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Cells to systems > Everything > Flashcards

Everything Flashcards

1
Q

Which four clinical signs contributed to your assumption that Harley was hypovolemic?

A

Weakness, collapse, tachycardia, weak pulse

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2
Q

In which cellular space is fluid accumulating in pitting oedema?

A

Interstitial / extracellular space

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3
Q

How does snake venom affect the cardiovascular system?

A

Release of fibrinolytic and thrombin-like enzymes to cause widespread clotting, depletion of fibrinogen and, later, widespread microhaemorrhages.

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4
Q

Define hypovolemia

A

Loss of fluid from the intravascular compartment; characterised by Na+ loss

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5
Q

Why were hypertonic fluids contraindicated in Harley’s case?

A

Because they work by drawing fluid out of the interstitial space into the blood to restore blood volume. However, Harley may have had snake venom in this compartment.

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6
Q

Would isotonic fluids help more with intravascular volume expansion or extravascular dehydration?

A

It would contribute equally.

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7
Q

What is one toxic mechanism of PLA2 in snake venom?

A

Inhibit the electron transfer chain and solubilise mitochondrial enzymes

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8
Q

Name three toxic components of snake venom

A

Hyaluronidase, collagenase, phospholipse, amino acid oxidases

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9
Q

Define petechiae

A

Small haemorrhages in the skin

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10
Q

Define ecchymoses

A

Converging petechiae visible in the mucous membranes

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11
Q

Two mechanisms by which snake venom can interrupt neuromuscular transmission are

A

Blocking (antagonising) the AChR, preventing release of ACh from pre-synaptic nerve

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12
Q

What is the major risk associated with giving antivenom to a dog?

A

Allergic reaction to the equine or sheep protein that would also be in the solution

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13
Q

How does snake venom spread around the body?

A

Spreads locally via diffusion, spreads to the blood via the lymphatics, spreads systemically via the blood

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14
Q

Why shouldn’t you shake antivenom?

A

Destroys the proteins within, also causes the liquid to foam making it difficult to draw up.

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15
Q

Describe the role of iodine in thyroid hormone production

A

Iodine converted to iodide in the GIT, which is then absorbed and travels to the thyroid. Here, it iodinates tyrosine residues on the thyroglobulin molecule to create mono-iodotyrosine and di-iodotyrosine.

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16
Q

What is the mechanism of action of a cyanogenetic goitrogen?

A

Acts to inhibit iodine uptake by thyroid, preventing synthesis of T3 and T4. Get overstimulation of thyroid with TSH in the absence of T3 and T4, leading to hyperplastic/hypertrophic thyroid.

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17
Q

What is the mechanism of action of a thiouracil goitrogen?

A

Prevent incorporation of iodine into thyroid hormones

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18
Q

Loose CT has a high or low ratio of cells to fibres?

A

High

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19
Q

Dense CT has a high or low ratio of cells to fibres?

A

Low

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20
Q

Three types of CT proper?

A

Loose, adipose, dense

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21
Q

Two types of extracellular material?

A

Amorphous and fibrous

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22
Q

Describe a mesenchymal cell (light microscope level)

A
  • stellate
  • cytoplasmic processes
  • oval/round nucleus
  • multipotent
  • small numbers in adults
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23
Q

Describe a fibroblast (light microscope level)

A
  • stellate or spindle
  • ovoid nucleus
  • abundant basophilic cytoplasm
  • synthesises collagen
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24
Q

Describe a fibrocyte (light microscope level)

A
  • flattened, elongated spindle shape
  • small
  • elongated nucleus
  • minimal cytoplasm as not active
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25
Q

What are some contents of mast cell granules?

A

Heparin, histamine, serotonin, proteases

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26
Q

Describe a B cell (light microscope)

A

Fat ovoid cell with abundant basophilic cytoplasm. Radially arranged chromatin in eccentric nucleus.

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27
Q

Do stereocilia have motility?

A

No

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28
Q

Name to lateral membrane specialisations for adherence

A

Desmosomes

Zona/macula adherens

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29
Q

What attaches epithelial cells to basement membrane?

A

Hemidesmosomes

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30
Q

Explain merocrine secretion

A

Vesicles containing secretory product open onto cell surface and discharge

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31
Q

Explain holocrine secretion

A

Entire secretory cell breaks down to release its product (e.g sebaceous glands)

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32
Q

Explain apocrine secretion

A

Part of apical cytoplasm is lost together with secretory product e.g sweat glands, mammary, prostate

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33
Q

In flexion, legs go backward or forward?

A

Backward

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34
Q

In extension legs go backward or forward?

A

Forward

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35
Q

A horse kick is an example of which kind of movement?

A

Abduction

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36
Q

Which joint is known as the ‘hock’? Which bones constitute the hock?

A

The tarsal joint - talus + calcaneus + centrale

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37
Q

Which is the main weight-bearing bone immediately distal to the stifle in a dog?

A

The tibia

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38
Q

How many sesamoids in a single paw? Where are they?

A

9 in total:
1 in digit 1
2 each in digits 2 - 5

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39
Q

Which phalanx is missing in digit 1?

A

Phalanx II

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40
Q

What is the name for the articular surface of the humerus and scapula?

A

The glenoid cavity

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41
Q

Which two bones meet at the antebrachial joint?

A

The radius, and the carpal bone Radiale

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42
Q

The most medial carpal bone is?

A

Ulnare

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43
Q

The large lateral foramen in the pelvis is called?

A

The obturator foramen. Contains nerves, femoral artery, etc

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44
Q

When viewed laterally, the femoral head points cranially or caudally? What about the distal condyles?

A

Cranially - the surface that articulates with the tibia and fibula points caudally

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45
Q

The surface between the lateral and medial femoral condyles on the distal caudal aspect of the femur is called?

A

The popliteal surface.

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46
Q

The malleolus structures of the tibia and fibula occur at the proximal or distal end? Which is larger - medial or lateral?

A

Distal. Medial is the larger.

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47
Q

When standing, the fibula is medial or lateral to the tibia?

A

Lateral.

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48
Q

The tibial tuberosity occurs on the cranial aspect and points medially or laterally?

A

Laterally

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49
Q

What is the vertebral formula for a dog?

A 
C 7
T 13 (T 11 is usually anticlinal)
L 7
S 3 (fused)
C 20 - 23
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50
Q

What does the head of the rib articulate with?

A

Both the caudal costal fovea of the cranial rib, and the cranial costal fovea of the caudal rib

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51
Q

What does the tubercle of the rib articulate with?

A

The transverse process of the caudal rib

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52
Q

The clavicle runs from__ to ___?

A

The clavicle runs from the shoulder joint to the cranial end of the sternum

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53
Q

Which bone is the hoof of a horse analogous to?

A

Metacarpal III

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54
Q

To which bones does ‘crus’ refer?

A

Tibia and fibula

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55
Q

To which bones does ‘manus’ refer?

A

The forepaw / hand structure

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56
Q

Define sesamoid.

A

A stiffening in a ligament that helps to reduce friction of joints and increase mechanical efficiency

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57
Q

What is the navicular bone?

A

A sesamoid bone present i horses and other heavy, hoofed animals. Occurs between P2 and P3

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58
Q

What is the difference between a condyle and a trochlea?

A

Condyles are usually rounded, trochleas are groove shaped. Both provide articular surfaces for the bone.

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59
Q

Are epicondyles usually rough or smooth?

A

Rough

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60
Q

Are tubercles found in forelimbs? What about trochanters?

A

Tubercles are tuberosities of the forelimb. Trochanters are tuberosities of the hindlimb

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61
Q

What is a splanchnic bone?

A

A bone that forms within viscera e.g penis bone in dogs

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62
Q

Name three major ligaments from cranial - caudal

A

Nuchal, supraspinous, sacrosciatic

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63
Q

Body water is approximately __% of body weight. __% bodyweight is intracellular and __% bodyweight is extracellular.

A

Body water is approximately 60% of body weight. 40% bodyweight is intracellular and 20% bodyweight is extracellular.

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64
Q

Of the extracellular body water (comprising a total of 20% bodyweight), ___ is interstitial fluid and ____ is plasma.

A

Of the extracellular body water (comprising a total of 20% bodyweight), 3/4 is interstitial fluid and 1/4 is plasma.

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65
Q

List two ions that are in high concentration intracellularly, and three that are low.

A

High: K+, Mg2+
Low: Na+, Cl-, Ca2+

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66
Q

What is the osmolality of all three body compartments?

A

~290mOsmol/kg ( or /L)

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67
Q

Dehydration represents a ____% loss of body water

A

Dehydration represents a 5 - 15% loss of body water

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68
Q

If the molarity of NaCl is 0.15M, what is the molality?

A

0.3 molal = 300mOsm

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69
Q

Define osmolality

A

The concentration of particles per kg

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70
Q

At 5 - 8% dehydration, what clinical signs would you expect?

