Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MOD > 1 Cell injury > Flashcards

1 Cell injury Flashcards

1
Q

3 methods cell injury can be visualised ? what can be visualised ?

A
  1. naked eye - gross appearance
  2. light microscope - microscopic features
  3. electron microscope - ultrastructural features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of cell injury ?

A

PINCHING

Physical agens
Infections
Nutritional imbalance
Chemical agents
Hypoxia
Immune-mediated processes
Neoplasia
Genetic derangement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which hypoxia is to do with cardiorespiratory failure ?

A

hypoxaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which hypoxia is to do with anaemia ?

A

anaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which hypoxia is to do with blocked vessel ?

A

ischaemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which hypoxia is to do with cyanide poisoning ?

A

histiocytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hypoxia may be …. or ….

A

generalised , localised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hypoxia may be generalised or localised, name 4 types of hypoxia …

A
  • Hypoxemic hypoxia = low arterial O2 concentration e.g. cardiorespiratory failure
  • Anemic hypoxia = decreased oxygen carrying capacity e.g. anaemia
  • Ischemic hypoxia = interruption to blood supply e.g. blocked vessel
  • Histiocytic hypoxia = unable to use oxygen due to disabled oxidative phosphorylation enzymes e.g. cyanide poisoning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List 6 physical agents that can cause cell injury

A

MET RACES
* mechanical trauma
* extremes of temperature (burns and deep cold)

  • radiation
  • Atmospheric pressure sudden change in
  • caustic agents, acids alkalis, e.g. domestic dishwasher agents. Iron tablets
  • electric shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Irreversible cell injury is usually encompassed by major … changes

A

Morphological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

5 examples of chemical agents or drugs that can cause cell injury

A

TD DOG

  • Trace amount of poison (arsenic, cyanide)
  • Daily exposure to air/pollutant/insecticide/ asbestos
  • Drugs (recreational e.g. cocaine, therapeutic)
  • Oxygen in high concentration
  • Glucose & salt in hypertonic concentrations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do infections cause cell injury / what microorganisms cause cell injury ?

A
  • viruses
  • bacteria
  • fungi
  • other infectious micro-organisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Neoplasia & cell injury :
* tumours may be ….. or …..
* local pressure effects by the …..
* ….. or ….. invasian by destruction of tissue by the tumour
* systemic effects, such as ….. and …..

A
  • benign, malignant
  • tumour
  • local , distant
  • malaise, weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Examples of immune-mediated that can cause cell injury

A
  • Autoimmune disease
  • Hypersensitivity reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Autoimmune disease happen because of reaction to what antigens ?

A

endogenous self-antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hypersensitivity reactions happen as a result of what ?

A

allergies are a result of vigorous (strong) immune reaction results in host tissue damage (asthma, anaphylaxis, urticaria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Examples of nutritional imbalance and how this can cause cell injury

A
  • hypoglycaemia
  • Dietary insufficiency = malnourished states in deprived population e.g. kwashiorkor, marasmus, self-imposed insufficiency e.g. anorexia
  • Dietary excess = obesity, diabetes, atherosclerosis, cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the genetic derangements causing cell injury ?

A
  • genetic abnormalities → chromosomes and genes
  • Inborn errors of metabolism → loss of production of an end product and/or build up of toxic intermediates of metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

substrates of adenosine triphosphate

A

oxygen , glucose, ADP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which ATP generating method produces more ATP ?

A

oxidative phosphorylation results in considerably more ATP than anaerobic processes of glycolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what happens at the cellular level for reversible injuries ?

A

decreased oxidative phosphorylation leading to decreased ATP production:

  • decreased functioning of Na+ pump = swelling/blebbing
  • detachment of ribosomes = lipid deposition
  • increased anaerobic glycolysis = clumping of nuclear chromatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what happens at the cellular level for irreversible injuries ?

A

CAP !!

Calcium ion influx, increased cytosolic calcium concentration

*activation of cellular enzymes

  • phospholipase -> decreased phospholipids = membrane damage
  • protease -> disruption of membrane and cytoskeleton proteins = membrane damage
  • endonuclease = nuclear damage
  • ATPase = decreased ATP

*increased mitochondrial permeability transition

  • decreased ATP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens to cells undergoing reversible injury when oxidative phosphorylation decreases ?

