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ESA 2 - Mine > MoD > Flashcards

MoD Flashcards

0
Q

How can cells become injured?

A 
Radiation
Extreme heat
Hypoxia
Microorganisms
Chemical agents
Trauma
Immune mechanisms
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1
Q

What is disease?

A

A state of failed homeostasis resulting in morphological and functional changes to cells

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2
Q

What are the 4 types of hypoxia?

A

Hypoxic hypoxia - low pO2 atmosphere, low O2 uptake in lungs

Anaemic hypoxia - lack of Hb to carry the O2, CO binding to Hb

Ischaemic hypoxia - lack of blood supply and therefore O2 delivery to a tissue

Histiocytic hypoxia - malfunctioning oxidative phosphorylation pathway (action of CN etc)

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3
Q

What is the result of hypoxia?

A

No respiration and no ATP generated as a result =
1). Increase in glycolysis
- production of lactate, pyruvate etc lowers pH = clumping of chromatin
2). Ribosomes detach from ER
- decreased protein synthesis
- lipid deposition
3). Na+/K+ ATPase fails
- intracellular Na+ mounts, K+ efflux occurs and NCX reverses to bring in Ca2+
= cellular swelling, blebs, myelin figures

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4
Q

What effect does high intracellular Ca2+ have on a cell?

A

Activates enzymes

1) . Proteases = digests cytoskeleton and proteins
2) . Phospholipases = damage membranes including ER and lysosomes
3) . ATPases = rid of the small ATP levels present
4) . Endonucleases = damages chromatin

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5
Q

What is oncosis?

A

The spectrum of morphological changes in a cell, prior to its death that occurs with swelling.

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6
Q

What is necrosis?

A

The morphological changes that a cell undergoes after it has been dead some time.

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7
Q

What are the reversible/oncosis related changes that can occur in cell injury?

A
  • Swelling - shows as reduced pink staining
  • Chromatin clumping
  • Blebs
  • Ribosomes detaching from the ER - shows as bits of darker pink
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8
Q

What are the irreversible/necrosis related changes that occur in cell injury?

A
  • karyolysis, pyknosis, karyorrhexis
  • myelin figures
  • further swelling
  • lysosome and ER rupture
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9
Q

What is coagulative necrosis and its appearance?

A

Protein denaturation > enzymatic activity

Ghost outline of cells preserves cell architecture

Heart, kidney

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10
Q

What is liquefactive necrosis and what does it look like?

A

Enzyme degradation > protein denaturation

More liquified and possibly creamy (pus may be present if acute inflammation is ongoing) with debris and neutrophils

Brain, lungs

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11
Q

What is caseous necrosis and what does it look like?

A

This is often found in cases of TB

Structureless with debris, often appears white and soft (like cheese) and with granulomas

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12
Q

What is fat necrosis and what does it look like?

A

This is destruction of adipose tissue.

Appears chalky white (due to fatty acid reaction with calcium) and the outline of adipocytes are present.

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13
Q

What is an infarct?

A

Tissue death caused by obstruction of the tissues blood supply

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14
Q

In what types of necrosis do the different types of infarct occur in?

A

Red infarct can occur in liquefactive

White infarct can occur in coagulative

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15
Q

What is a white infarct and where/why does it occur?

A

Where there is little haemorrhage into the area of tissue death.

Occurs due to occlusion of an end artery and due to solidarity of the tissue (as white infarcts occur in solid organs) limiting haemorrhage into it.

Heart, spleen, kidneys (usually wedge shaped)

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16
Q

What is a red infarct and where/why does it occur?

A

This is where extensive haemorrhage occurs.

Occurs if

  • the tissue has collateral blood supply (two arteries supplying it)
  • the tissue is not solid (poor stromal support)
  • the tissue has many anastomoses (2 arteries share a capillary bed)
  • increased venous pressure
  • congestion has been in the tissue previously

Occurs in the brain, lungs

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17
Q

What are the 2 reactions that form free radicals?

