Cp Final Study Set

Front 1

General functions of circulatory system

Back 1

1. Delivery of O2, nutrients, hormones, electrolytes, and water to cells

2. Removal of CO2 and metabolic wastes

Front 2

Common basic structure of whole circulatory system

Back 2

Concentric rings of tissue:

Tunica Intima

Tunica Media

Tunica Adventitia

Front 3

What is the Tunica Intima?

Back 3

Single layer of endothelial cells on a basement membrane (with a small amount of connective tissue)

Front 4

What is the Tunica Media?

Back 4

Concentric rings of smooth muscle with elongated blue nuclei

Front 5

What is the Tunica Adventitia?

Back 5

Connective tissue support/scaffolding for vessels, helping anchor them to rest of organ/tissue

Front 6

What constitutes the microcirculation?

Back 6

Arterioles, metarterioles, capillaries, post-capillary venules

Front 7

The microcirculation is the site for...

Back 7

Fluid, nutrient and waste exchange

Front 8

Capillary wall is a __________________ due to _________________, creating....

Back 8

Semi-permeable membrane

Interendothelial pores

Osmotic pressure through plasma proteins

Front 9

What is the interstitium?

Back 9

Space between the cells and the microcirculation containing ECM

Front 10

ECM (extracellular matrix) is made up of?

Back 10

Collagen fibres embedded within a protein polysaccharide gel

Front 11

Interchange of water between the vascular and interstitial compartments is tightly regulated by?

Back 11

The Starling Equilibrium

Front 12

Starling equilibrium is achieved when there is a balance between?

Back 12

Net filtration and Net absorption

Front 13

2 types of Starling forces

Back 13

Hydrostatic pressure (forces fluid out)

Colloid Osmotic pressure (draws fluid in)

Front 14

Net filtration pressure equation

Back 14

(Plasma hydrostatic [arteriolar] + Tissue oncotic) - (Plasma oncotic + Tissue hydrostatic)

Front 15

Net absorption pressure equation

Back 15

(Plasma hydrostatic [venular] + Tissue oncotic) - (Plasma oncotic + Tissue hydrostatic)

Front 16

What happens when fluid balance is disturbed?

Back 16

EDEMA

Front 17

Define edema

Back 17

Accumulation of excess fluid in interstitial tissue spaces or body cavities

Front 18

Dependent edema

Back 18

Edema of ventral areas (limbs, under jaw) due to gravity

Front 19

Severe, generalized subcutaneous edema in a still born puppy due to congenital heart defect, is called?

Back 19

Anasarca

Front 20

Term for edema fluid accumulation in body cavities?

Back 20

Effusion

-Hydrothorax

-Ascites (hydroperitoneum)

-Hydopericardium

Front 21

4 Mechanisms of Edema

Back 21

1. Increased intravascular hydrostatic pressure

2. Decreased plasma oncotic pressure

3. Lymphatic obstruction

4. Increased vascular permeability

Front 22

Increased Intravascular Hydrostatic Pressure

-Localized caused by?

-Generalized caused by?

Back 22

Localized - Occlusions or obstructions to venous outflow (tumor, abscess, thrombus, intestinal accidents)

Generalized - Heart failure resulting in venous pressure

Front 23

Left vs Right sided heart failure sequella?

Back 23

Left - Backflow into the lungs leading to pulmonary edema

Right - Backflow on the systemic and portal venous systems leading to bottle jaw/ventral subcutaneous edema

Front 24

Explain why decreased plasma oncotic pressure leads to edema?

Back 24

-Albumin exerts major portion of plasma oncotic pressure, therefore hypoalbuminemia decreases this pressure and fluid leaks out

-Hypoalbuminemia results from reduced production or excessive loss

Front 25

Lymphatic obstruction aka ________________

is always ___________

-Caused by?