A

Tacky MMs, reduced skin turgor

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71
Q

Define osmolarity

A

Concentration of particles per litre. It is independent of particle size or weight.

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72
Q

What is fick’s law? Which biological process does it describe?

A

(Surface area of membrane x difference in concentration across the membrane) / thickness of membrane

Describes osmosis of particles in the context of bulk flow

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73
Q

In what situation might your blood become hypotonic?

A

Secretory diarrhoea - where ions are being lost but not water e.g cholera

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74
Q

Describe continuous capillaries, including where they are found

A

10-15nm clefts between enothelial cells and caveolae. Found in the muscle, skin, lung, fat, connective tissues

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75
Q

Describe fenestrated capillaries including where they are found

A

Have fenestrae as well as clefts and caveolae. Found in kidneys, intestines, endocrine glands, joints

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76
Q

Describe discontinuous capillaries including where they are found

A

Have wide clefts (100 - 1000nm) between adjacent endothelial cells that are permeable to large molecules. Also have large fenestrations. Found in the bone marrow, liver, spleen.

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77
Q

Which capillary type has caveolae?

A

Neural

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78
Q

Which of Starlings forces contributes least to the overall flow?

A

The colloid pressure of the interstitial fluid

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79
Q

If a particle moves via diffusion-limited exchange, will increasing blood flow increase its exchange?

A

No

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80
Q

Which kind of endothelial gap are plasma proteins most likely to penetrate?

A

Caveolae

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81
Q

What sort of epithelium does an initial lymphatic have?

A

Simple squamous

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82
Q

List the four major functions of the lymphatic system.

A
  1. Control of blood and ECF volume by returning excess filtered fluid and proteins
  2. Main pathway for fat absorption as well as lipid soluble vitamins A, D, E, K
  3. Pathway for immune cell circulation
  4. Role in turnover of extracellular matrix proteins e.g hyaluronan and glycosaminoglycans
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83
Q

Lymph enters the initial lymphatic by:

A

Mechanical deformation of the valves, causing them to open

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84
Q

How does lymph move?

A
  • deformation of tissues (extrinsic pump - may include pulse pressure changes, peristalsis, respiration)
  • contraction of collecting lymphatic smooth muscle (intrinsic pump)
  • presence of valves in collecting lymphatic to prevent backflow
  • pumps create suction to draw lymph from initial lymphatics into collecting
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85
Q

What constitutes a lymphangion?

A

A segment of collecting lymphatic bounded by an upstream and downstream valve with a smooth muscle wall.

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86
Q

List four causes for lymphoedema.

A
  1. High hydrostatic pressure in veins
  2. Low oncotic pressure of blood
  3. Inflammation
  4. Obstruction of lymphatic drainage
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87
Q

Which structures are drained by the R lymphatic duct

A
  • head and neck
  • thoracic cavity
  • upper limb R side
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88
Q

What are the three main types of membrane lipid?

A
  1. Phospholipids (phosphoglycerides, sphingolipids, glycosphingolipids)
  2. Cholesterol - the more there is the less flexible the less permeable the membrane will be
  3. Glycolipids - external leaflet only
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89
Q

List and describe the four factors affecting membrane fluidity

A
  1. Membrane lipid tail length - the longer the tails, the less fluid
  2. Degree of unsaturation of fatty acid tails - the more saturated, the less fluid as unsaturated tails have a kink, meaning they don’t pack together as tightly
  3. Amount of cholesterol present - reduces both fluidity and permeability though is necessary structural component
  4. Temperature - increasing temp increases fluidity
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90
Q

Give two examples of mechanically-gated ion channels.

A
  1. Ion channel in the inner ear opened by sound waves
  2. Ion channels in smooth muscle opened by stretch
  3. pacinian corpuscle?
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91
Q

Fatty acids with one or more double bonds in their hydrocarbon tail are ____?

A

Unsaturated.

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92
Q

What is the difference between integral and peripheral plasma membrane proteins?

A

Integral proteins traverse the membrane (except integral monotopic), are ampipathic.

Peripheral proteins are non-covalently bound to one side of the bilayer, often to an integral membrane protein.

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93
Q

What makes up the glycocalyx? What is its function?

A

The sugar moieties of cell membrane glycoproteins or glycolipids. Mediates cell-cell interactions such as surface recognition and attachment.

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94
Q

Contrast pinocytosis and endocytosis.

A

Pinocytosis is not receptor mediated, requires energy and is continuous. Endocytosis only occurs in presence of the correct ligand. Endocytic vesicles have clathrin or caveolin structure.

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95
Q

What is serum?

A

Plasma without the clotting factors. Obtain by collecting sample without anticoagulant

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96
Q

How to get plasma?

A

Collect blood in EDTA tube and spin.

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97
Q

Describe CO2 transport in the blood.

A 
11% free in plasma
89% in RBC
- 21% bound to Hb
- 64% as HCO3- ion inside RBC (has high carbonic anhydrase concentration)
- 4% dissolved in RBC cytoplasm
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98
Q

Lifespan of cat RBC?

A

~ 80 days

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99
Q

Lifespan of dog RBC?

A

~ 100-120 days

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100
Q

Lifespan of horse, cow, sheep RBC?

A

~ 150 days

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101
Q

What is the lifespan of a platelet? What cell do they come from?

A

Megakaryocytes in the bone marrow produce membrane blebs that become platelets. 8 - 10day life span

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102
Q

What do the dense granules of platelets contain?

A

ADP, serotonin, Ca2+

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103
Q

What do the alpha granules of platelets contain?

A

Thrombospondin, fibrinogen

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104
Q

Name three sites of haematopoiesis in the adult

A
  1. The red marrow region (ends) of long bones
  2. Pelvic flat bones
  3. Vertebrae
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105
Q

Name the cells of the myeloid lineage (7 types)

A 
Erythrocytes (++ erythropoietin)
Thrombocytes (++ thrombopoietin)
Basophils
Eosinophils
Monocytes
Dendritic cells
Neutrophils
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106
Q

What special kind of cell replication do megakaryocytes undergo to produce platelets?

A

Endomitotic replication

- replicate DNA and expand cytoplasm but don’t divide

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107
Q

Which glycoprotein is responsible for regulating erythropoiesis? Where is it produced and by which cell type?

A

Erythropoietin - produced in the renal cortex and medulla by renal peritubular cells (fibroblast-like)

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108
Q

What are the three main effects of EPO on erythropoiesis?

A
  1. Increases mitotic rate of haematopoietic progenitor cells
  2. Reduces maturation time for erythroblasts
  3. Increases rate of RBC release from bone marrow
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109
Q

Give a brief summary of blood clotting

A

Exposed collagen of injured blood vessels activates platelets, and they aggregate at the site. Prothrombin is converted to thrombin, which then converts soluble fibrinogen to fibrin, which forms a mesh of fibres over platelet plug.

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110
Q

What are the sites of haematopoiesis in the embryo? What about the foetus?

A

Embryo - yolk sac, liver, spleen

Foetus - liver, spleen, bone marrow

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111
Q

Reticulocytes are erythrocytes that still possess which structures?

A

Mitochondria and ribosomes

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112
Q

What are three cytokines secreted by macrophages?

A

IL-1, IL-6, IL-8, TNFalpha

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113
Q

What lineage are dendritic cells?

A

Some are from myeloid while others are from lymphoid lineage

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114
Q

Which granulocyte is typical of hypersensitivity/allergic response?

A

Basophil

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115
Q

What do acute phase proteins do?

A

Activate complement, opsonise pathogens

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116
Q

Name four cells that aren’t usually seen in the blood

A

Plasma cell, macrophage, dendritic cell, mast cell - all activated forms usually present in tissue

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117
Q

Which two classes of leukocytes are AGRANULOCYTES?

A

Monocytes, lymphocytes

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118
Q

Name three antimicrobial peptides of the innate immune system

A
  1. cryptidins
  2. defensins
  3. cathelicidins
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119
Q

What do the primary granules of neutrophils contain?

A

Peroxidase, lysosyme, hydrolytic enzymes

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120
Q

What do the secondary granules of neutrophils contain?

A

Collagenase, lactoferrin, phospholipase

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121
Q

What are the three mechanisms by which neutrophils kill pathogens?

A
  1. Phagocytosis and formation of a phagolysosome
  2. Extracellular release of granule contents and protease contents
  3. Release of neutrophil extracellular traps (NETs) along with myeloperoxidase and neutrophil elastase
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122
Q

What are three antibacterial proteins neutrophils produce?

A

Lactoferrin, lysosyme, defensins

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123
Q

What is the lifespan of a neutrophil in the blood? What about the tissues?

A

4 - 10h in the blood, 1 - 2 days in tissue

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124
Q

What are some of the secretory products of basophils? Are they effective at killing bacteria?

A

Histamine, heparin, serotinin, hyaluronic acid. They are inefficient bacteria killers, and cannot phagocytose in any significant way

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125
Q

What are two cytokines secreted by basophils?

A

IL-4 and IL-13

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126
Q

How do mast cells degranulate?

A

Multivalent antigen binds two IgEs on their cell surface at once, cross linking causes degranulation

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127
Q

List six PAMPs

A
  1. LPS present on gram negative cell wall
  2. Bacterial porins in outer membrane of gram negative cell wall
  3. Peptidoglycan
  4. Lipotechoic acids found in gram positive cell wall
  5. Flagellin
  6. Double stranded RNA (viral )
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128
Q

Which MHC molecule do CD8 T cells express?

A

MHC I

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129
Q

Which MHC molecule to CD4+ T cells express?

A

MHC II

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130
Q

What do Th17 cells do?

A

Activation of epithelial cells and fibroblasts, recruit neutrophils

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131
Q

List three TLRs and their ligands

A
  1. TLR2 => peptidoglycan
  2. TLR4 => LPS
  3. TLR5 => flagellin
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132
Q

What is an autacoid? What are some possible actions of autacoids

A

Autacoids are biological factors which act locally for a brief duration near the site of synthesis. May have systemic effect if a significant concentration is reached. Effects include modulation of smooth muscle tone and length, increasing glandular secretion and sensitising nerves for pain and itch

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133
Q

List three mediators of vasodilation.

A

Any of: histamine, prostaglandins, NO, bradyknin, substance P

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134
Q

List three mediators of increased vascular permeability

A

Any of: histamine, complement, leukotrienes, chemokines

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135
Q

List three mediators of neutrophil attachment

A

Any of: IL-1, TNFalpha, leukotrienes, chemokines

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136
Q

List three mediators of fever

A

IL-1, TNF alpha, PGE2

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137
Q

Give two causes of tissue necrosis in acute inflammation

A
  1. Released ROS

2. neutrophil metalloproteinases and collagenases

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138
Q

Give three factors that stimulate histamine release

A
  1. IgE binding mast cell, cross-linking
  2. complement C3a and C5a action
  3. Physical trauma
    Also
    Substance P
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139
Q

What drug might you use for atopic dermatitis, uriticaria, stings??

A

H1 blocker

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140
Q

What four sensations does histamine induce?

A

Redness, wheal, flare and itch

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141
Q

Give two examples of autacoids

A

Histamine

Bradykinin

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142
Q

Give three actions of bradykinin

A
  1. Stimulates vasodilation
  2. Promotes vascular permeability
  3. Stimulates pain sensation via causing substance P release
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143
Q

What are the three kinds of eicosanoid

A

Thromboxanes, prostaglandins and leukotrienes

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144
Q

What are the three major processes leading to acute inflammation?

A
  1. Vasodilation
  2. Increase in vascular permeability
  3. Cellular recruitment and activation
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145
Q

Describe serous inflammation

A

The least severe kind. Minimal increase in vascular permeability. Modified transudate e.g burns, blisters

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146
Q

Describe catarrhal inflammation

A

Serous exudate formed on a mucosal surface. Has mucous, inflammatory cells, debris. Occurs in intestine, respiratory tract.

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147
Q

Describe fibrinous inflammation

A

Caused by larger increase in vascular permeability - fibrinogen included in the effusion, polymerises into fibrin. Occurs on serosal and mucosal body surfaces.

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148
Q

Describe suppurative inflammation

A

Production of large amounts of purulent exudate including neutrophils, pathogen, necrotic tissue. Characteristic response to pyogenic bacteia. May occur in lumen, body cavity, or within an abscess.

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149
Q

Define phlegmon

A

Spreading, diffuse, suppurative inflammation present in loose CT e.g cellulitis

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150
Q

Define empyema

A

Accumulation of pus within a body cavity especially pleura

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151
Q

List three ‘stop’ signals for inflammation

A

Resolvins, lipoxins, protectins, IL-10, TGF beta

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152
Q

What are the three major characteristics of chronic inflammation?

A
  1. Change to inflammatory cell population (more lymphocytes and macrophages, less neutrophils)
  2. Inflammatory tissue damage e.g necrosis
  3. Tissue repair and regeneration e.g fibrosis, scarring, granulation tissue
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153
Q

Are abscesses acute or chronic inflammation?

A

They may be either.

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154
Q

Three features of lymphoplasmacytic inflammation

A
  1. Perivascular cuffing
  2. lymphoid follicles
  3. autoimmune, hypersensitivity reaction common
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155
Q

Typical pathogens to cause pyogranuloma? What cell types predominate?

A

Actinomyces, Actinobacillus. Would typically be macrophages and neutrophils

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156
Q

Typical pathogens to cause caseating granuloma? What cell types would predominate?

A

M. bovis
Typically macrophages, lymphocytes, plasma cells, fibrovascular connective tissue
Possibly mineralised

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157
Q

What are three mechanisms for tissue damage during chronic inflammation?

A
  1. Bacterial or viral toxic damage
  2. Damage by inflammatory mediators e.g proteases and ROS
  3. Direct cell-mediated destruction
  4. Tissue ischaemia due to thrombosis and vascular damage
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158
Q

Describe granulation tissue

A

Loose oedematous connective tissue containing fibroblasts and leukocytes interspersed by capillaries arranged perpendicular to the surface

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159
Q

What are the three phases of granulation tissue?

A
  1. Inflammatory phase
    - clearance of debris
    - replacement with fibrin coagulum, which serves as scaffold for next phase
  2. Proliferative phase has two components: angiogenesis and fibroplasia, occuring simultaneously
  3. Maturation phase
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160
Q

Describe angiogenesis in the context of granulation tissue

A

Hypoxic conditions stimulate VEGF, FGF and angiopoietin release form local endothelial cells, macrophages, platelets. Get activation of endothelial cells and collagenase production allowing breakdown of basement membrane. The cells proliferate into the hypoxic area, secreting proteases to assist. Canalise and anastamose with others to form loops with progressive re-arrangement and maturation.

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161
Q

Describe fibroplasia in the context of angiogenesis

A

Fibroblasts migrate along the fibrin scaffold under the influence of PDGF, FGF and TGFbeta. Initially secrete extracellular matrix as fine reticulin type III collagen network, replacing the fibrin coagulum.

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162
Q

Describe the maturation phase of granulation tissue formation

A

Collagen III replaced with collagen I, re-organised along lines of tension. Wound contracts and tensile strength increases. Fibroblasts atrophy, microvasculature regresses.

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163
Q

Describe primary intention healing

A

Wound edges are in direct opposition. Minimal granulation tissue formation. Epithelium covers defect via mitosis and migration, fuses in midline under scab. Granulation tissue forms from day 3, by day 5 collagen fibres are present. Smaller defects = less granulation tissue = faster healing.

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164
Q

When does secondary intention healing occur?

A

In incidences of extensive tissue loss where the defect is too large for epithelial migration

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165
Q

List 5 factors that influence healing

A
  1. Presence of infection and necrosis
  2. Nutrition e.g vitamin C deficiency inhibits collagen maturation
  3. Movement and pressure on the wound
  4. Persistent foreign body
  5. Impaired blood supply
  6. Hormones such as glucocorticoids can inhibit collagen synthesis
  7. Concurrent disease
  8. Age
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166
Q

Why are cells showing hydropic degeneration pale?

A

They have lost much of their intracellular protein due to membrane damage, and so less to take up the stain

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167
Q

What are myelin figures?

A

Aggregates of phospholipids that have detached from the cell membrane

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168
Q

List three causes of pathological glycogen accumulation in the liver

A
  1. Steroid hepatopathy
  2. Diabetes mellitis
  3. Glycogen storage disorder
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169
Q

What is an example of an inherited lysosomal storage disorder? It is possible to acquire the same condition later in life?

A

Alpha-mannisidosis (a type of glycoproteinoses) in cattle and cats - defective catabolism of CHO component of N-linked glycoproteins. See swollen neuronal cell bodies with foamy cytoplasm and peripheral nuclear displacement.

It is possible that an animal could ingest swainsonine via a plant which inhibits alpha-mannosidase, producing the same condition.

170
Q

What are mallory bodies?

A

Retained misfolded protein bodies in hepatocytes.

171
Q

Define amyloid.

A

An insoluble, extracellular, fibrillar glycoprotein deposit

172
Q

What is fibrinoid change?

A

Entry and accumulation of plasma proteins +/- complement +/- immunoglobulin secondary to vascular endothelial injury. Accumulation in the tunica intima, tunica media and perivascular connective tissues. Especially small arteries and arterioles

173
Q

What is collagenolysis? What are some causes?

A

Lysis of collagen fibrils. Causes include mast cell tumours, insect bites, eosinophilic collagenolytic granulomas

174
Q

Give some examples of pathological apoptosis.

A
  • secondary to radiation damage
  • atrophy of glandular parenchymal cells secondary to blockage of duct
  • viral infections
  • malignant tumour cell killing by immune system
175
Q

Why is there no inflammatory response to apoptosis?

A

Expression of phosphatidylserine molecules on exterior of cell - this is recognised by neighbouring cells and is a stimulus for phagocytosis

Inflammatory mediators such as arachadonic acid are not released

176
Q

What is karryorhexis?

A

Blebbing, budding or fragmentation of the nucleus following rupture of the nuclear envelope

177
Q

Outline the cellular mechanism for oncosis

A

Deprivation of oxygen or nutrients causes cell to switch to anaerobic metabolism and swell with water drawn in by increased lactic acid concentration
Eventually get failure of the Na/K ATPase pump
Get sodium flowing into the swollen cell down its concentration gradient
Damage to the cell and organelle membranes catalyses Ca2+ release from mitochondria/influx from extracellular space causing activation of ATPases, endonucleases, proteases and phospholipase, all of which play a role in breakdown of cell contents

178
Q

Define pyknosis

A

Shrunken, darkly staining nuclei

179
Q

Define karyolysis

A

Fading of nucleus due to activation of RNAses and DNAses

180
Q

When does coagulative necrosis occur?

A

When hypoxia or intracellular acidosis has lead to denaturation of both structural AND enzymatic proteins, preventing proteolysis of the dead cells.

181
Q

Define dry gangrene

A

Coagulative necrosis induced by ischaemia. Tissue eventually mummifies due to dehydration

182
Q

Define wet/gas gangrene

A

Tissue necrosis (usually coagulative) that is then colonised by bacteria causing liquefaction and putrefaction

183
Q

What does liquefactive necrosis refer to?

A

Rapid enzymatic degradation of dead cells involving both autolysis and heterolysis. Characteristic of pyogenic bacterial infection.

184
Q

What is malacia?

A

Liquefactive necrosis in the brain, characterised by softening of the tissues usually due to hypoxic damage leading to oncosis. Tissues are pale, soft and swollen

185
Q

What is caseous necrosis?

A

Following oncosis, dead tissue is converted to grossly dry, granular, cream-white friable tissue +/- mineralisation

186
Q

Two histological features of fat necrosis are?

A

Dystrophic mineralisation of calcium salts and released fat

Precipitation of free cholesterol into needle-like crystals

187
Q

Define dystrophic mineralisation

A

Deposition of calcium salts into tissues that have undergone oncotic necrosis - regardless of normal Ca:P concentrations.

188
Q

Define metastatic mineralisation

A

Deposition of calcium salts into living tissues when Ca:P ratio is abnormal or there is a defect in Ca:P metabolism

189
Q

Normal TP range in most mammals?

A

60 - 80 g/L

190
Q

What is the difference between multiunit and visceral smooth muscle?

A

Multiunit is innervated by a single nerve terminal, never contracts spontaneously.
Visceral occurs in bundles, connected by gap junctions, and may contract spontaneously. Depolarisation of one cell will spread to the others - functional syncytium

191
Q

Which parts of the sarcomere get smaller when it contracts?

A

I band (actin only) and H band (myosin only)

192
Q

What does the A band of the sarcomere encompass? Is it lighter or darker in H&E?

A

The absolute length of the myosin myofibrils, which does not change . Darker in H&E

193
Q

What does the Z line represent?

A

Line of attachment for actin filaments

194
Q

With which muscle fibre type are postural muscles associated?

A

Type I - red cells
Thinner, more myoglobin and mitochondria
Myosin has low ATPase activity > slower contraction

195
Q

Which region of the sarcomere do intercalated discs likely correspond to?

A

Z line

196
Q

Name three components of the intercalated disk, and what they do

A
  1. Fascia adherens - anchors actin to nearest sarcomere
  2. Macula adherens desmosome to stop separation of cardiomyocytes during contraction
  3. Gap junctions to allow electrochemical charge to spread from cell - cell
197
Q

What is the function of astrocytes?

A

Provide mechanical and metabolic support to neurons

198
Q

What is the function of oligodendrocytes?

A

Synthesise myelin sheath of CNS axons

199
Q

What is the function of microglia?

A

Phagocytic function

200
Q

What is the function of ependymal cells?

A

Simple cuboidal/low columnar epithelial cells that line ventricles of brain and central canal of spinal cord. Often ciliated.

201
Q

Is the I band lighter or darker in H&E?

A

Lighter

202
Q

How do K+ and Cl- both contribute to the equilibrium potential of a neuron?

A

The intracellular concentration of K+ is higher than extracellular
There are constitutively open K+ channels in the neuron cell membrane
K+ leaks out of these down its concentration gradient
Cl- cannot leave, so its electrical charge hols some K+ inside the cell
The balance between K+ leaving and staying form the equilibrium potential for potassium (-70mV)

203
Q

What event contributes to the falling phase of the AP?

A

Opening of voltage-gated K+ channels, and rush of K+ out of the neuron

204
Q

What is the refractory period? What are its phases?

A

The period of time post-depolarising that the neuron is unresponsive to further stimulation. Composed of the Absolute refractory period (all Na+ channels are inactivated) and the Relative refractory period (some Na+ channels may be opened with further stimulation). Ensures the AP only travels in one direction

205
Q

Define graded potential

A

Local change in RMP which occurs over short distance. May summate or cancel each other out. Amplitude is variable - is related to the magnitude of the stimulus

206
Q

Define EPSP and IPSP

A

EPSP is a small wave of Na+ ion influx as a result of ion channel activation. IPSP is the same but inhibitory - may increase neuron permeabilty to Cl- or K+, hyperpolarising it.

207
Q

Compare temporal and spatial summation of EPSPs

A

Temporal summation occurs when two or more EPSP are generated within a short timeframe. They may summate to an AP

Spatial summation occurs when two or more EPSP are generated within a small enough time frame and close proximity - may summate to an AP

208
Q

What is the effect on ion permeability caused by activation of m1AChR?

A

K+ permeability of the cell is decreased - brings membrane closer to threshold

209
Q

What is the effect on ion permeability caused by activation of m2AChR?

A

K+ permeability of the cell is increased, brings membrane further from threshold

210
Q

Give some factors that might affect the amount of NT released into the synapse

A

Effectiveness of Ca2+ channels in the presynaptic membrane
Integrity of the SNARE complex
Function of choline acetyltransferase

211
Q

What is an axoplasm?

A

An artery for protein transport from the perikaryon down the axon. Slow and fast systems exist.

212
Q

How many molecules of ACh need to bind the nAChR to cause activation?

A

Two

213
Q

Smaller or larger motor units offer finer muscle control?

A

Smaller

214
Q

How might the somatic nervous system achieve a gentle contraction?

A

By recruiting only the proportion of muscle fibres (e.g half) of the total muscle that it needs.

215
Q

List the three outer layers of muscle and what they enclose.

A 
Epimyseum = lies immediately beneath the fascia. Encloses the entire muscle
Perimyseum = encloses fascicles (bundles of fibres )
Endomyseum = encloses individual fibres
216
Q

Which molecule in the contractile apparatus has a Ca2+ binding site?

A

Troponin - binding causes conformational change in TROPOMYOSIN which then moves from the actin-binding site allowing myosin access

217
Q

Which molecule of the contractile apparatus is rope-like?

A

Tropomyosin

218
Q

What happens after myosin binds actin?

A

Myosin is ‘loaded’ with the energy from splitting an ATP, and still has an ADP + P attached. When it binds actin, a conformational change occurs - the power stroke - pulling actin over the myosin and shortening the sarcomere. ADP and P are released.

219
Q

What causes myosin to release the actin?

A

A new ATP molecule binds the myosin, and the myosin head releases the actin. Hydrolysis of the ATP molecule provides the energy to ‘cock’ the myosin head again.

220
Q

How does this relate to rigor mortis?

A

No new ATP to bind myosin - actin stays bound, muscle remains contracted (stiff)
Furthermore, no ATP to pump Ca out of sarcoplasm, so contraction continues

221
Q

What are the three roles for Ca2+ in skeletal muscle contraction?

A
  1. Influx of Ca2+ at the presynaptic terminal to allow fusion of NT vesicles with presynaptic membrane
  2. Released from the SR in response to AP arriving at the T tubules. Binds troponin C causing tropomyosin to release actin, allowing myosin to bind
  3. Pumped back into the SR via Ca2+ ATPases, allowing tropomyosin to reassociate with actin and muscle to relax
222
Q

What are the three roles of ATP in skeletal muscle contraction?

A
  1. Provides energy for myosin power stroke
  2. Binding to myosin allows release of actin and muscle relaxation
  3. Drives the Ca2+ ATPase that pumps Ca2+ back into the SR
223
Q

A small amount of ATP is stored in skeletal muscle, and used within the first 6 seconds. What are the next three sources of ATP for skeletal muscle ?

A
  1. Creatinine kinase forms ATP from creatinine phosphate and ADP - first 10 sec
  2. Glycolysis used to generate ATP - low level production, durable over longest time. Starts at 30 seconds
  3. ATP generated via anaerobic glycolysis (glucose oxidised to lactic acid) from 70 seconds onward, tires after about 2min
224
Q

Slow twitch fibres have ____ oxidative capacity, ___ glycolytic capacity, ___ mitochondria, _____ blood supply, ____ contraction force, ____ resistance to fatigue

A

Slow twitch fibres have high oxidative capacity, low glycolytic capacity, plentiful mitochondria, better blood supply, lesser contraction force, greater resistance to fatigue

225
Q

Fast twitch fibres have ___ oxidative capacity, ____ glycolytic capacity, _____ mitochondria, _____ blood supply, ____ contraction force, ____ resistance to fatigue

A

Fast twitch fibres have less oxidative capacity, more glycolytic capacity, fewer mitochondria, lesser blood supply, greater contraction force, poor resistance to fatigue

226
Q

List three differences between cardiac and skeletal muscle contraction

A
  1. Contraction is not initiated by neuronal input, though is modulated by it
  2. All myocytes are interconnected electrochemically by gap junctions at intercalated disk
  3. AP has longer duration
227
Q

What is the function of pacemaker cells in heart?

A

They are rhythmically active, capable of depolarising by themselves and passing the AP along to Purkinje fibres and cardiomyocytes. Regulate the baseline HR.

228
Q

How does extracellular Ca2+ influence cardiomyocyte contraction?

A

The presence and concentration of Ca2+ contributes to the strength of contraction

229
Q

Other than [Ca2+], what influences heart contraction strength?

A

ANS innervation
Hormones e.g adrenaline
Extent of cardiac stretch

230
Q

What are dense bodies?

A

Sites of attachment for actin
They are attached to the cell membrane
They transduce the contraction of the sarcomeres to the smooth muscle cell as a whole - actin contracting pulls on the dense bodies making the cell smaller

231
Q

Which muscle type doesn’t have T tubules?

A

Smooth - has caveoli instead

232
Q

Multiunit smooth muscle has ____ gap junctions, _____ response to stretch, _____ response to hormonal influence

A

Multiunit smooth muscle has fewer gap junctions, poor response to stretch, minimal response to hormonal influence

233
Q

Visceral/single unit smooth muscle has ____ gap junctions, ____ response to stretch, hormones and local pacemaker potentials.

A

Visceral/single unit smooth muscle has more gap junctions, strong response to stretch, hormones and local pacemaker potentials.

234
Q

All muscle fibres are innervated in ____ smooth muscle, but only a few are innervated in _____ smooth muscle.

A

All muscle fibres are innervated in multi unit smooth muscle, but only a few are innervated in single unit smooth muscle.

235
Q

List the three ways smooth muscle cells achieve an increase in intracellular Ca2+

A
  1. Voltage gated Ca2+ channels at the cell membrane
  2. Ligand gated Ca2+ channels at the cell membrane
  3. Ca2+ channels at the ER (activated later, by second messenger systems)
236
Q

Describe cross bridge cycling in smooth muscle

A

Ca2+ binds to calmodulin which activates myosin light chain kinase. Myosin light chain kinase uses ATP to phosphorylate myosin, changing its conformation and increasing myosin’s affinity for actin. Myosin ATPase then cycles, allowing binding of actin, power stroke and release.

237
Q

Which enzyme is upregulated by circulating cortisol and corticosteroids to cause hepatic lipidosis?

A

Glycogen synthetase

238
Q

What is required for amyloidosis to develop?

A

A source of inflammation in the body, increasing SAA production
Production of a defective SAA protein

239
Q

What do muscle spindles detect? Where are they located?

A

Stretch of skeletal muscle. Located within the fleshy part of the muscle

240
Q

What do golgi tendon organs detect? Where are they located?

A

Tension of skeletal muscle. Located at the junction of muscle and tendon.

241
Q

What are the three sources of sensory innervation conveyed by afferent neurons to the spinal cord?

A

Skeletal muscles of the area
Other nearby muscles especially the antagonist
Tendons, joints, skin and other structures directly affected by the muscle’s action

242
Q

What are the fibres inside a muscle spindle called?

A

Collectively, they are known as ‘intrafusal’ fibres, and the fibres of the surrounding skeletal muscle are ‘extrafusal’. There are two types of intrafusal fibres - Nuclear bag fibres, which detect the onset of stretch, and nuclear chain fibres which detect sustained stretch.

243
Q

Describe the stretch reflex in one sentence

A

Stretch of a muscle is detected by muscle spindle and through the stretch reflex the stretching muscle is stimulated to contract, and the antagonist is stimulated to relax

244
Q

Describe the tendon reflex in one sentence

A

Excessive tension of a muscle is detected by the golgi tendon organ at the musculo-tendonous junction, and relayed to the spinal cord causing inhibition of further APs to the original muscle, relaxing it, and propagation of new APs to the antagonist muscle, causing it to contract

245
Q

True or false - drug concentration can affect its selectivity.

A

True

246
Q

At the cellular level, do antagonists have efficacy?

A

No

247
Q

What is potency? Is it affected by affinity?

A

Potency is the amount of drug that is required to have the effect. It is usually affected by affinity (higher affinity, more potent) though not always. Specific for a given tissue type.

248
Q

What is EC50?

A

The dose of the drug at 50% of its maximum effect. Specific to tissue type.

249
Q

As antagonists have no efficacy, how would you measure their potency?

A

By adding them to a solution then adding the agonist at varying doses. The higher the dose of agonist required to outcompete the antagonist, the more potent the antagonist is. Requires competitive, reversible binding of drug to target. The concentration of agonist required to regain the full response = pA2 or pKb

250
Q

Pharmacodynamics relates to:

A

Affinity, selectivity, potency and efficacy. Know where drug acts and predict response.

251
Q

Pharmacokinetics relates to:

A

How often to dose based on ADME, potency and efficacy. Know long term consequences of use

252
Q

Which sympathetic nerve is unusual in that it does not synapse at the SNS ganglion chain?

A

The ACh nerve innervating the adrenal gland

253
Q

Which SNS nerve is unusual in that it uses ACh as its post-ganglionic transmitter?

A

The nerves innervating sweat glands

254
Q

From which area of the spine do SNS neurons arise?

A

Thoraco-lumbar

255
Q

From which areas of the spine to PNS neurons arise?

A

Cranial, sacral

256
Q

How does the SNS indirectly affect the body?

A

Via release of adrenaline from the adrenal gland. This is how it modulates arteriolar diameter and bronchiolar diameter

257
Q

Which receptor does NA have greatest selectivity for?

A

alpha1 adrenergic

258
Q

Which receptors does adrenaline have greatest selectivity for?

A

beta1 and beta2 adrenergic

259
Q

What is meant by the ‘alpha’ effect of adrenaline in the blood?

A

A rise in BP due to adrenaline’s actions on the alpha1 receptors to cause vasoconstriction, and beta1 receptors to increase HR.

260
Q

What is meant by the ‘beta’ effect of adrenaline in the blood?

A

PNS homeostatic innervation of the heart brings HR back down, and this unmasks the effect of adrenaline binding the beta2 adrenoceptors to cause vasodilaton. BP falls as adrenaline has higher affinity for the beta2 than alpha1.

261
Q

What happens when NA is given IV?

A

Get spike in BP due to its action on alpha1 adrenoceptors to cause vasoconstriction. There would be some action on the beta1 adrenoceptors too, however this is not obvious due to the PNS-mediated homeostatic mechanism which reduces HR to combat the rise in BP. Thus we see a reasonable spike in BP with minimal change in HR. NA can’t cause adrenaline release from the adrenal gland, as its being given in the blood.

262
Q

What happens when give adrenaline + phentolamine IV?

A

Get large drop in BP due to adrenaline action on beta2 adrenoceptors. Homeostatic mechanism mediated by SNS is to raise HR to bring BP back up. We get adrenaline’s effect on beta1 receptors + this homeostatic mechanism to produce a greater increase in HR than adrenaline alone.

263
Q

What is phentolamine?

A

An alpha-adrenoceptor antagonist. Not commonly used medically as not very specific ??

264
Q

What happens when we give noradrenaline and phentolamine IV?

A

No change in BP, as this was mediated by alpha1 which has been blocked. We do see a small increase in HR due to NA’s action on beta-1 - absence of PNS homeostatic response unveils this small effect.

265
Q

What is propanolol? What effect might it have on NA and A administered IV?

A

A beta adrenoceptor antagonist - would block increase in HR and vasodilation of peripheral arterioles as mediated by adrenaline or noradrenaline in the blood.

266
Q

List the contents of a noradrenaline vesicle. Other than NA, are any of them physiologically significant?

A

Noradrenaline, neuropeptide Y, ATP, dopamine-B-hydroxylase. There is evidence to suggest that NPY and ATP can participate in signaling if NA is not present or functional.

267
Q

Which drugs prolong NA effect at the synapse? What is the mechanism?

A

90-95% of NA is taken up by the presynaptic nerve. Blocking this pathway can prolong the effects of NA. Drugs that do this are cocaine, desipramine. Causes rapid accumulation of NA in the cleft

268
Q

What other effects might you get from cocaine?

A

Increased dopamine signalling in the CNS as the uptake receptor for NA and dopamine is the same
Effects on peripheral NS including tachycardia

269
Q

Which enzyme breaks down NA at the presynaptic nerve?

A

Monoamine oxidase (MAO)

270
Q

Which enzymes metabolise NA in the peripheral tissues?

A

MAO

Catechol-o-methyltransferase

271
Q

Which drugs might you use to cause slow accumulation of NA in the cleft? What is the mechanism?

A

MAO inhibitors will cause slower, more progressive NA accumulation than cocaine or desipramine. E.g moclobemide.

272
Q

What are the two mechanisms by which indirectly acting sympathomimetics increase NA effect? What are some examples?

A

Have affinity for the NA reuptake carrier at the presynaptic nerve

  1. Enter the nerve terminal, cause release of NA vesicles
  2. As they work, compete with released NA for uptake, prolonging its effect in the synapse

Examples are amphetamine, ephedrine

273
Q

What is phenylephrine?

A

An alpha adrenoceptor agonist

274
Q

What is isoprenaline?

A

A beta adrenoceptor agonist

275
Q

What is the effect on NA dose required to increase BP and HR in the presence of phentolamine?

A

Phentolamine is an alpha adrenoceptor antagonist.

You need more NA to produce BP increase, though no effect on HR.

276
Q

What is the effect on NA dose required to increase BP and HR in the presence of propanolol?

A

Propanolol is a beta adrenoceptor antagonist.

You need more NA to produce an increase in HR, though no effect on BP

277
Q

What feature of isoprenaline limits its clinical use?

A

It isn’t very specific for beta2 adrenoceptors - so if used to cause bronchodilation, get a certain amount of cross-reactivity with beta1 adrenoceptors causing heart palpitations

278
Q

Which drug is commonly used to help asthmatics with their asthma?

A

Salbutamol, and beta2 agonist. Has higher specificity than isoprenaline. Causes fewer heart palpitations, though still get some.

279
Q

What is an alpha-2 adrenoceptor agonist? What is the effect produced?

A

Clonidine - has affinity for alpha 1, but mostly alpha2. Causes inhibition of NA release at the presynaptic neuron, dampening down SNS transmission. Causes sedation as passes into CNS to inhibit neurological activity there.

280
Q

Which alpha1 antagonist is preferred to phentolamine? Why?

A

Prazosin - more specific for alpha1. Provides relief for hypertension, though can permit wide blood pressure fluctuations when posture changes, causing dizziness and potentially fainting

281
Q

What does yohimbine do? What is its use in veterinary medicine? What other names is it known by?

A

Yohimbine is an alpha2 antagonist - prevents inhibitory signalling. May be used to reverse Clonidine sedation. Also called xylazine a.k.a Rompun.

282
Q

List three effects of alpha1 adrenoceptor activation.

A
  1. Vasoconstriction
  2. Constriction of sphincters in GIT
  3. Dilation of pupil via constriction of radial muscle
283
Q

List three effects of beta1 adrenoceptor activation

A
  1. Increase in HR
  2. Renin secretion by the kidneys
  3. Glycogenolysis in the liver
284
Q

List two effects of beta2 adrenoceptor activation.

A
  1. Vasodilation of skeletal muscle arterioles

2. Bronchodilation via relaxation of adjacent smooth muscle

285
Q

What is one effect of beta3 adrenoceptor activation?

A

Lipolysis in adipocytes

286
Q

As a drug IV, is NA useful?

A

Not really - has greatest affinity for alpha1, followed by beta1, but has limited potency from the blood

287
Q

An a drug IV, is adrenaline useful?

A

Has similar affinity for alpha1, beta1, and beta2. Endogenous location is bloodstream, so has high potency in IV dose. Stimulates HR, blood flow, cellular metabolism and improves airway function - lifesaving!

288
Q

Beta1 and beta2 adrenergic receptors are both Gs GPCR. What determines the difference in their effects?

A
  1. The location of the receptor in the body (what tissue type, and in what density)
  2. The affinity of the ligand for the receptor
289
Q

What is the presynaptic neurotransmitter at the adrenal gland?

A

ACh

290
Q

If you pre-treat with atropine and give a large dose of ACh, what is the outcome on BP?

A

Atropine is a mAChR antagonist - so the drop in BP caused by ACh will be prevented. At high doses, circulating ACh may act on the nAChR at the adrenal gland, and cause release of adrenaline from the adrenal gland. Therefore expect big jump in BP due to action of adrenaline.

291
Q

If you give moderate ACh dose IV, what is the outcome on BP?

A

Drops, due to ACh acting on mAChR in the heart to reduce rate and contractility

292
Q

Which is the dominant AChR available to circulating ACh?

A

mAChR

293
Q

List four effects of mAChR antagonists on a living organism

A
  1. Tachycardia - lost PNS tone
  2. Inhibition of SLUD
  3. Dilation of pupil
  4. Agitation, restlessness, coma, depression (CNS effects)
294
Q

List two clinical applications for atropine

A
  1. Bradycardia

2. Carbamate poisoning

295
Q

What sort of drug is hyoscine?

A

A mAChR antagonist

296
Q

What sort of drug is ipratopium?

A

A mAChR antagonist

297
Q

What sort of drug is pilocarpine?

A

a mAChR agonist

298
Q

What sort of drug is carbachol?

A

a mAChR agonist

299
Q

What sort of drug is bethanecol?

A

a mAChR agonist

300
Q

What sort of drug is physostigmine?

A

A reversible AChE antagonist

301
Q

What sort of drug is neostigmine? Provide two uses.

A

A reversible AChE antagonist.

  1. Treatment of myasthenia gravis (prolong ACh at synapse)
  2. Reversal of non-depolarising neuromuscular blockers (increases available ACh which then outcompetes)
302
Q

What are the two categories of nAChR antagonist?

A
  1. Neuromuscular blocking drugs (action at NMJ)

2. Ganglion blocking drugs (action at sympathetic ganglion)

303
Q

What are the two categories of NMJ blocking drugs (nAChR antagonists). Give a drug for each category.

A
  1. Non-depolarising blockers - vecuronium, tubocurare

2. Depolarising blockers - suxamethonium

304
Q

What is an example of a nAChR antagonist that blocks at the ganglion?

A

Hexamethonium

305
Q

Which drugs may be reversed with neostigmine?

A

Vecuronium, d-tubocurare

306
Q

Give an example of an nAChR agonist?

A

Nicotine

307
Q

What sort of G protein is mAChR 3? What signal transduction mechanism does it activate?

A

Gq protein

  • PLC breaks PIP2 into IP3 + DAG
  • DAG activates PKC
  • IP3 mobilises Ca2+, which causes downstream effects such as GIT contraction
308
Q

What sort of G protein is mAChR 2? What signal transduction mechanism does it activate?

A

Gi protein

  • inhibits adenylate cyclase activity to reduce cAMP production
  • lower cAMP levels in cytosol reduce HR and force
309
Q

How does ACh cause vasodilation, when acting from the blood?

A

Binds M3 on vascular endothelial cells
Downstream signaling switches on NO synthetase causing NO production
NO diffuses to vascular smooth muscle, causes relaxation > vasodilation

310
Q

Give five examples of autacoid molecules.

A 
1. Histamine
2 Bradykinin
3. Prostaglandins
4. Leukotrienes
5. Thromboxane
6. Eicosanoids
311
Q

Give four cell types that produce histamine. Is it stored for release, or made on demand?

A

Mast cells, basophils, ECL cells in stomach, histaminergic neurons. Stored in granules.

312
Q

What sort of receptor are the histamine receptors?

A

GPCRs

313
Q

What are some clinical uses for H1 antagonists?

A 
Hay fever tx
Atopic dermatitis
Urticaria
Anaphylaxis
Angioderma
Bites and stings
314
Q

What is a clinical use for H2 antagonists? Name two such drugs

A

Reduce HCl secretion in the stomach - ranitidine, cimetidine

315
Q

Why must bradykinin synthesis occur after an initial increase in vascular permeability in inflammation? What other molecules are involved ?

A

Because Hageman factor, is only activated once outside the blood. Hageman factor is required to convert prekallikrien to kallekrien, which can then convert Kininogen to bradykinin.

316
Q

What sort of receptors are bradykinin receptors?

A

GPCRs - has B1 and B2

317
Q

What does icatibant do? what condition might it be used for?

A

B2 bradykinin receptor antagonist - used to reduce effects of excessive circulating bradykinin in inherited angioderma

318
Q

Eicosanoids are synthesised de novo (not stored). What is the signalling mechanism for this?

A

Influx Ca2+ into cell > PLA2 releases AA from phospholipids in cell membrane > COX acts on AA to produce prostanoids, LOX acts on AA to produce leukotrienes

319
Q

In which cells is LOX mostly found?

A

Leukocytes

320
Q

Which prostaglandin is produced by most cells of the body?

A

PGE2

321
Q

Give an example of two prostanoids acting in synergy

A

PGE2 and PGI1 both increase sensation and duration of pain (hyperalgesic)

322
Q

What kind of receptor are eicosanoid receptors?

A

GPCRs

323
Q

How do NSAIDs work? Give an example

A

Aspirin - Inhibit COX

324
Q

How do glucocorticoids work? Give an example

A

Dexamethosone
Bind intracellular receptor to change gene expression
Inhibit PLA2 and COX
- inhibit synthesis of prostanoids and leukotrienes
Inhibit cytokine synthesis and adhesion molecule expression

325
Q

How long is the pre-implantation period? What event typically occurs at the end?

A

Fertilisation - 1 weeks

Blastocyst hatches from zona pellucida

326
Q

In which week do the three germ layers appear? What is one other event from that week?

A

Week 2. Also should have implantation

327
Q

What is one major event of the third week?

A

Formation of the extra-embryonic membranes

328
Q

What are the three requirements for implantation?

A
  1. Blastocyst hatches from zone pellucida
  2. Pregnancy recognised by mothers body
  3. Formation of the extra-embryonic membranes
329
Q

Define morula

A

Solid ball of blastomeres within the zona pellucida. Formed through cleavage.

330
Q

Define blastocyst

A

Blastomeres are arranged within the zona pellucida to form blastocoele containing inner cell mass and fluid

331
Q

What four forces facilitate rupture of the zona pellucida?

A

Blastocyst growth
Fluid accumulation in blastocoele
Enzymatic degradation via trophoblast enzymes
Blastocyst contraction

332
Q

What other names is the inner cell mass known by?

A

Embryonic disc = epiblast = embryo proper

333
Q

Where does the hypoblast layer come from?

A

The proliferating inner cell mass. Once the hypoblast has formed, the ICM is called the epiblast.

334
Q

Which structure indicates the beginning of gastrulation?

A

The primitive streak (formed from epiblast cells). It also gives the embryo polarity for the first time.

335
Q

Where do endoderm cells come from?

A

A coelom forms between the epiblast and hypoblast layers. Epiblast cells migrate medially, through the primitive streak and through the coelom to the hypoblast layer. They push the hypoblast cells laterally, and become the endoderm

336
Q

Where do mesoderm cells come from?

A

As for endoderm, except they remain in the coelom and migrate laterally to fill it

337
Q

Where does ectoderm come from?

A

The remaining epiblast cells after mesoderm and endoderm have formed

338
Q

Where is somatic mesoderm relative to the somites? ?What does it occur beside

A

lateral to somites

Ectoderm

339
Q

Where is splanchnic mesoderm relative to the somites? ?What does it occur beside

A

Lateral to somites

Endoderm

340
Q

What structures does the ectoderm form in the adult?

A

Epidermis
Nervous tissue
Brain and spinal cord
Peripheral nerves and other neural crest derivatives

341
Q

What structures does the mesoderm form in the adult?

A

Connective tissues
Muscle
Epithelial linings of cardiovascular, urinary and reproductive systems

342
Q

What structures does endoderm form in the adult?

A

Epithelial linings of GIT and respiratory system
Digestive organs
Glands of digestive system

343
Q

What major event occurs simultaneously to gastrulation?

A

Formation of the notochord (primitive streak)

344
Q

What events begin as a result of notochord formation?

A

Head, nervous system formation

Somite formation

345
Q

What is the ultimate fate of the notochord?

A

Becomes nucleus pulposus of the intervertebral discs

346
Q

List the four extra-embryonic membranes

A

Chorion, amnion, yolk sac, allantois

347
Q

What is the function and origin of the chorion?

A

Trophectoderm and mesoderm
Mediates attachment to uterus
Eventually fuses with allantois

348
Q

What is the function and origin of the amnion?

A

Trophectoderm and mesoderm

Fluid filled sac that protects the embryo via shock absorption

349
Q

What is the function and origin of the yolk sac?

A

Endoderm
Provides nutrients for the embryo
Contributes primitive germ cells

350
Q

What is the function and origin of the allantois?

A

Primitive gut
Fluid filled sac that collects waste from the embryo
Eventually fuses with the chorion to form the allantochorionic membrane which is the foetal contribution to the placenta

351
Q

What is neurulation?

A

Notochord-induced transformation of the ectoderm into nervous tissue. Confers first appearance of gut, heart and nervous system

352
Q

What is neuroectoderm?

A

Tall, columnar ectodermal cells over the notochord which form at the beginning of neurulation. Form a neural plate with neural folds at either end and a neural groove in the centre.

353
Q

What event/s complete formation of the neural tube?

A

Closure of the anterior and posterior neural pores

354
Q

What is the position of the neural crest cells?

A

Dorsolateral to the neural tube, beneath the ectoderm.

355
Q

What are some products of the neural crest cells?

A

Pigment cells of skin
Neurons and glial cells of the PNS
Adrenal medulla cells
Meninges, bone, fascia and teeth in head

356
Q

What major event is occuring at the same time as neurulation?

A

Cranial and caudal folding of the embryo. The cranial fold forms subcephalic pocket

357
Q

What are the three placodes? what tissue do they form from?

A

Ectoderm

  • nasal placode > nasal chambers
  • optic /lens placode > lens
  • otic placode > inner ear
358
Q

Which tissue forms somites?

A

Paraxial mesoderm

359
Q

What do the somites give rise to?

A

First 7: mesodermal structures in the head

Caudal to those: axial skeleton and its associated musculature, overlying dermis

360
Q

What does the intermediate mesoderm form?

A

Occurs lateral to the somites - forms urinary and reproductive system

361
Q

What is the fusion of somatic mesoderm and ectoderm called?

A

Somatopleure

362
Q

What is the fusion of splanchnic mesoderm and endoderm called?

A

Splanchnopleure

363
Q

What structure occurs between the somatopleure and the splanchnopleure? what does it give rise to?

A

The extra-embryonic coelom- gives rise to the cavities of the body (pleural, pericardial, peritoneal)

364
Q

Define agenesis

A

Developmental abnormality where there is not enough tissue - something has not formed.

365
Q

Define aplasia

A

Failure of a structure to develop in utero

The most severe form of hypoplasia

366
Q

Define segmental aplasia

A

Aplasia of tubular structure e.g intestine, uterus

367
Q

What other term could be used to describe segmental aplasia of the intestine?

A

Intestinal atresia

368
Q

Define hypoplasia

A

Failure of an organ or tissue to reach its full size

369
Q

Give two veterinary example of hypoplasia

A

Hypoplasia of uterus i female calves due to ‘freemartinism’ masculinising them

Cerebellar hypoplasia due to BVDV infection or FIP infection in utero

Congenital micropthalmia in piglet due to hypovitaminosis A in utero

370
Q

What is a common feature of unilateral hypoplasia, dysplasia, aplasia of paired structures?

A

Hyperplasia/hypertrophy of the unaffected structure

371
Q

Define dysplasia

A

Abnormal development resulting in disorganisation of cells and hence architectural distortion of a tissue or organ. Effect on function is chaotic though may require microscope to identify

372
Q

Under what circumstances may dysplasia occur post-natally?

A

Infection with a virus in first few weeks of life in species that are still undergoing development e.g kitten, puppy

373
Q

Define atresia

A

Absence or closure of a normal opening

374
Q

What are the potential consequences of atresia ani?

A 
Distension of distal rectum and colon
Possibly mucosal ulceration and perforation
Leading to septic peritonitis 
Grossly see abdominal distension
Extreme discomfort
375
Q

Define atrophy

A

Decrease in cell size or tissue mass after normal growth has been achieved
Cell decreases size and metabolic activity in order to survive in presence of external stressor

376
Q

Define hypertrophy

A

Increase in cell size, or increase in tissue mass due to increase in cell size
All cells

377
Q

Define hyperplasia

A

Increase in tissue mass due to increase in cell number

Labile and stable cells only

378
Q

Define metaplasia

A

Transformation of a mature, differentiated cell type into another cell type

379
Q

Provide two examples of physiological atrophy

A
  1. Involution of lymphoid organs (thymus at puberty, LNs in old age)
  2. Involution of corpus luteum in ovary during oestrous
  3. Involution of uterus following parturition, involution of mammary secretory parenchyma following lactation
380
Q

What are the seven major mechanisms of pathological atrophy?