A

ATP levels decrease

  1. sodium pump decreases -> influx of Ca2+, H2O, Na+, efflux of K+ -> ER swelling, cellular swelling, loss of microvilli, blebs
  2. increased anaerobic glycolysis -> decreased glycogen, increased lactic acid (-> decrease pH) -> clumping of nuclear chromatin
  3. detachment of ribosomes -> decreased protein synthesis -> lipid deposition -> results in atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what’s the difference at cellular level with reversible and irreversible injury ?

A

cellular level →
* ER swelling, cellular swelling, loss of microvilli , formation of blebs
* clumping of nuclear chromatin
* lipid deposition because detachment of ribosomes = decreased protein synthesis

irreversible injury →
* influx of calcium
* membrane damage, nuclear damage , decreased level of ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

3 sources of ATP production ?

A
  1. mitochondria = oxidative phosphorylation (aerobic)
  2. glycolysis pathway (anaerobic)
  3. glycogenolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which ultrastructural organelles and changes that are responsible for the morphological changes ?

A
  • cell membranes - plasma membrane & organelle membranes
  • nucleus - DNA
  • proteins - structural (enzymes)
  • mitochondria - oxidative phosphorylation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Ultrastructural changes to cell of reversible injury

A
  • plasma membrane blebbing, blunting and loss of microvilli
  • swelling of the mitochondria and appearance of small densities
  • dilation of ER (endoplasmic reticulum) detachment of ribosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

light microscopic changes to cell of reversible injury

A
  • cell swelling
  • vacuolar change
  • fatty change
  • surface blebs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Ultrastructural changes to cell of irreversible injury

A
  • breakdown of plasma membrane
  • degradation of cellular organelles
  • formation of myelin figures
  • pyknosis, karyorrhexis and karyolysis of nuclei
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

light microscopic changes to cell of reversible injury

A
  • increased eosinophilia
  • cytoplasm has moth eaten appearance
  • nuclear dissolution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the 3 characteristic nuclear changes that occur in irreversible cell injury ?

A
  1. pyknosis = nuclei condenses
  2. karyorrhexis = nuclei fragmentation
  3. karyolysis = nuclei dissolved
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Necrosis involve what changes ? that occur when ?

A

morphological changes that occur after a cell has been dead some time, not a type of cell death i.e. it’s an appearance and not a process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the changes of necrosis due to ?

A

progressive degradative action of enzymes on the lethally injured cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are the 2 main processes seen in necrosis ?

A
  1. denaturation of intracellular proteins
  2. enzymatic digestion by lysosomes inherent to the dying cell and lysosomes of leukocytes that are part of inflammatory reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

In necrosis:
The host response may take …. to develop. The ….. microscopic evidence of necrosis may not become apparent until ….. hours.

A
  • hours
  • earliest
  • 4 to 12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are the 5 types of necrosis ?

A
  1. coagulative
  2. liquefactive
  3. caseous
  4. fat
  5. fibrinoid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What does necrosis of tissues have several of ?

A

morphologically distinct patterns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

why are the several morphologically distinct patterns of necrosis of tissues important to recognise ?

A

they may provide clues about the underlying cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Cogaulative necrosis is a result of what ?

A

protein denaturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

microscopy features of coagulative necrosis ?

A
  • ghost cells
  • neutrophils can infiltrate but NOT a prominent feature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Gross features of coagulative necrosis

A
  • firm
  • pale wedge of tissue
  • can become soft later
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

coagulative necrosis ?
* …… form
* occurs in ….. organs

A
  • commonest
  • most
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are free radicals ?

A

highly reactive molecules with unpaired electron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Alkalis result in …. of fat cells which is followed by ….

A
  • saponofication
  • liquefaction necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

5 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

In normal state what concentration are free radicals present at ?

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are free radicals required for ?

A
  • killing bacteria
  • cell signaling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

In excess what do free radicals do ?

A
  • attack lipids in cell membranes
  • damage mitochondrial proteins
  • damage carbohydrates and nucleic acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

which cell may free radicals be produced ? [check and alter Q + A]

A

leucocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are free radicals also known to be ?

A

mutagenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what 2 events are free radicals involved in ?

A

pathological & physiological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

List 5 methods where free radicals may be produced

A
  • chemical and radiation injury
  • ischaemia - re-perfusion injury
  • cellular ageing
  • high oxygen concentraiton
  • killing of pathogens by phagocytes (ROS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Increased free radicals (oxidative stress) is sourced from activated …1… in response to 4 factors :
…2…
…3…
…4….
…5…

A
  1. leukocytes
  2. toxins
  3. UV light
  4. ionising radiation
  5. pollutant exposure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

When are there decreased scavenging of free radicals ?