A

Haber Weiss
- O2- + H2O2 + H+ —–> O2 + *OH + H2O

Fenton reaction
- Fe2+ + H2O2 —–> OH- + *OH + Fe3+

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18
Q

Why are free radicals bad?

A

Damage DNA
Lipid peroxidation
Cause proteins to be denatured

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19
Q

What are some cellular defences against ROS?

A
  • SOD and catalase (O2- —-> H2O2 —-> H2O + O2
  • glutathione and NADPH
  • Vit A, C, E and flavenoids (beta carotene)
  • zinc and selenium in membrane as scavengers
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20
Q

What is ischaemia reperfusion injury caused by?

A

A build up of ROS, neutrophils and compliment proteins

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21
Q

What products do dying cells release?

A

K+

  • hyperpolarisation of cells which makes it harder to fire A.P
  • usually diluted before it reaches the heart but can be much larger in huge trauma, tumour lysis syndrome and tourniquet shock

Enzymes
- can be detected for diagnosis

Myoglobin

  • released from damaged striated muscle (trauma, burns, exercise)
  • plugs up renal tubules and can lead to renal failure = brown urine
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22
Q

What is calcification?

A

The accumulation of hydroxyapatite crystals in tissue, especially abnormal in soft tissue.

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23
Q

What is dystrophic calcification and where does it often occur?

A

Calcification in areas of dying tissue with no abnormality in Ca2+ levels or metabolism (= local)

Atherosclerotic plaque, ageing or damaged heart valves, TB infected lymph nodes

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24
Q

What is metastatic calcification and how does it occur?

A

This is where calcium is deposited into tissues due to hypercalcaemia as a result of abnormal metabolism.

Can occur as a result of

  • increased PTH secretion due to ectopic producing tumour or parathyroid tumour
  • bone destruction
  • vitamin D related disorder
  • renal failure
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25
Q

What are the basic steps of apoptosis?

A

Normal cell
Cell chromatin condenses
Cell shrinks
Formation of apoptotic bodies

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26
Q

What is the intrinsic pathway of initiation and execution of apoptosis?

A

Mitochondria increase permeability of membrane to allow leakage of cytochrome C

Cytochrome C reacts with APAF1 and caspase 9 to form an apoptosome

Apoptosome activates further caspases

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27
Q

What inhibits he release of cytochrome C from mitochondria?

A

BCl2

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28
Q

What is the extrinsic pathway for initiation and execution of apoptosis?

A

External death ligands bind to death receptors on the cell

This activates caspases

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29
Q

What is the third stage of apoptosis and how does it occur?

A

Degradation and phagocytosis

Apoptotic bodies have portions of cytoplasm and other organelle fragments inside them. They have an undamaged membrane containing molecules that induce their phagocytosis

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30
Q

What do caspases do?

A

Degrade the DNA and cytoplasmic proteins

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31
Q

Name some physiological and pathological pathways in which apoptosis occurs.

A

Physiological

  • sculpting in embryogenesis
  • some organs response to hormones (uterus etc)

Pathological

  • accumulation of misfolded proteins cause ER stress = apoptosis
  • virus induced
  • damage to DNA
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32
Q

Name some abnormal protein accumulations.

A

Mallorys hyaline - keratin build up in liver in alcoholic liver disease as it can’t process them.

Alpha1antitrypsin - in alpha1antitrypsin disorder the liver misfolds the enzyme = can’t leave ER so stays there and no longer inhibits tissue breakdown in other organs

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33
Q

Name some abnormal pigment accumulations.

A

Exogenous - coal dust, tattoo ink.

Endogenous

  • haemosiderin - derived from Hb, can be released due to leakage from stores, or deposited due to systemic overload.
  • –> may be caused by hereditary haemochromatosis, where the intestine absorbs too much iron and deposits in in organs
  • lipofuscin - brown pigment due to ROS causing lipid peroxidation, found with ageing
  • bilirubin - deposited in tissues if produced in excess causing jaundice
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34
Q

Name lipid accumulations.