Back 25

Lymphedema

Localized

-Damage or obstruction by trauma, surgery, inflammation or neoplasia

Front 26

Clear to slightly yellow fluid with low protein and low cells is called ________________

Inflammatory edema fluid with high protein and high cells is called _______________

Back 26

Transudate

Exudate

Front 27

How is Increased Vascular Permeability different from the other mechanisms? What is it caused by?

Back 27

It's an exudate rather than a transudate

Opening of interendothelial gaps due to (examples: inflammation, vasculitis, infections, toxins, insect bites)

Front 28

1. Enlarged mammary glands most common in ______________ cows

2. Evaluation of enlarged mammary glands should include __________ & ___________ histories

3. Most common causes of udder swelling are ___________________, ____________ & __________

4. Congenital anomalies (such as....) won't show up until ____________

Back 28

1. Periparturient

2. Medical & Reproductive histories

3. Onset of lactation, udder edema, and mastitis

4. (stenotic or absent teat canals) parturition/lactation

Front 29

What is the milk producing unit in the udder?

Back 29

Alveolus

Front 30

External pudendal vein returns to heart through the?

Superficial epigastric vein (milk) vein returns to heart through the?

Back 30

Caudal vena cava

Cranial vena cava

Front 31

Non-infectious cause of udder swelling:

Onset of Lactation (pathway)

Back 31

-Development of milk secretion tissue in the udder

-Edema associated with the transition to lactation

-Engorgement of tissues

Front 32

Mammogenesis during the DRY PERIOD?

(Drying off process - what happens?)

Name Steps

Back 32

1. Milking is stopped

2. Intramammary luminal pressure in udder increases and becomes greater than the blood pressure

3. Milk biosynthesis ceases

4. Alveoli furthest from gland cistern degenerate first

5. Involution progresses to the alveoli closer to the gland cistern

6. Adipose cells occupy the empty intra-luminal space

7. With complete involution only the duct system remains

Front 33

Mammogenesis during LATE PREGNANCY

Back 33

-Estrogen alone stimulates mammary duct growth

-Progesterone alone stimulates formation of alveoli

-Synergistically, progesterone and estrogen induce lobule-alveolar development

Front 34

Non-infectious causes of udder swelling:

Udder Edema

Back 34

Dietary

Congestive heart failure

Poor conformation

Reduced plasma proteins

Lymphatic obstruction

Front 35

Most common cause of non-inflammatory mammary gland swelling

Back 35

Udder Edema

Front 36

Most common cause of INFECTIOUS mammary gland swelling?

Back 36

Mastitis

Front 37

Categories of mastitis

Back 37

Contagious

Environmental

Front 38

Contagious mastitis caused by? Source of infection?

Back 38

Cause: Gram +ve bacteria (Strep. agalactiae and Staph. aureus and Mycoplasma)

Source of infection: Udder

Front 39

Environmental mastitis results in the ??

Caused by??

Source of infection??

Back 39

Most severe inflammatory reaction and swelling in the udder

Caused by: Gram -ve bacteria (E.coli & Klebsiella)

Source of Infection: Environment

Front 40

Where is the first detectable sign of udder swelling when caused by inflammation?

Back 40

Gland secretions with an elevated somatic cell count (number of WBCs)

Front 41

(Steps) Pathway of environmental mastitis infection?

Back 41

1. Coliform bacteria pass through streak canal and invade mammary gland

2. Bacteria rapidly proliferate & reach peak in 5-16 hours

3. Phagocytosis & killing of coliforms by neutrophils/macrophages releases LPS endotoxin from bacterial cell walls

4. Secondary endogenous release of inflammatory mediators such as prostaglandins & leukotrienes, and interleukins from macrophages are responsible for symptoms of acute coliform mastitis

Front 42

Staph. aureus mastitis details

Back 42

-Spreads rapidly from cow to cow

-Primary source: infected udder

-Transfer thru milking practices

-Chronic subclinical mastitis

-75-80% of dairies have some infection

-Poor response to treatment

-Damage to alveoli (can be gangrenous)

Front 43

Some teat malformations?