A
  • decreased levels of scavenging enzyme (catalase, peroxidase)
  • decreased vitamins A , C, E (antioxidants)
  • decreased glutathione
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

heat shock proteins (HSPs) are what class of molecular chaperones ?

A

chaperonins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What 3 functions do HSPs fulfill ?

A
  1. Provide optimal condition for denatured protein folding
  2. Prevent protein aggregation
  3. Label misfolded proteins as degradation at proteasome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Give one example of HSP

A

Ubiquitin

58
Q

What does the heat shock response aim to do?

A

What does the heat shock response aim to do?

59
Q

What is heat shock or the cellular stress reponse triggered by ?

A

any form of injury, not just heat

60
Q

Apart from stressed cells where else are HSPs also present ?

A

lower concentrations in unstressed cells

61
Q

all cell from any organism that have been so far tested when submitted to stress what happens to the protein synthesis ?

A

turn down their usual protein synthesis and turn up the synthesis of HSPs

62
Q

If Heat shock proteins aren’t secreted where do they remain ?

A

within the cell where they are concerned with protein repair (similar to DNA repair)

63
Q

when are HSPs important ?

A

when the folding step in protein synthesis goes astray or when proteins become denatured during cell injury

64
Q

What does the anti-oxidant system consist of ?

A
  • enzymes e.g. superoxide dismutase, catalases , peroxidases
  • free radical scavengers that neutralise free radicals e.g. vitamins A, C, E, glutathione
  • storage proteins that sequester transition metals in the extracellular matrix
65
Q

Examples of storage proteins that sequester transition metals in the extracellular matrix

A
  • transferrin and ceruloplasmin
  • sequester iron and copper
  • catalyse the formation of free radicals
66
Q
  1. Infarction is a cause of necrosis which 2 types
  2. what are the 2 main types of infarction ?
  3. what do the consequences range from ?
A
  1. coagulative + liquefactive necrosis
  2. white (ischemic) & red (haemorrhagic) infarct
  3. none to death
67
Q

Aetiology of infarcation ?

A
  • thrombosis
  • embolism
  • arterial torsion
  • external compression of vessel
68
Q

Liquefactive necrosis :
1. usually seen in which organ ?
2. seen in …..resulting in abscess (swollen area within body tissue, containing accumulation of pus) formation
3. …… of tissues by …….

A
  1. brain
  2. infections
  3. degradation , enzymes
69
Q

what is the necrotic material in liquefactive necrosis frequently like ? why is it like that ? what is it called ?

A
  • creamy yellow because of presence of dead leukocytes
  • called pus (accumulation of neutrophils and other cellular debris)
70
Q

gross appearance of caseous necrosis

A

cheese like

71
Q

Most common cause of caseous necrosis ?

A

tuberculosis

72
Q

caseous necrosis :
…1… debris surrounded by histiocytes resulting in a …2…. inflammation

A
  1. amorphous
  2. granulomatous
73
Q

refer to ? and may include what ?

In caseous necrosis….
“Amorphous debris surrounded by histiocytes resulting in a granulomatous inflammation”

  • what is amorphous debris ?
A
  • refers to irregularly shaped, non-specific material
  • may include dead cells, cellular debris and other components associated with tissue damage or infection
74
Q

In caseous necrosis….
“Amorphous debris surrounded by histiocytes resulting in a granulomatous inflammation”

  • what is granulomatous inflammation ?
  • what are granulomas ?
A

specific type of chronic inflammation characterised by formation of granulomas

granulomas = organised collections of immune cells surrounding a central core of foreign material or debris

75
Q

What is fat necrosis ?

A
  • destruction of adipocytes
  • consequence of trauma or secondary to release of lipases from damaged pancreatic tissue
76
Q
  1. what does fatty necrosis cause?
  2. what does the caused substance react with to form …?
A
  1. fatty acids
  2. react with calcium to form white deposits in fatty tissue
77
Q

Where is fat necrosis seen and what can it mimic ?

A
  • seen in breast tissue, pancreas
  • mimic breast tumour on radiology and is biopside to exclude cancer
78
Q

Where is fibrinoid necrosis usually seen ?

A

In immune reactions involving blood vessels : vasculitis

79
Q

In fibrinoid necrosis what has leaked out of vessels ?

A

deposits of “immune complexes” together with fibri

80
Q

What’s the appearance of fibrinoid necrosis in H&E stains ? what is it “called” by pathologists ?