A

TAG build up in liver = steathosis

Cholesterol build up = stored as membrane bound droplets as its insoluble. This can then be absorbed by macrophages to form foam cells.

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35
Q

What are the effects of an aspirin overdose?

A

Increases resp centre = alkalosis which body tries to amend = acidosis

Interferes with carb, fat and protein metab = lactate/pyruvate/ketone body production = acidosis

Decreases platelet aggregation and inhibits stomach from producing mucus = GI bleeding

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36
Q

What is acute inflammation?

A

An innate, early and stereotyped response of living tissue to injury.

37
Q

What can cause acute inflammation?

A 
Hypersensitivity reaction 
Microbial infection
Direct trauma
Chemical agents
Physical agents
38
Q

What are the 3 basic stages of acute inflammation?

A

Vascular change 1 (v. short vasoconstriction followed by dilation)
Vascular change 2 (increased vessel permeability)
Cellular phase

39
Q

What are the macroscopic features of acute inflammation?

A

Rubor - redness
Dolor - pain
Calor - heat
Tumor - swelling

40
Q

What occurs in vascular change 1 of acute inflammation?

A

1) . Brief vasoconstriction to restrict any blood loss.
2) . Vasodilation of arterioles then capillaries occurs to increase blood flow and therefore delivery of platelets, complement, neutrophils and chemical mediators. It also increases temperature of the body in an attempt to slow bacterial enzyme action.

41
Q

What occurs in the 2nd vascular change of acute inflammation?

A

1). Dilated vessels increase in permeability
= exudate leakage because
–> dilation = increased hydrostatic pressure
–> permeability leaks proteins = increased colloid osmotic pressure outside the vessel

Therefore oedema occurs.

42
Q

What does the leakage of exudate result in?

A

Increased lymphatic drainage (ridding of microbes quicker)
Dilution of toxins
Increase n chemical mediator, fibrinogen etc delivery to tissues.
Stasis of blood in the vessel due to an increase in viscosity.

43
Q

What chemical mediators increase blood flow in the vessel?

A

Histamine

Prostaglandins

44
Q

What chemical mediators increase vessel permeability?

A 
Histamine
Leukotrienes
TNF
IL-1
VEGF
45
Q

What occurs in the cellular phase of acute inflammation?

A

Neutrophils move into the tissues and phagocytose debris and pathogens in the inflamed area.

46
Q

How do neutrophils enter tissues in the cellular phase of acute inflammation?

A

1) . They express ligands that are complementary to chemoattractants such as c5a, LTB4 and bacterial peptides.
2) . These chemo attractants form a gradient towards the tissue, which the neutrophils therefore follow via chemotaxis.
3) . Roll along endothelium until they alter their cytoskeleton to form a pseudopod, and digest the basement membrane to pass into the tissue.

47
Q

What do the neutrophils do once in the tissue in acute inflammation?

A

They phagocytose pathogens, aided by opsonins such as c3b and Fc.

Do this by forming a phagosome, which then fuses with lysosomes to form a secondary lysosome. This kills the pathogen by:

  • O2 dependant - use of H2O2, O2- or OHCl*
  • O2 in dependant - use of hydrolases, lysozymes, defensins and bactericidal permeability increasing protein.
48
Q

Where does histamine come from?

A

Mast cells, basophils and platelets.

49
Q

What is histamine released in response to?

A 
IL-1
Physical trauma
C3a
C5a
Immunological reaction
50
Q

What is the difference between a transudate and exudate?

A

Exudate is protein rich as it is fluid lost to inflammation.

Transudate is low in protein as it is fluid lost simply to hydrostatic pressure.

51
Q

What chemical mediators are involved in phagocytosis?

A

C3b

Fc

52
Q

What chemical mediators act as chemoattractants in neutrophil migration?