Back 43

-Web Teat

-Blind Teat

Front 44

How can we evaluate teat obstructions?

Back 44

-Ultrasound

-Theloscopy

Front 45

All causes of udder swellings??

Back 45

-Onset of lactation

-Udder edema

-Mastitis

-Injury

-Obstruction of milk collection system

-Tumors

Front 46

Define micturition

Back 46

Normal process of passive storage and active voiding or urine

Front 47

Disorders of micturition

Back 47

Incontinence - problem with urine storage

Urine Retention - problems with bladder emptying

Front 48

Define stranguria

Back 48

Straining to urinate

Front 49

Define pollakiuria

Back 49

Producing small amounts of urine, frequently

Front 50

Define dysuria

Back 50

Difficulty urinating

Front 51

Define polyuria

Back 51

Producing lots of urine

Front 52

Define anuria

Back 52

No urine production

Front 53

Define oliguria

Back 53

Small amounts of urine production

Front 54

3 layers of bladder wall?

Back 54

1. Mucosa with distensible Transitional Epithelium and lamina propria

2. Thick smooth muscle (Detrusor Muscle)

3. Fibrous adventitia

Front 55

Transitional epithelium is also called

Back 55

Urothelium

Front 56

Bladder Innervation: Para-sympathetic

1. Source

2. Neurotransmitter

3. Activity patterns

4. Effects/Receptor

Back 56

1. Pelvic nerve

2. ACh, ATP, NO

3. Inputs from PMC during voiding phase; typically inhibited during storage phase

4. Detrusor contraction (M3); Presynaptic inhibition of NE (M2); Relaxation of bladder neck (NO)

*PMC: Pontine Micturition Center

Front 57

Bladder Innervation: Sympathetic

1. Source

2. Neurotransmitter

3. Activity patterns

4. Effects/Receptor

Back 57

1. Hypogastric nerve

2. Norepinephrine, Neuropeptide Y

3. Activated by inputs from urethra during storage phase; inhibited during voiding phase

4. Detrusor relaxation (B3); Contraction of bladder neck (a1); Presynaptic inhibition at parasympathetic ganglia (a2)

Front 58

Bladder Innervation: Somatic (skeleto-motor)

1. Source

2. Neurotransmitter

3. Activity patterns

4. Effects/Receptor

Back 58

1. Pudendal nerve

2. ACh

3. Activated by inputs from urethra, pons & cerebral cortex; inhibited via interneurons by inputs from PMC during voiding phase

4. Tonic contraction of external urethral sphincter (nicotinic)

Front 59

Bladder Innervation: A(delta) - afferent

1. Source

2. Neurotransmitter

3. Activity patterns

4. Effects/Receptor

Back 59

1. DRG

2. L-glutamate

3. Activated during normal bladder distension & contraction

4. Signal physiologic bladder fullness; trigger the normal micturition reflex

Front 60

Bladder Innervation: C-type-afferent

1. Source

2. Neurotransmitter

3. Activity patterns

4. Effects/Receptor

Back 60

1. DRG

2. L-glutamate, substance P, CGRP, ATP, NO

3. High threshold of activation; silent C-afferents activated by inflammation

4. Spinal micturition reflex in spinal cord injury; release of mediators from urothelium

Front 61

Unique features of Micturition

Back 61

-Highly dependent on CNS

-Depends on voluntary control & learned behaviour

-2 modes of operation (on/off switch)

Front 62

What happens during Storage reflex

Back 62

Relaxation of bladder

Contraction of internal and external urethral sphincters

Front 63

What happens during Voiding reflex

Back 63

Contraction of bladder

Relaxation of urethral sphincters

Front 64

2 major categories of micturition disorders

Back 64

1. Disorders associated with a large or distended urinary bladder (urine retention)

2. Disorders associated with a small or normal-sized urinary bladder (incontinence)

Front 65

Urine retention is usually secondary to...