A

bright pink and amorphous
“fibrinoid”

81
Q

White infarct :
1. found in what organs ?
2. what limits haemorrhage into necrotic area from adjacent capillaries ?
3. insufficiency in what ?
4. involves what artery ?
5. 3 common sites:

A
  1. solid
  2. robust stromal support
  3. arterial
  4. end
  5. heart, spleen , kidney
82
Q

In what organs is red / haemorrhagic infarct found ?

A

organs with/ that have :
* dual blood supply
* those with numerous anastomoses between capillary beds
* have loose stromal support

83
Q

What results in the arterial insufficiency in red infarct ?

A

raised venous pressure leading to increased capillary pressure and tissue pressure

84
Q

Clinical term to describe visible necrosis ?

A

gangrene

85
Q

Wet gangrene is necrosis modified by what ?

A

bacteria

86
Q

Dry gangrene is necrosis modified by what ?

A

air

87
Q

gas gangrene is necrosis modified by what ?

A

gas forming bacteria

88
Q

3 types of gangrene:

A
  1. wet
  2. dry
  3. gas
89
Q

What type of cell death is apoptosis ?

A

energy dependent programmed

90
Q

Apoptosis can be …. or ….

A

physiological , pathological

91
Q

3 features/ characteristics of apoptosis :

A
  • non-random inter-nucleosomal cleavage of DNA
  • distinct morphological features
  • doesn’t result in inflammatory response
92
Q

4 Examples of physiological apoptosis

A
  • embryogenesis and fetal development (loss of webbing)
  • hormone dependent involution (endometrium shedding at menstruation)
  • cell deletion in proliferating cell populations (regulation of immune system or intestinal crypts)
  • death of cells that have served their function (neutrophils and lymphocytes)
93
Q

Apoptosis in pathologic conditions ?

A
  • neoplasia
  • autoimmune conditions
  • immunodepletion from activation of CD4 by AIDS - HIV proteins
94
Q

Relationship between neoplasia and apoptosis ?

A

failure of normal apoptosis

95
Q

Relationship between autoimmune conditions and apoptosis ?

A

failure of induction of apoptosis in lymphoid cells directed against host antigens

96
Q

Relationship between immunodepletion and apoptosis?

A

AIDS - HIV proteins may activate CD4 on uninfected T helper lymphocytes resultin in apoptosis leading to immunodepletion

97
Q

What is apoptosis regulated by ?

A
  • many genes
  • inhibitors
  • inducers
98
Q

What inhibitors regulate apoptosis ?

A
  • growth factors
  • extracellular cell matrix
  • sex steroids
  • some viral proteins
99
Q

What inducers regulate apoptosis?

A
  • growth factor withdrawl
  • loss of extracellular matrix attachment
  • glucocorticoids
  • viruses
  • free radicals
  • ionising radiation
100
Q

Mechanism of apoptosis involves the activation of what ?

A

cascade of caspases

101
Q

what is the full name for caspases ?

A

cysteine-dependent aspartate-directed proteases

102
Q

What do the 2 pathways of apoptosis (extrinsic and intrinsic) result in ? which does what ?

A
  • activated caspase 3
  • cleave proteins
  • causing: chromatin condensation, nuclear fragmentation and blebbing
103
Q

What is the extrinisc pathway in the mechanism of apoptosis ?

A

external “death receptors” (TNF receptors or Fas receptors) are activated by a ligand

104
Q

what is the intrinsic pathway in the mechanism of apoptosis ?

A

withdrawal of growth factors or hormones causes molecules to be released from mitochondria (e.g. Bcl2, Bax, p53)

105
Q

What’s the difference in what the 2 pathways in the mechanism of apoptosis are initiated by ?

A

extrinsic - initiated by external death receptor signalling

intrinsic - triggered by internal cellular stressors

106
Q

What eventually happens to a apoptotic cell ? but there is no…

A

It’s phagocytised by macrophages or histiocytes or by neighbouring cells but there is no acute inflammation

107
Q

How do the 2 pathways of apoptosis differ ?

A

in their induction and regulation

108
Q

Difference between necrosis + apoptosis in the pattern feature

A

N: contiguous groups of cells
A: single cells

109
Q

Difference between necrosis + apoptosis in the cell size feature

A

N: enlarged (swelling)
A: reduced (shrinkage)

110
Q

Difference between necrosis + apoptosis in the nucleus feature

A

N: pyknosis - karyorrhexis - karyolysis
A: fragmentation into nucleosome size fragments

111
Q

Difference between necrosis + apoptosis in the plasma membrane feature

A

N: disrupted, early lysis
A: intact; altered structure, especially orientation of lipids

112
Q

Difference between necrosis + apoptosis in the cellular contents feature

A

N: enzymatic digestion, may leak out of cell
A: intact, may be released in apoptotic bodies

113
Q

Difference between necrosis + apoptosis in the adjacent inflammation feature

A

N: frequent
A: No

114
Q

Difference between necrosis + apoptosis in the physiologic or pathologic role feature

A

N: invariably pathologic
A: often physiologic, means of eliminating unwanted cells; may be pathologic after some forms of cell injury especially DNA damage

115
Q

Biochemical findings related to cell death-Molecules released because of cell injury and death ?