A

LTB4
C5a
Bacterial peptides

53
Q

What are the 4 methods of vascular leakage and the chemical mediators that cause each?

A

1) . Cytoskeletal reorganisation - TNF and IL-1
2) . Endothelial contraction - histamine and leukotrienes
3) . Injury - direct or induced by action of leukocytes (ROS, enzyme leakage)
4) . Increase in transcytosis across endothelial cytoplasm - VEGF

54
Q

What is vascular leakage helpful in acute inflammation?

A

Delivery of cells and fibrin = LOCALISATION OF PROBLEM

55
Q

What are the main local complications of acute inflammation?

A

Pain
Loss of function
Swelling (could block tubes)
Exudate (could compress organs, cause pericarditis/serotinitis etc)

56
Q

What are the systemic complications of acute inflammation?

A

Acute phase response (fever, decreased appetite, increased use and temp, increased blood conc of fibrinogen, CRP, alpha1 anti trypsin etc, leukocytosis)

57
Q

What chemical mediators control leukocytosis and are released by fever?

A

Fever - releases prostaglandins, TNFalpha and IL-1

Leukocytosis occurs due to TNFalpha and IL-1

58
Q

What can the results of acute inflammation be?

A

1) . Complete resolution if cellular architecture is undamaged
2) . Continued acute inflammation with chronic inflammation in severe persistant or repeated irritation.
3) . Develops into chronic inflammation with fibrous repair

59
Q

How does acute inflammation stop?

A 
Mediators have short half life so run out
Mediators are diluted/washed away via exudate
Mediators degraded (e.g. by heparinase) or bound to antiproteases.
Lipoxins, endothelium and other chemicals inhibit changes acute inflammation cause.
60
Q

What causes lobar pneumonia?

A

Streptococcus pneumonaie

61
Q

What occurs in lobar pneumonia and how does this give the symptoms it does?

A

Bacteria cause acute inflammation in the alveoli = increase in vascular permeability by VEGF, IL-1, TNF, histamine, leukotrienes etc.

This causes exudate to fill the lungs, decreasing gas exchange = breathlessness, dry cough, hypoxia.
Fever also occurs as part of the acute phase response

62
Q

What can cause acute appendicitis?

A

Blockage of the appendix (e.g. By gallstones)

Hypersensitivity reactions

63
Q

What can the bad consequences of appendicitis be?

A

1) . Perforation of the appendix = leakage of purilent exudate = peritonitis/pericarditis
2) . Abcess may form = septicaemia
3) . Ulceration due to loss of usual mucosal surface.

64
Q

When does an abcess occur?

A

When acute inflammation in solid tissue pushes its layers apart by producing exudate

65
Q

What occurs in the centre of an abcess?

A

Liquefactive necrosis (pus)

66
Q

Why can accesses be a problem?

A

They can compress or place pressure on other structures
= pain
= damage and therefore scarring of adjacent structures

67
Q

What does alpha1 antitrypsin deficiency cause?

A

Deficiency in alpha1 antitrypsin = usually inhibits elastase
Therefore loss of it = elastic tissue broken down quicker

= emphysema in lung
= scarring in liver (liver sclerosis = thickens due to fibrosis)

68
Q

What is chronic inflammation?

A

A chronic response of living tissue to injury with associated fibrosis.

69
Q

How can chronic inflammation arise?

A

1) . De novo
- some autoimmune conditions
- chronic low level irritation
- chronic infection

2) . From acute inflammation
- that has severe persistence or repeated irritation
- that is taking too severe to be resolved in a few days

70
Q

What cells are present in chronic inflammation?

A 
Macrophages
Lymphocytes
Fibroblasts/myofibroblasts
Plasma cells 
Eosinophils
71
Q

What is the function of plasma cells and when do they become present?

A

A B lymphocyte that has differentiated to produce antibodies

Present 7-14 days into an immune response = considerable chronicity

72
Q

What is the function of eosinophils in chronic inflammation?

