pathologic
• A - often physiologic (eliminating unwanted cells), pathologic (some forms of cell injury - DNA damage)

36
Q

What are molecules that are released as a result of cell injury and death?

A
  • Potassium
  • Enzymes
  • Myoglobin
37
Q

What can happen to the body as a result of molecules released as a result of cell injury?

A
  • Can cause local inflammation
  • May have general toxic effects on body
  • May appear in high concentrations in blood and can aid in diagnosis
38
Q

Explain rhabdomyolysis

A

This can be serious without myoglobin as a breakdown product of muscle causing damage to the kidneys/renal failure -> dialysis
Typical brown urine in myoglobinuria

39
Q

What are mechanisms of intracellular accumulations?

A 
• Abnormalmetabolism
• Alterationsinproteinfolding
and transport
• Deficiency of critical enzymes
• Inability to degrade phagocytosed particles
40
Q

What can intracellular accumulations be?

A
  • Water and electrolytes • Lipids
  • Carbohydrates
  • Proteins
  • Pigments
41
Q

What are the names of some disease as a result of endogenous pigments (abnormal accumulations)?

A
  • Haemosiderin
  • Haemosiderosis
  • Hereditary haemochromatosis
  • Bilirubin
42
Q

What is pathological calcification - metastatic?

A
  • Parathyroid overactivity – tumour or hyperplasia
  • Vitamin D overdosage
  • Malignant tumours e.g. breast and lung, bone
  • Paget’s disease •Prolonged immobilisation

MoD (11 decks)

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