Back 65

-Decreased detrusor contractility

-Increased urethral outflow resistance

Front 66

Urinary incontinence is usually secondary to...

Back 66

-Decreased urethral outflow resistance

-Increased detrusor muscle contractility (nerve damage)

-Inability of bladder to expand in capacity

-Bladder spasms

Front 67

Neurogenic causes of urine retention with a distended bladder

Back 67

-LMN disease (detrusor & sphincter areflexia)

-UMN disease (detrusor areflexia & sphincter hypertonus)

-Detrusor-urethral dyssynergia (functional urethral obstruction)

Front 68

LMN disease results in

(distended bladder disorder)

Back 68

Large, flaccid distended bladder; easily expressed

Front 69

UMN disease results in

(distended bladder disorder)

Back 69

Large, firm distended bladder: difficult to express

Front 70

Non-neurogenic causes of urine retention with a distended bladder

Back 70

Physical outflow tract obstruction

Front 71

Causes for physical outflow obstruction (urinary)

Back 71

Physical entity blocking outflow

Neoplasia, calculi (dogs)

Mucus plugs, calculi (cats)

Calculi (horses & bulls)

*Large distended bladder that is difficult to express and catheterize

Front 72

Clinical signs of physical outflow obstruction?

Back 72

-Stranguria (no actual urine production)

-Urine dribbling

-Restlessness/vocalization

-Abdominal pain

Front 73

Urinary incontinence disorders with a small to normal urinary bladder

Back 73

Increased detrusor contractility

-Bladder/urethral irritation & inflammation

-UTI, FLUTD (feline lower urinary tract disease)

-Pollakiuria, Dysuria, Stranguria, Hematuria

Decreased outflow resistance

-aka: USMI - Urethral Sphincter Mechanism Incompetence

-Seen in spayed, medium to large breed dogs

-Decreased estrogen levels lead to decreased urethral muscle tone & urine leakage/incontinence

Front 74

Congenital causes for decreased urethral outflow resistance

Back 74

-Ectopic ureters

-Patent urachus

*Seen an constant urine dribbling

Front 75

Diestrus

1. Structures on ovaries

2. Dominating hormone

3. Cervix

Back 75

1. Corpus luteum

2. Progesterone

3. Closed

Front 76

Estrus

1. Structures on ovaries

2. Dominating hormone

3. Cervix

Back 76

1. Follicles (and a corpus albicans)

2. Estrogen

3. Open

Front 77

Describe the mare's general estrous cycle

Back 77

Seasonally Polyestrous

Long day breeders

21-22 days

Diestrus is 14 days

Estrous period shorter during peak of season

Front 78

Seasonality is influenced by

Back 78

Melatonin levels (pineal gland/darkness)

Nutrition, Temperature, Opioids

Front 79

Fall transition for mare's seasonality - what happens?

Back 79

-FSH and LH levels start to decline

-LH declines first

-Follicular growth without ovulation

-Mares have an autumn follicle

Front 80

What is an autumn follicle?

Back 80

-Follicle with large diameter

-Follicle persists

-No concurrent uterine edema or signs of estrus

*Can not be manipulated

Front 81

Methods to manipulate seasonality?

Back 81

-GnRH

-recombinant FSH

Front 82

General canine estrous cycle

Back 82

-Monestrous, non-seasonal

-2 estrous periods a year

-Dormitory effect

Front 83

Canine Estrous Cycle:

Length of...

-Diestrus

-Anestrus

-Proestrus

-Estrus

Back 83

Diestrus - 2 months

Anestrus - 4 months

Proestrus - 9 days (0-27dys)

Estrus - 9 days (4-24dys)

Front 84

Signs of anestrus in a bitch

Back 84

-Not receptive to mating

-Small vulva

-Deep anestrus (FSH and LH low)

-Parabasal cells with occasional small intermediate cells

Front 85

Signs of proestrus in a bitch

Back 85

-Male interested in female, but female is NOT interested in male

-Follicles grow due to increase in estrogen

-Vaginal mucosa is smooth (edematous) and vulva swells

-Testosterone peaks at end of proestrus

-Progesterone low until late proestrus

Front 86

Signs of estrus in a bitch

Back 86

-Female is receptive to mating

-Estrogen peaked in proestrus, levels decline in estrus

-Progesterone increases

-LH surge and ovulation occurs

Front 87

Vaginal cytology during estrus in a bitch

Back 87

-Increase in cornified cells

-RBCs decrease

-Ovulate primary oocyte

Front 88

Signs of disestrus in a bitch

Back 88

-Female is not receptive to mating; no longer attracts males

-Estrogen is low

-Progesterone increases rapidly to peak 3-4 weeks after diestrus onset

Front 89

Vaginal cytology for first day of diestrus in a bitch

Back 89

Abrupt decline in cornified cells

>50% intermediate cells

WBCs present

Metestrum cells

Front 90

Define feedlot

Back 90

An area or building where cattle (or other livestock) are fattened rapidly for market

Front 91

Factors that may influence feedlot profitability

Back 91

-Economic factors (purchase, sale, feed, interest)

-Management factors (ADG, FE, carcass quality)

Front 92

Role as veterinary consultant at a feedlot

Back 92

Optimize production & Maximize profits by developing, implementing and evaluating herd health management programs adapted to each individual feedlot

Front 93

What does a good herd health management program do?

Back 93

-Provides for healthier, better performing cattle

-Avoid unnecessary use of vaccines, anthelmintic and antibiotics

-Helps insure you are producing a safe, wholesome product

Front 94

Heard health management programs include

Back 94

-Preventative medicine programs (vaccination, on-arrival antibiotics, metaphylaxis)

-Therapeutic management programs (treatment protocols for disease syndromes)

Front 95

Implementation of herd health programs includes

Back 95

-Training and education of feedlot employees

-Ongoing disease diagnostics (necropsies)

-Record keeping system (computer software)

Front 96

Evaluation/Revision of herd health programs includes

Back 96

Data analysis on:

-Morbidity/mortality

-Treatment response

-Performance

Front 97

Given a feedlot problem case, what are the steps required to respond to case?

Back 97

1. Data analysis

-calculate feedlot performance

2. Investigate cause

-differential diagnosis, additional tests, final diagnosis

Front 98

Feed efficiency calculation

Back 98

Units of feed DM consumed / Units of animal weight gain

OR

Units of animal weight gain / Units of feed DM consumed

Front 99

Define Residual Feed Intake (RFI)

Back 99

Difference between actual feed intake and the feed an animal is expected to consume based on its body weight and ADG

Front 100

What does a negative RFI mean?

Back 100

Higher efficiency as cattle are consuming less than expected

Front 101

List some factors that impact DMI

Back 101

-Animal factors (genetics, BW, body fat, gender, age, breed)

-Feeding management (energy density of diet, feedbunk management)

-Implants & feed additives (ionophores)

-Environmental factors (ambient temperature, mud)

-Health status of animal

Front 102

2 types of feedbunk management

Back 102

1. Slick bunk management

2. Ad-libitum management

Front 103

Slick bunk management: goal and risk

Back 103

Goal: to have a clean bunk in slightly less than a 24 hour period

Risk: Reduction in intake if too much restriction; potential for grain overload

*More widely adopted

Front 104

Ad-libitum management: goal and risk

Back 104

Goal: To always have feed in the bunk

Risk: wasted-feed, increased labour, potential for digestive disorders

Front 105

How do ionophores impact ADG and F:G

Back 105

Act in rumen to increase energy availability by changing the proportion of VFAs

*More propionic acid, less acetic and butyric acid

Front 106

How does monensin work?