A

Tackle

  • Hypersensitivity reactions
  • Parasite infection
  • Some tumours
73
Q

What is the function of fibroblasts in chronic inflammation and how are they recruited?

A

Produce collagen required for fibrosis

Recruited by macrophages

74
Q

What is the function of lymphocytes in chronic inflammation and where does each type mature?

A

B

  • mature in bone marrow
  • differentiate to produce antibodies

T helper

  • mature in thymus
  • activate B cells and macrophages

T killer

  • mature in thymus
  • cytotoxic function to kill virus infected cells
  • activated by cytokines released by macrophages
75
Q

What can macrophages be inactivated by?

A

Kupffer cells of liver

Monocytes in blood

76
Q

What are the functions of macrophages in chronic inflammation?

A

1) . Phagocytosis
- can also do this by forming giant cells

2) . Synthesis of
- cytokines (which activate T killer cells)
- proteases
- complement
- blood clotting factors

3). Antigen presentation

77
Q

Describe the 3 types of giant cell.

A

LANGHAN

  • horse shoe shaped
  • common in TB

TOUTON

  • clock face shaped
  • foamy cytoplasm surrounds macrophages
  • common in fat necrosis

FOREIGN BODY TYPE
- disorganised nuclei

78
Q

Why do giant cells form?

A

To tackle debris/pathogens too large or stubborn for a single macrophage to phagocytose

79
Q

What are the conditions caused by fibrosis due to chronic inflammation?

A

Chronic colecystitis

Gastric ulceration

80
Q

What is chronic colecystitis?

A

Gall stones block the bile duct, damaging the mucosal surface (ulceration) and obstructing bile flow.
This causes repeated acute inflammation, resulting in it becoming chronic.

81
Q

What is gastric ulceration and its causes?

A

Acute caused by drugs, chronic by helicobacter pylori.

Leads to chronic inflammation in the stomach which alters its mucosal surface = acid > mucosa
= ulceration

82
Q

How is gastric ulceration treated?

A

Antibiotic (amoxicillin) or a PPI inhibitor (proton pump = decreased acid)

83
Q

How is chronic colecystitis treated?

A

Surgery to remove the gallstones

84
Q

What are the conditions due to chronic inflammation that result in altered function of the affected part?

A

Thyrotoxicosis (Graves’ disease)

Inflammatory bowel disease

85
Q

What is thyrotoxicosis (graves disease)?

A
  • autoimmune production of antibodies which stimulate TSH receptors = increased T3/4
  • the antibodies a produced by plasma cells that originate from a chronic inflammatory response
86
Q

What are the 2 types of inflammatory bowel disease?

A

Ulcerative colitis

  • idiopathic
  • diarrhoea, rectal bleeding
  • more superficial
  • treat via immunosurpressants or colonectomy

Crohn’s disease

  • idiopathic
  • diarrhoea, rectal bleeding
  • transmural so may cause fistulae (abnormal connection of 2 mucosal surfaces) and strictures (tube narrowing)
  • treat with hydration, specific diet and immunosurpressants
87
Q

In what disease does chronic inflammation lead to atrophy?

A

Atrophic gastritis
- chronic inflammation where lymphocytes/plasma cells produce autoantibodies that kill stomachs parietal cells
= impair function as these produce HCl

88
Q

What immunological disorder is due to chronic inflammation?

A

Rheumatoid arthritis

  • chronic inflammation destroys joints in a localised manner.
  • systemically, it can lead to amyloidoses.

Temperature via non steroidal antiinflammatories or a disease modifying antirheumatic (block action of damaging chemicals produced by antibodies)

89
Q

In what disorder does chronic inflammation lead to a loss in function and fibrosis?

A

Cirrhosis

Can be caused by alcohol, drugs, infection by hepatitis B/C, immune attack or fatty liver disease. = chronic inflam.

This leads to fibrosis forming nodules and therefore loss of function.

Treat via lifestyle changes or a transplant.

ESA 2 - Mine (4 decks)

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