A
  • Potassium
  • Enzymes
  • Myoglobin
116
Q

As calcium enters damaged membranes other molecules leak out, what effects does this have ?

A
  • can cause local inflammation
  • may have toxic effects on body e.g. potassium
  • may appear in high concentrations in blood and can aid in diagnosis
117
Q

In myocardial infarction name 3 molecules are released by injured and dying cells ?

A
  • troponin I
  • CK-MB (creatine kinase-MB)
  • myoglobin
118
Q

After how many hours after onset of chest pain does troponin I reach it’s peak relative concentration close to 40 ? [slide 62 graph]

A

after 20 hours

119
Q

Rhabdomyolysis can be serious with …1….as a breakdown product of muscle causing damage to the …2… and even ….3…. failure requiring …4…

Typical …5… urine in myoglobinuria

A
  1. myoglobin
  2. kidneys
  3. renal
  4. dialysis
  5. brown
120
Q

Abnormal cellular accumulations happen as a result of what injury?

A

sub-lethal or chronic injury

121
Q

When do abnormal cellular accumulations occur ?

A

when metabolic processes are deranged

122
Q

Abnormal cellular accumulations:
may be …..

A

reversible

123
Q

Abnormal cellular accumulations:
can be ….. or ……

A

harmless , fatal

124
Q

4 mechanisms of intracellular accumulations :

A
  • abnormal metabolism - normal substance accumulates at an increased rate e.g. fatty liver
  • alterations in protein folding and transport
  • deficiency of critical enzymes - e.g. lysosomal storage disease (hurler’s syndrome, tay sachs)
  • inability to degrade phagocytosed particles
125
Q

5 examples of substances that undergo intracellular accumulations ?

A
  • water and electrolytes e.g. cerebral oedema
  • lipids e.g. fatty liver
  • carbohydrates
  • proteins
  • pigments
126
Q

example of abnormal fluid accumulation

A

hydropic swelling: oedema in brain

127
Q

example of abnormal lipid accumulation

A

steatosis

128
Q

examples of abnormal proteins accumulation

A
  • mallory hyaline body-damaged protein
  • alpha - 1 antitrypsin globules
129
Q

what is rhabdomyolysis ?

A

destruction of muscle to produce myoglobin

130
Q

Classic triad for symptoms of rhabdomyolysis ?

A
  • muscle pain
  • weakness
  • dark coca cola/brown urine (myoglobinuria)
131
Q

what is steatosis ?

A

Abnormal condition of fat accumulation (increased fat at the cellular level often affecting the liver)

132
Q

Endogenous pigment accumulation causes

A
  • Lipofuscin
  • Haemosiderin (iron accumulation)
  • Hereditary haemochromatosis
133
Q

Lipofuscin endogenous pigment

A

Age Pigment
Lysosomes with degradation products (residual body)

134
Q

Haemosiderin endogenous pigment

A

Iron pigment from breakdown of blood or ingestion of iron

Golden brown pigment seen in macrophages

Bruising

135
Q

Haemosiderosis
when does an overload of iron in the body result from ? most common in patients with what condition ?

A

Iron overload

An overload of iron in the body resulting from repeated blood transfusions.

Hemosiderosis occurs most often in patients with thalassemia.

Abnormal deposit of hemosiderin

136
Q

Hereditary haemochromatosis

A

Hereditary - autosomal recessive
Excessive absorption of iron from GI tract

137
Q

Bilirubin can accumulate in what pathologies?

A

Liver disease
Hemolytic anemia

138
Q

Pathological calcifications causes

A
  • Parathyroid overactivity e.g., tumour/hyperplasia
  • Malignant tumours e.g., breast/lung/bone
139
Q

Other causes of calcification apart from the pathological causes being parathyroid overactivity and malignant tumours

A
  • Vitamin D overdosage
  • Paget’s disease
  • Prolonged immobilisation
140
Q

Cellular ageing

A

Telomeres shorten

MOD (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions