Brainscape's Knowledge GenomeTM

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


See full index

DVM 2 - 1 > HLI 4 > Flashcards

HLI 4 Flashcards

1
Q

What are autacoids, duration of action, examples and functions

A
  • Chemical mediators which are synthesised and function in a localised area or tissue – ‘local hormone’
  • Typically short lived and rapidly degraded
  • Complex effects mediated through multiple receptor types
    ○ e.g. histamine, serotonin, eicosanoids
  • Key mediators of inflammatory processes
  • Important targets for anti-inflammatory therapies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Histamine where stored, what released by and what response is it essential in

A
  • Found in most tissues, stored at high concentrations in lungs, skin, GI tract (clinical signs)
  • Cellular level: stored in mast cells, basophils, ECL cells (stomach), histaminergic neurons (brain)
  • Histamine release stimulated by antigen binding to IgE
    ○ Essential role in type I hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 4 receptors for histmine and there locations

A 
H1 receptors: 
- Smooth muscle, endothelium, brain 
H2 receptors:
- Gastric mucosa, cardiac muscle, brain, mast cells (negative feedback)
H3 receptors: 
- Brain: pre-synaptic 
H4 receptors:
- Leukocyte chemotaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Histamine effects on gastric secretion and examples of drugs

A
  • Histamine stimulates the secretion of gastric acid through action on H2 receptors located on parietal cells
  • Histamine is stored in enterochromaffin-like (ECL) cells in gastric fundus
  • Covered during Digestive System lectures
    ○ e.g. cimetidine, ranitidine - anti-histamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Effects on smooth muscle and cardiovascular of histamine

A

Effects on smooth muscle
- Acting on H1 receptors, contracts smooth muscle in ileum, bronchi, bronchioles and uterus
- Contraction of most smooth muscle except blood vessels (vasodilation)
Effects on cardiovascular system
- Vasodilation via H1 receptors in vascular smooth muscle
- ↑ heart rate and contractility via cardiac H2 receptors
- ↑ vascular permeability via H1 receptors on endothelial cells

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

Histamine effects on the neurological system

A
  • Neurotransmitter in the brain
  • H1 post-synaptic receptors:
    ○ Stimulates sensory nerves to cause itch
  • H3 pre-synaptic receptors:
    ○ Inhibit the release of a number of neurotransmitters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is histamine used in veterinary medicine

A
  • Histamine itself not used therapeutically due to multiple effects
  • H1 and H2 antihistamines are widely used in small & large animal veterinary clinical work for the following indications:
    ○ Allergic reactions (bites/stings, allergic skin disease) - H1
    ○ Gastric ulceration (treatment and prevention) - H2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

H1 antihistamines function and side effects

A

Function
- Relaxation of bronchiolar and intestinal smooth muscle
- Inhibition of vasodilation and increased vascular permeability
Inhibition of itch sensation by prevention of sensory nerve stimulation
- antimotion sickness
Side effects
- sedation - as H1 receptors found on the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the differences between first and second generation H1-antihistamines and which more effective in veterinary medicine

A

First generation antihistamines
- (e.g. diphenhydramine, chlorpheniramine)
- These drugs cross the BBB and therefore produce CNS side-effects (sedation)
• Second generation antihistamines
- (e.g. loratadine, cetirizine)
- Less lipid soluble, so limited ability to cross the BBB (blood-brain barrier) , reduced central effects (sedation)
- Used widely in humans, limited efficacy in veterinary patients and not widely used
○ Due to importance of sedation in the patients - scratch-itch cycle and they only make it worse, really need to reduce the itch sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

H2 antihistamines functions and examples

A
  • Reduce gastric acid secretion from parietal cells
    ○ e.g. cimetidine, ranitidine: remember DVM1!
  • Also mast cells - negative feedback, histamine release acts back on the mast cells to stop further production of histamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What chemicals are involved in bee stings and the main chemical and where it is present

A
  • Profound oedematous, very rapid and localised response - dictated by autacoids (act as local hormones)
    Serotonin
    • Serotonin = 5-hydroxytryptamine (5-HT)
    • Present in high concentrations:
    1. GI tract (enterochromaffin cells, enteric neurons)
    2. Platelets
    3. CNS (neurotransmitter)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List 4 main functions of serotonin

A
  • Regulation of gut motility
  • Platelet aggregation
  • Body temperature
  • Sleep, aggression and mood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the functions of seratonin in the CNS and smooth muscle

A 
CNS:
- Control of vomiting 
- Mood, sleep, appetite 
Smooth muscle contraction (all throughout the body including blood vessels unlike histamine)
- GI tract
- Uterus
- Vascular 
Platelet activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Metoclopramide what is it, main use and effects and side effects

A

Serotonin antagonist
- used to control vomiting
1) antimetic effect - serotonin antagonism
2) prokinetic effect - increase movement - can be issue with obstructive disease don’t want to perforate the gut but stop vomiting
CNS side effects - hyperactivity to depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cisapride what is it, what used for

A

Serotonin veterinary applications

- used in the treatment of GI stasis, constipation/megacolon in cats

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

Selective serotonin reuptake inhibitors (SSRIs) mechanism and function and uses

A
  • Reduces pre-synaptic recycling of 5-HT → increased 5-HT activity in synapse
  • Promotes function of serotonin as prevent breakdown in synaptic cleft
  • Used in the treatment of aggression, separation anxiety, compulsive behaviours
  • Combined with behavioural modification
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Eicosanoids what made from main precursor and the two main types

A

Generated from phospholipid precursors on demand (not stored like histamine)

  • produced by most cell types - broad regulatory activities
  • Arachidonic acid is the main precursor found within the plasma membrane
  • Principle eicosanoids are:
    1. Leukotrienes
    2. Prostanoids (prostaglandins and thromboxanes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What occurs in the arachidonic acid pathway ad the enzymes involved

A
  • Arachidonic acid which is then activated upon by two enzymes
    ○ LOX and COX (two types)
    ○ COX 2 - inducible form
  • LOX - leads to leukotrienes and lipoxins
  • COX - Prostanoids
    ○ Different types of COX enzymes will result in different prostanoids produced
    ○ Certain enzymes are upregulated in different tissues and situations resulting in different prostanoids being produced
    § COX-2 is thought to be upregulated during inflammatory responses resulting in pro-inflammatory prostanoids being produced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Prostanoids roles in inflammation

A
  • Some are powerful vasodilators
  • Potentiate the effects of other mediators (e.g. histamine) which increase vascular permeability
  • Potentiate the effects of other mediators which sensitise nerves to noxious stimuli
  • Some are pyrogenic
  • Some have anti-inflammatory effects under specific circumstance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

List some specific functions of prostaglandin E2 and F2alpha and thromboxane A2

A

PGE2 (prostaglandin)
- pyrogenic, GI system, increased mucus secretion, decrease acid secretion, contraction of pregnant uterus
PGF2α (prostaglandin)
- produced in the uterus and cause luteolysis, contraction of uterine muscle in parturition
Thromboxane A2
- from platelets, platelet aggregation and vasocosntrction

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

What is prostaglandin F2alpha clinical uses

A

• Manipulation of reproductive cycle in cattle
- Synchronisation of oestrus for fixed-timed artificial insemination (in combination with ovulation-inducing drug)
- Induction of abortion during early pregnancy (e.g. neighbour’s bull jumped the fence!)
• Abortifacient – pregnant women should not handle drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Leukotrienes what made by, key roles and how used

A 
made by white blood cells (leuko) 
Key roles:
- Potent chemoattractants
- Activation of leukocytes
- Bronchoconstrictors
Used in human medicine for treatment of bronchoconstriction (asthma, COPD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the two main types of corticosteroids and the mains ones main function

A
  1. Mineralocorticoids - aldosterone - important for salt and water metabolism, promote reabsorption of Na+
  2. Glucocorticoids
    - Different to mineralocorticoids but do have some of the same effects
    Eg: Cortisol
  3. Anti-inflammatory
  4. Immunosuppressants
  5. Metabolic effects
  6. Negative feedback
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Cortisol mechanism of action

A
  1. a steroid molecules diffuses into a cell and bind to a receptor molecule
  2. as a result the receptor undergoes a change
  3. That allows it to bind to a short stretch of DNA called a response element (RE) near a gene
    ○ Lots of different RE’s that it can bind to resulting in so many different products and therefore effects
  4. The binding modifies the expression of that gene - leads to repression or induction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the main 4 glucocorticoid effects

A
  1. Metabolic
    1. Negative feedback
    2. Anti-inflammatory
    3. Immunosuppressant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the metabolic effects of glucocorticoid and mechanism

A
  • decrease uptake and ultisiation of glucose and increase gluconeogenesis
    -> leading to hyperglycaemia
    ALSO
  • increase appetite but increase lipolysis and protein catabolism = muscle wasting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the negative feedback effects of glucocorticoids and treatment

A
  • Administered corticosteroid suppresses endogenous steroid synthesis → adrenocortical atrophy
  • Abrupt cessation of long-term therapy can precipitate an ‘Addisonian crisis’ - body doesn’t have enough acutely
  • Can make the animal very ill
  • Treatment dose is tapered to allow for recovery of adrenocortical function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the anti-inflammatory effects of glucocorticoids treatment

A
  • Inhibits PLA2 → reduced eicosanoid production
  • Reduce expression of COX-2 (inducible form) - anti-inflammatory
  • Suppress mast cell degranulation (↓ histamine release)
  • Potent effects on leukocyte trafficking (see immunosuppressive effects)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the immunosuppressive effects of glucocorticoids treatment

A
  • Inhibits extravasation and infiltration of leukocytes
  • Inhibits inflammatory actions of leukocytes (e.g. phagocytosis in macrophages)
  • Reduces cytokine production
  • Partial/complete suppression of a complex range of immune functions
    ○ Dose-dependent effect
    ○ Need to give certain dose depending on whether we want anti-inflammatory effect or pro-inflammatory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the effects on neutrophils, macrophages and lymphocytes in terms of glucocorticoid treatment

A 
NEUTROPHILS 
↓ chemotaxis 
↓ margination 
↓ bactericidal activity
MACROPHAGES
↓ chemotaxis
↓ phagocytosis
↓ Ag presenting and cytokine production
LYMPHOCYTES
↓ proliferation
↓ T-cell responses
↓ IL-2 production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

List 5 clinical uses of synthetic glucocortcoids

A

1) allergic skin disease - dermitis, flea
2) allergic respiratory disease - asthma
3) arthritis
4) lymphoma
5) Addison’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the potency and duration of action of the glucocorticoids

A
  • Structure of steroid base determines potency

- Solubility of ester determines duration of action

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

Prednisolone sodium succinate and methylprednisolone acetate what type of drug and duration of action

A

Corticosteroid
Prednisolone sodium succinate - short action, released for minutes
Methylprednisolone acetate - long acting, released for days to weeks

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

Dexamethasone sodium phosphate and Dexamethasone phenylpropionate what type of drug and duration of action

A

Corticosteroid
Dexamethasone sodium phosphate - short acting released for minutes
Dexamethasone phenylpropionate - long acting, released for days to weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the 2 main common clinical signs from cortcisteroid side effects

A
  1. Polyphagia, polydipsia, polyuria - within the first few days
  2. Thinning of the skin, hair loss, poor wound healing within weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

5 main side effects of corticosteroids

A
  1. Impaired wound healing
  2. Immunosuppressive doses will increase the risk of secondary infections (bacterial, fungal parasitic)
    - Why we use them but always risk
  3. Gastric ulceration
  4. Diabetes mellitus
  5. Abortion in late pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some contraindications of glycocorticoids

A

1) concurrent NSAID use
2) diabetes mellitus
3) pregnancy
4) gastric ulceration

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

List 3 main principles of corticosteroid therapy

A

1) Lowest effective dose - slowly decrease the concentration overtime and ask the owner to tell at what dose does the clinical signs come back
2) Shortest course
3) Limit frequency (e.g. alternate day oral administration enables adrenocortical recovery period between each dose)

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

Azathioprine and Cyclosporin what type of drug and mechanisms

A

Both immunosuppressant drugs - corticosteroid
Azathioprine
- Interferes with synthesis of purine nucleotides → inhibits DNA synthesis
- Inhibits clonal proliferation during induction phase of the immune response
Cyclosporin
Inhibits T-lymphocyte function by inhibiting cytokine production (IL-2, IFN-ɣ) – helper T-cell activation is blocked - used with atopic skin disease

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

What are the 3 primary aims of pharmacological control of inflammation

A

1) - Relief of presenting signs
e.g. pain, swelling, lameness, itch
2) - Maintenance of function
•e.g. improving mobility and range of motion
3) - Arrest of tissue damaging processes
•e.g. reduction in inflammatory cell infiltration/accumulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the 3 primary actions of NSAIDs and main mechaism

A
  1. Anti-inflammatory
  2. Analgesic
  3. Antipyretic
    - All actions relate to inhibition of the actions of COX → inhibit production of prostanoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the mechanism of antipyretic effect of NSAids

A

NSAIDs inhibit this synthesis of PGE2 in the hypothalamus which is a pyretic

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

what is the mechanism of the analgesic effect of NSAIDS

A
  • Reduce production of prostaglandins that sensitise nociceptors to inflammatory mediators (e.g. bradykinin)
    therefore reduce the requirement for opioid analgesia (severe pain relief)
44
Q

NSAIDs effect on coagulation

A
  • Prostaglandins and prostacyclin are anti-aggregatory and vasodilatory
  • Thromboxane is pro-aggregatory and vasoconstrictory
    → Predominant effect depends on the tissue
45
Q

Aspirin what type of drug, primary action and other effects

A

NSADI

  • Primary action: Irreversible inactivation of COX
  • Anti-platelet effect due to inactivation of platelet COX → inhibition of TXA2 synthesis → ↓ platelet aggregation (for the life of the platelet; 5-10 days)
46
Q

What are the two main side effects of NSAIDS and the mechanism behind them

A

1) Renal toxicity
- - Inhibit synthesis of prostaglandins (PGE2 and PGI2) which are important in maintaining vasodilation (needed for blood flow thorugh kidney -> ischemic kidney disease)
- hypovlaemia risk
2) GI side-effects
- Inhibition of gastric COX-1 → ↓ synthesis of PGs that inhibit acid secretion and protect the mucosa
- PG analogues such as misoprostol can reduce GI side-effects

47
Q

What are the main functions for COX-1 and COX-2 and what is important

A 
COX-1
- Involved in tissue homeostasis
- Production of regulatory prostaglandins:
○ gastric cytoprotection
○ platelet aggregatation
○ renal blood flow autoregulation
COX-2 
- induced by pro-inflammatory stimuli
IMPORTANT - Both isoforms have bi-functional roles
48
Q

Whar are NSAIDS most commonly used for and give an example and why its different

A
  1. Osteoarthritis: dogs, cats, horses
  2. Control of post-operative pain
    Trocoxil (Mavacoxib)
    - Used monthly - long duration of action
    ○ Eliminated slowly
    ○ May get longer duration of adverse effects - unable to withdraw it
    § Instead give analogue if gastric side effects develop before it leaves the system
    - Most NSAIDS need to be given daily
49
Q

Contraindications with NSAIDS list 5

A

1) pregnant
2) pre-exising renal disease
3) liver disease
4) coagulation disorders
5) Any haemodynamic compromise: dehydration, hypovolaemia, hypotension, cardiac disease

50
Q

Contraindications with NSAIDS list 6

A

1) pregnant
2) pre-exising renal disease
3) liver disease
4) coagulation disorders
5) Any haemodynamic compromise: dehydration, hypovolaemia, hypotension, cardiac disease
6) corticosteroid use as well - DOUBLE INHIBITION

51
Q

Are NSAIDS used for pre-operative administration

A

concern due to renal side effects but if young, healthy and routin procedures okay

52
Q

NSAIDS and cats

A
  • Limited ability to glucuronidate NSAIDs → Increased potential for toxicity as longer duration of action
  • many NSAIDS only licensed for single dose
  • now Metacam for longer term pain management (Arthritis)
53
Q

Integument what are the 2 reasons it is important and type within

A

1) Function
1. protection: physical protection, radiation protection, antimicrobial action, immunity (innate)
2. control of fluid permeability & barrier to chemicals
3. sensory activity: cutaneous nerve endings and sensory organs
4. nutritional: Vitamin D3 and mammary gland
5. social: sexual attraction, territorial marking and species identification.
2) Indicator of health – direct observation and palpation
- rough hairs, alopecia (loss of hairs), jaundice, cyanosis

54
Q

Describe the layers and appendages of the skin

A

1) Layers:
1. Epidermis - ectoderm derived stratified squamous epithelium
2. Dermis - mesoderm derived connective tissue
○ Under dermis is the hypodermis (subcutis)
§ Contains lots of fat and cutaneous trunci
2) Appendages
1. Keratinized - scales, horns and hoofs
2. Glands - sebaceous glands, tubular glands, special glands (scent and regional)

55
Q

Epidermis what type of epithelium, what components

A
  • Stratified squamous keratinised epithelium
  • Avascular, nutrients and oxygen are supplied by underlying dermal vessels
  • Varies in thickness depending on region and function
56
Q

List the 5 layers of the epidermis

A

1) stratum basale
2) stratum spinosum
3) stratum granulosum
4) stratum lucidum
5) stratum corneum

57
Q

Stratum basale and stratum spinosum what type of epithelium, what made of and function

A

1) stratum basale: single layer of cuboidal to columnar cells, undergo mitosis and rests on a basement membrane that is anchored to the dermis
2) stratum spinosum: polygonal cells become squamous toward the surface, desmosome junctions between adjacent cells
○ Cells gradually shrink and flatten as progress towards the surface layer
○ Tonofilaments are anchored to the inner surfaces of the desmosomes.
§ Type of intermediate filament - cytoskeleton for the skin
§ This arrangement contributes to the cohesion of the cells and the layer’s resistance to abrasion.

58
Q

Stratum granulosum, stratum lucidum and stratum corneum what type of epithelium and hwere present

A

Stratum granulosum: narrow layer of flattened cells that marks the transition from variable to dead cells ○ Only present in soft keratinised structures
Stratum lucidum: clear translucent layer of keratinised cells (no organelles or nuclear remnants) ○ Only present in some non-air areas (digital pads, teats and planum nasal) and soft keratinised structures
Stratum corneum: layer of flattened dead cells joined together, no organelles or nuclei present
Keratinisation complete, keratin intensely eosinophilic

59
Q

List the 4 cells of the epidermis and their functions

A

1) Keratinocytes -> Progressive keratinisation of the cells as they give rise to flakes or keratin which accumulate in the stratum corneum
2) Melanocytes -> responsible for skin and hair colour
3) Langerhan cells - dendritic cells for antigen presentation
4) Merkel cells - sensory cells associated with tactile stimulation and nerve cells

60
Q

What are the 3 layers of the keratinocytes and what occurring at each layer

A

1) Proliferative - mitosis occurs at the cells of statum basale (attached to basement membrane)
2) Active - cells of stratum spinosum synthesise keratin that contributes to cohesion of the cells
3) Inactive - cell sof upper layer of stratum spinosum flatten and die forming with other molecules a waterproof seal

61
Q

What are dermal papillae and epidermal pegs

A

Epidermal pegs fits into the dermal papillae
- Epidermal pegs are extensions of the epidermis into the dermis
- Dermal papillae are extension of the dermis into the epidermis
These features are more pounced in areas where the skin is greatly thickened (digital pads)
They reflect patterns in epidermal surface leading to fingerprints

62
Q

what are the 2 connective tissues layers of the dermis

A

1) Papillary -> glands and hair are located, fine fibres

2) Reticular -> deeper layer, course collagen, reticular and elastic fibres, less cellular than papillary

63
Q

What are the 3 dermal vascular plexuses and where found

A

1) superficial plexus in papillary dermis
2) intermediate plexus in upper reticular layer
3) deep plexus at dermis/hypodermis junction

64
Q

List and describe the 3 constituents of the dermis

A

1) Cells - immune cells at the epidermis and dermis, friboblasts and fibrocytes
2) intercellular substances - fibres: collagen, reticular and elastic
3) appendages -> keratinised - scales, hair, horn
glands - tubular, sebaceous

65
Q

Hypodermis what is it, function and what is it grossly

A
  • Loose connective tissue layer beneath and merging with the dermis
  • Not part of the skin but anchors it to the underlying structures
    Grossly = superficial fascia
66
Q

Footpads what are the 3 layers

A

1) Subcutaneous cushion of connective tissue
2) Dermis with high prominent papillary layer
3) Epidermis with a stratum lucidum and thickened stratum corenum

67
Q

Horns what layers within

A
  • Has a epidermis, dermis and hypodermis
    ○ epidermis has a thick hard stratum corneum: tubular horns & intertubular horns
  • Horny shell + bony core
68
Q

What does the claw in the dog consist of and what is present in the digital pad

A
  • Claw plate and a sole
    ○ Claw plate consists of strongly united flattened cornified cells of stratum corenum which are often heavily pigmented
    ○ A fold in the skin called the claw fold covers the proximal portion of the claw plate
  • also dermis within that bleeds when cut
    Digital pad (merocrine sweat glands)
69
Q

List and describe the 4 modes of secretion with sebaceous and tubular glands

A
  1. merocrine: small secretory product or granule + cell membrane via exocytosis, viscous
  2. apocrine: large granule + a rim of cytoplasm + cell membrane, higher protein (albumin) in the sweat
  3. holocrine: entire cells are released as a the secretory product;
    ○ sabaceous glands of the skin are typical holocrine glands (sebum)
  4. cytocrine: secretory material is transferred from one cell to the cytoplasm of another cell.
    ie: melanin from melanocytes to keratinocytes
70
Q

Tubular glands what type of glands, where located, how innervated and what mode of secretion

A

Sweat glands

  • Usually restricted to primary hair follicles and located in the dermis
  • Innervation via sympathetic nervous system
  • Secrete by merocrine or apocrine mode depending on species and location
71
Q

sweat glands where found in different animals and what glands found in the eye and eyelids

A

sweat glands
- digital pads (carnivores),
- nasolabial or nasal regions of ruminants and pigs
- frog of ungulates (horse)
Ø Ear canal: ceruminous glands (cerumen) & large sebaceous glands - ear wax
Ø Eyelids: tarsal glands & Meibomian glands (at the rim of the eyelids)

72
Q

List 4 glands found in carnivores, 2 in sheep and 1 in goat

A 
Carnivores 
1) anal sac
2) circumanal glands 
3) supracaudal glands (dorsal to the surface of the tail) 
4) mammary glands 
Sheep
1) infraorbital sinus 
2) interdigital glands 
Goat 
1) horn glands
73
Q

What are the 3 main regions of the hair

A

Shaft - free part
Root - located within the hair follicle, surrounded by inner and outer root sheaths and includes the hair bulb
Hair bulb - terminal hallow knob of epithelium over the dermal papilla and is located at the bottom of the hair follicle (part of the root)

74
Q

What are the 3 types of hair

A
  1. Straight, rather stiff guard hairs:
    - “topcoat”
    - Primary hairs
  2. Fine, wavy wool hairs:
    - “undercoat”
    - Secondary hairs
  3. Stout tactile hairs:
    - restricted distribution
    - associated with touch receptors
75
Q

What are the 3 structures within a hair shaft and what made of

A
  1. medulla: a solid column of cuboidal cells within the hair shaft - the cells degenerate and form a system of air filled spaces
  2. cortex: contain melanin acquired from melanocytes, fibrillar keratin in an amorphous matrix (keratin-associated proteins (KAP)
  3. cuticle: the outermost single layer of overlapping flat keratinised cells; free edges of the cells are directed upward
76
Q

How does sulphur rich food effect hair growth

A
  • Help increase sulfur - more disulphide bonds, stronger binding hair
77
Q

What are the 3 root sheaths of hair follicles and what made from

A

1) Internal root sheath - cuticle inner layer most important
- The cells become thinner and fuse with external root sheath just below the opening of the sebaceous gland
2) External root sheath - several layers of cells resembling those of the stratum spinosum of the epidermis
- Separated from the dermal root sheath by a thick basement membrane and associated reticular fibres which have a hyaline (glossy) appearance
3) Dermal root sheath - cells and fibres arranged parallel to hair

78
Q

Arrector pili muscles what type of cells, where located and function

A
  • smooth muscles cells
  • attaches to the dermal root sheath of the follicle and the superficial layer of the dermis and angled towards the surface
  • contract to form dead-air space to provide insulation to help to maintain internal body temperature in cold weather - piloerection
79
Q

Variations in hair follicles what are the 2 main types and describe, what does each create

A

1) primary / secondary
○ Primary - deep set and possess sebaceous and tubular glands and an arrector pili muscle - produce primary hairs
○ Secondary - smaller and more superficial, may have a sebaceous gland but lack tubular glands and arrector pili muscle - produce secondary hairs
2) simple / compound -
○ Simple - single hair that leaves the follicular canal
○ Compound - several follicles grouped together which fuse at the sebaceous gland duct and hairs emerge onto surface via a single opening - one primary with several secondary hairs

80
Q

What is the main type of hair follicles on horses and ruminants and carnivores

A

Horses & ruminants: simple hair follicles evenly distributed
carnivores: most of the follicles are compound follicles

81
Q

Merkel cells what are they, function and location

A

nerve fibres flow to these cells via the trabecula
Involved with tactile stimulation
located in the external root shealth

82
Q

What are 3 main key phases of the hair cycle and what occurs in each

A
  1. Anagen (growth phase)- repetitive cycles of growth
    - Growth of new hair follicle at the space of the old
  2. catagen (recession phase) - apoptosis-driven regression
    - Bottom 2/3rd of follicle die via apoptosis, the stem cells at the bottom of the follicle don’t undergo apoptosis
    3) telogen (resting phase) - regeneration depends on the retention of germ cells and hair remains in the canal until pushed out by new growth
83
Q

List 5 things the hair cycle is controlled by

A
  • Hair length: the longer the growing phase the longer the hair
  • daily period of light
  • ambient temperature (seasonal change)
  • nutrition
  • hormones, particularly estrogen, testosterone, adrenal steroids, thyroid hormone
84
Q

What is the main gland associated with hair, mode of secretion, what produces and function

A

Sebaceous gland
- Simple or compound alveolar/acinar gland located adjacent to a hair follicle and surrounded by a sheath of dermal connective tissue
- produced sebum that is composed of cholesterol and triglycerides
Function - bacteriostatic, fungistatic, waterproofing,

85
Q

What are the 2 shapes of wool and how first emerge

A
  • When wool fibres emerge from the skin they are individually curly but usually they emerge aggregated together in a form referred to as a staple.
  • staple: “the fiber of cotton or wool considered with regard to its length and degree of fineness”
  • crimp: a natural wave formation visible in wool.
86
Q

Nutritional effects on wool name 3

A

1) supply of energy and protein
2) pregnancy, enviromental stress, hormones
3) copper and zinc deficiencies

87
Q

Immunisuppressant drugs what used for and name 3 examples

A
  • Used in the treatment of hypersensitivity & autoimmune diseases
  • Examples: Cyclosporin, Azathioprine, Cyclophosphamide
88
Q

Cyclosporin what type of drug, how exert effects and disease most used for

A

Immunosuppressant drug
- Inhibits T-lymphocyte function by inhibiting cytokine production (IL-2, IFN-ɣ) → helper T-cell activation is blocked
- in keratoconjunctivitis sicca (dry eye), atopic skin disease
○ More prevalent in dogs and used topical

89
Q

Oclacitinib (Apoquel TM) what type of drug, how exert effects and what diseases used for

A
  • May be termed immunomodulatory rather than immunosuppressive
  • Inhibits cytokines that are dependent on JAK1 enzyme activity - pro-inflammatory cytokines
    treatment of pruritis in allergic & atopic dermatitis in dogs
90
Q

List 4 characteristics of neoplastic cells

A

1) Uncontrolled proliferation - main characteristic targeted with drugs
2) De-differentiation and loss of function
3) Invasion into adjacent tissue
4) Metastasis – spread to distant site

91
Q

what are the two main forces that regulate the cell cycle and genes within

A

1) Positive forces -> proto-oncogenes - growth factors, intracellular growth signalling pathways
2) Negative forces -> tumour suppresor genes - primary line of defence - DNA repair genes, RB protein

92
Q

What are the 2 checkpoints in the cell cycle and list and describe function of 2 tumour suppressor genes and which checkpoint they act

A

1) G2/M: check newly syntehsised DNA is error free
2) G1/S check template DNA is undamaged before replication
Tumour suppressor genes
1) p53
- When DNA damage is detected, p53 halts progression of cell from G1 phase to S phase (checkpoint 1)
- Activates DNA repair enzymes, if not fixable induces apoptosis
- Often non-functional in neoplastic cells
2) Rb (Retinoblastoma) gene
- Controls progression of cell from G1 phase to S phase (Checkpoint 1)

93
Q

What is chemotherapy and the goal

A

Chemotherapy = the use of anti-neoplastic drugs to kill neoplastic cells
- Goal: increase length and quality of life in veterinary patients - QUALITY OF LIFE IS VERY IMPORTANT IN VETERINARY MEDICINE

94
Q

What are the 3 things chemotherapy is best used for

A

1) Treatment of systemic disease - cannot surgically remove all of them
2) Palliation (ease) for metastatic or non-resectable disease
3) Reducing tumour size to make more amenable to surgical excision or radiation therapy

95
Q

When are chemotherpay drugs most effective and why and what is important for effective treatment and what generally used with

A

1) Tumour is small (microscopic) - due to the first order kinetics - larger number of cells will be remaining after every treatment -> constant percentage of cells is killed each dose
2) It is rapidly growing -> anti-neoplastic drugs target this, growth rate falls as tumour grows, less responsive to drugs - IMPORTANT EARLY DIAGNOSIS
Generally used with surgery

96
Q

what do traditional neoplastic drugs depend on therefore what side-effects relate to and what is dose based on

A

SELECTIVE TOXICITY - differences in normal and cancer cells -> RAPID DIVISION -> side effects relate to rapidly dividing cell populations (GI, bone marrow, hair follicles)
Dose based on body surface area (BSA) which is an estimate of metabolic rate

97
Q

List 4 ways resistance can occur to anti-neoplastics and how to know if primary or acquired

A
  1. ↓cell permeability/uptake or ↑ efflux of drugs
  2. ↑ production of enzymes which degrade the drug
  3. ↑ capacity to repair or bypass drug effects
  4. ↓ binding of drug to receptors or target enzymes
    - Often cannot know the difference - assume primary if doesn’t work the first time give drug but cannot know
98
Q

What protein has been implicated in multi-drug resistance and how

A

P-glycoprotein
- Efflux pump used to remove toxic substances
- There are naturally occurring inhibitors however:
- Increased numbers - increase the resistance to cells to anti-neoplastic cells
○ Upregulated in neoplastic cells

99
Q

List 4 ways to implement chemotherapy that helps overcome resistance

A

1) multi-drug protocols
2) drugs used with difference mechanisms of action
3) drugs given at max dose with acceptable side-effects
4) non-overlapping adverse effects of each drug -> decrease toxicity to the patient

100
Q

List 7 classes of anti-neoplastic drugs and an example of each

A

1) Alkylating agents e.g. cyclophosphamide
2) • Antimetabolites e.g. azathioprine
3) • Platinating agents e.g. cisplatin
4) • Mitotic spindle inhibitors e.g. vincristine
5) • Cytotoxic antibiotics e.g. doxorubicin
6) • Hormones e.g. glucocorticoids
7) • Tyrosine kinase inhibitors e.g. toceranib

101
Q

Alkylating agents what type of drug, example and mechanism of action

A

Anti-neoplastic drug
Cross-link DNA and inhibit replication
• DNA damage leads to cell apoptosis
• Example: cyclophosphamide

102
Q

Antimetabolites what type of drug, example and mechanism of action

A

Anti-neoplastic drug
azathioprine (immunosupression as well)
- Interferes with synthesis of purine nucleotides → inhibits DNA synthesis

103
Q

Platinating agents what type of drug, example and mechanism of action

A

Anti-neoplastic drug
Produces inter and intra- crosslinks in DNA (binds to guanine residues)
• Example: cisplatin

104
Q

Mitotic spindle inhibitors what type of drug, mechanism of action and example

A

Anti-neoplastic drug
Bind to tubulin in the mitotic spindle → prevent cell division
• Active in G2 and M phases of cell cycle
• Example: vincristine

105
Q

Cytotoxic antibiotics what type of drug, mechanism of action and example

A

Anti-neoplastic drug
Inhibits topoisomerase II, an enzyme involved in DNA cleavage, unwinding and rejoining
Example: doxorubicin - red liquid

106
Q

Hormones how used for anti-neoplastics and example

A

Example: glucocorticoids

  • Can cause apoptosis of lymphocytes
  • Cell cycle non-specific
107
Q

Tyrosine kinase inhibitors what type of drug, mechanism and example

A

Anti-neoplastic drug
Inhibit tyrosine kinase receptors involved in malignant transformation of cells
• Example: toceranib

DVM 2 - 1 (31 decks)

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