A
  1. Decreased blood supply
  2. Decresaed workload
  3. Loss of innervation
  4. Loss of endocrine stimulation
  5. Obstruction of secretory or drainage ducts
  6. Inadequate nutrition or wasting diseases
  7. Ageing
381
Q

Provide an example of decreased blood supply causing atrophy

A

PSS

Pressure atrophy

382
Q

Provide an example of decreased workload causing atrophy

A

Disuse atrophy of limb in a cast for extended period

383
Q

Provide an example of loss of innervation causing atrophy

A

Atrophy of the left dorsal cricoarytenoid muscle in laryngeal hemiplegia in horses due to damage of the left recurrent laryngeal nerve
* fastest form of atrophy*

384
Q

Provide an example of loss of endocrine stimulation causing atrophy

A

Atrophy of the prostate gland following castration of male dog
Atrophy of adrenal cortex due to long term corticosteroid therapy and reduced ACTH secretion

385
Q

Provide an example of duct obstruction causing atrophy

A

Obstruction of pancreatic duct causing parenchymal atrophy. May be compounded by increase in pressure reducing bloodflow.

386
Q

Provide an example of inadequate nutrition or wasting disease causing atrophy

A

Chronic conditions such as cancer cause atrophy of adipose, muscle, viscera especially liver, pancreas and myocardium

387
Q

Provide an example of aging causing atrophy

A

Of reproductive organs and CNS in old animals and people

388
Q

What is lipofuschin?

A

Lipofuschin is polymers of lipids and phospholipids complexed with proteins

389
Q

Why does lipofuschin accumulate in atrophic and aged cells?

A

It is the residue formed from peroxidation and polymerisation of unsaturated fatty acids and the phospholipid component of cell membranes. Is indigestible. The more organelle breakdown, the more lipofuschin there will be

390
Q

Name three ultrastructural features of atrophic cells

A
  1. Reduced size and number of organelles
  2. Reduced number of secretory vesicles
  3. Additional autophagosomes that may contain lamellar lipofuschin
391
Q

List four features of atrophic tissue under light microscope

A
  1. False appearance of hypercellularity due to crowding of small cells
  2. Increased prominence of ducts, connective tissue
  3. Fatty infiltration
  4. Lipofuschinosis
392
Q

List five gross features of atrophic organs

A

MAY BE

  1. Smaller, lighter
  2. Firmer
  3. May be pale due to fat or fibrosis deposit
  4. May be brown-yellow due to lipofuschinosis
  5. May have wrinkled CT capsule
393
Q

What is serous atrophy of fat?

A

When fat stores are being mobilised so quickly the fat becomes gelatinous, translucent, sometimes pale pink due to oedema and increased prominence of local capillaries

394
Q

Under what circumstances is serous atrophy of fat seen? Which organ will commence this process last (i.e in most severe demand)

A

Extreme starvation/cachesis

Serous atrophy of the bone marrow is only seen in most advanced stages

395
Q

List three mechanisms for villous atrophy

A
  1. Significant loss of surface epithelial cells e.g viral infection, transient hypoxia
  2. Necrosis or impaired mitosis of crypt stem cells e.g viral infection, prolonged hypoxia >2h
  3. Dysregulation of crypt cell proliferation and enterocyte maturation e.g lymphoma, food hypersensitivity
396
Q

List two consequences of villous atrophy

A
  1. Reduced SA for absorption > malnutriton

2. Reduced absorption of food > osmotic drag of water into lumen > diarrhoea

397
Q

What pathogen is responsible for progressive atrophic rhinitis in pigs? Which species are affected, and which age?

A

Pasteurella multocida +/- other bacteria

Typically 6 - 12 week piglets

398
Q

What clinical signs might a pig with atrophic rhinitis display?

A 
Sneezing
Nasal discharge
Haemorrhage
Nasal deformity
Failure to thrive
Predisposition to secondary bacterial infection
399
Q

What is the pathogenesis of atrophic rhinitis

A

P. multocida cyclotoxin causes:
- atrophy of the renal mucous secreting glands
- resorption of nasal turbinate bone
-. reduced formation of new bone
- proliferation of fibroblasts
- deposition of collagen
Leading to progressive atrophy of the nasal turbinates and deviation of snout to more severely affected side.

400
Q

Define abiotrophy. Give an example

A

Genetically programmed, premature or accelerated degradation of mature cell types causing atrophy of affected organ or tissue

Autosomal recessive cerebellar abiotrophy in dogs, lambs, piglets and calves
- especially purkinje cells

401
Q

What ultrastructural features are associated with cellular ageing?

A 
Irregular nuclear shape
Vacuolation of mitochondria
Reduced ER
Distorted golgi
Accumulation of lipofuschin
402
Q

What are advanced glycation end products? Why do they accumulate? what is one veterinary example?

A

The result of non-enzymatic glycosylation reactions causing cross-linking of adjacent proteins. Accumulation of abnormally folded proteins. Due to reduced proteasome function of older cells.
E.g Age-related glycosylation of lens proteins causes senile cataracts

403
Q

Give two examples of physiological hypertrophy

A
  1. Hypertrophy of pancreatic acinar cells in response to high protein diet
  2. Hypertrophy of uterine smooth muscle cells in response to oestrogen in late pregnancy
404
Q

Give two examples of pathological atrophy

A
  1. Hypertrophy of cardiac muscle in response to chronic high BP > narrowing of lumen, reducing stroke volume and cardiac output. Prone to hypoxic damage and energy defecit
  2. Hypertrophy of intestinal smooth muscle proximal to ab obstruction or stricture > reduced lumen size
405
Q

Which two factors impose the upper limit on hypertrophy?

A

Distance for O2 diffusion into tissues

Size of cell permits efficient metabolic rate

406
Q

List four signals for hyperplasia

A
  1. Hormonal stimulation
  2. Cytokine signalling
  3. Growth factor signalling
  4. Increased expression of growth factor receptors
407
Q

List three advantages of hyperplasia

A
  1. Repair of injured tissues
  2. Compensate for lost cells
  3. Respond to increased workload
  4. Protect a structure that is being damaged
408
Q

What is the difference between hyperplasia and neoplasia?

A

Hyperplastic response will stop once cause has been removed or tissue mass has been restored

409
Q

What are the common stimuli for hyperplasia?

A

Increased hormonal stimulation

Compensation ( increased workload )

410
Q

Provide two examples of physiological hyperplasia

A
  1. Mammary gland hyperplasia in late pregnancy under influence of oestrogen, progesterone and prolactin
  2. Mild hyperplasia of adrenal cortices in response to sustained stress causing increased ACTH secretion
411
Q

Provide two examples of pathological hyperplasia

A
  1. Goitre due to low iodine
    - see fronds of hyperplastic follicular epithelium, no colloid in follicles
  2. Mammary fibroadenomatous hyperplasia in young, intact female cats due to endogenous progesterone
  3. Benign prostatic hyperplasia in dogs due to testosterone
412
Q

What is the general outcome of metaplasia?

A

Usually change of a specialised, vulnerable cell type into a less specialised, more resistant type - typically within the same germ line. Most common in epithelia e.g squamous metaplasia of upper alimentary tract mucous cells. Generally confers loss of function

413
Q

What is the most common kind of metaplasia?

A

Squamous metaplasia.

414
Q

What does glandular metaplasia usually involve? Give an example

A

Transformation of epithelial cells into mucous secreting cells e.g chronic inflammation of the gastric fundus causes mucous metaplasia of the gastri epithelium e.g parasitism. Get reduced HCl secretion and impaired digestion.

415
Q

What does mesenchymal metaplasia usually involve? Give an example.

A

Metaplasia of one connective tissue type into another e.g metaplastic bone formation in pulmonary connective tissues of old dogs and cattle

416
Q

What does dysplasia mean in the acquired sense? When is it most commonly seen?

A

A proliferative response of cells and tissues in which there is abnormal tissue architecture and cellular atypia

Most commonly in chronically ill/inflamed epithelium

417
Q

What are 5 possible features of dysplasia under the light microscope?

A
  1. Disorderly tissue architecture, irregular cell orientation
  2. Loss of normal regular progression from deep germinative to superficial mature cells
  3. Increased mitotic rate, mitoses in more superficial cell layers
  4. Cellular pleiomorphism
  5. Hyperchromatic cells
418
Q

Give an example of acquired dysplasia

A

Dysplasia of transitional mucosa of bladder in chronic cystitis, dysplasia of mammary epithelium in chronic mastitis

419
Q

What can anaplasia refer to in the acquired sense? Is it reversible?

A

Loss of differentiation - irreversible

420
Q

Give three microscopic features of anaplasia

A

Hyperchromatic, irregular nuclei with prominent nucleoli
High mitotic rate
Abnormal mitoses present

Cells to systems (4 decks)

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