Back 106

Works on gram +ve bacteria and causes loss of K+ out of the cell, with Na+ and H+ moving into the cell. Energy is required to export H+ out of cell and thus the bacterial cells expend so much energy doing this, that they die due to less energy availability for growth & metabolism.

Front 107

What do B-agonists do?

Back 107

Repartitioning agent that basically changes fat deposition to protein/muscle deposition

Front 108

Which implant strategy is best when optimum efficiency is the only goal, regardless of carcass quality?

Back 108

High-dosage implants with re-implantation frequently

Front 109

3 ways to alter growth?

Back 109

1. Genetics

2. Nutrition

3. Growth Promoting Agents

Front 110

Type of muscle/fat growth:

1. Embryonic stage

2. Fetal stage

3. End of fetal stage (7-9.5 months)

Bonus: when are total # of muscle fibres fixed?

Back 110

1. Primary (type 1) myogenesis

2. Secondary (type 2) myogensis)

3. Adipogenesis & Muscle fibre hypertrophy

*6 months

Front 111

How does growth of skeletal muscle occur post-natally?

Back 111

Satellite cells below sarcolemma are stimulated, start dividing and fuse with skeletal muscle and incorporate their nuclei into nuclei of skeletal muscle cells

Front 112

Beef:

British breeds vs Continental breeds

Back 112

Continental: Charolais, Limousin, Simmental

-Large frame

-Late fattening (internal fat > subcutaneous)

-Higher DMI, BW and ADG

British: Angus, Hereford, Shorthorn

-Small frame

-Early fattening (^ fat on high energy diets)

-Fat (internal fat < subcutaneous fat)

Front 113

Types of implants for beef

Back 113

1. Estrogens

2. Androgens

3. Combination

Front 114

Mechanisms of Endocrine Disease

Back 114

Insufficient (hypo function)

Excessive hormone production (hyper function)

Front 115

Mechanisms of Endocrine Disease: Hypofunction types

Back 115

Primary

Secondary

Front 116

Primary Hypofunction causes

Back 116

-Biochemical defect in synthetic pathway (uncommon!)

-Failed to develop

-Destruction (immune-mediated OR neoplasia)

Front 117

Secondary Hypofunction causes

Back 117

-Destructive lesion in one organ leads to hypo function of another

-Failure of trophic hormone production

-Usually pituitary lesion (nonfunctional tumour)

*RARE

Front 118

Mechanism of Endocrine Disease: Hyperfunction types

Back 118

Primary

Secondary

Front 119

Primary Hyperfunction causes

Back 119

-Neoplasm of endocrine gland (common)

-Autonomously secrete a hormone in excess of body's ability to use/degrade

Front 120

Secondary Hyperfunction causes

Back 120

-Lesion in one organ results in stimulation and hyper secretion of hormone in target organ

-Excess production of trophic hormone

-Pituitary neoplasm (functional)

Front 121

Adrenal gland medulla secretes?

Back 121

Catecholamines

-Epinephrine

-Norepinephrine

Front 122

Outer to inner zone of adrenal gland cortex

Back 122

Zona glomerulosa

Zona fasiculata

Zona reticularis

Front 123

Zona glomerulosa secretes

Back 123

Mineralcorticoids (aldosterone!!)

Front 124

What controls the zona glomerulosa?

Back 124

RAAS (renin angiotensin aldosterone system)

Front 125

Functions of Aldosterone

Back 125

Acts on distal convoluted tubules

-Excretion of potassium

-Retention of sodium

*Decreases blood pressure

Front 126

Zona fasiculata

-What does it secrete?

-Release regulated by?

Back 126

Glucocorticoids (cortisol)

ACTH

Front 127

What does cortisol do?

Back 127

-Spares glucose (gluconeogenesis, lipolysis, protein catabolism)

-Suppress inflammation/immunity

-Negative effect on wound healing (reduces fibroplasia)

Front 128

Zona reticularis

-What does it secrete?

-Secretion regulated by?

Back 128

Sex hormones (progesterone, estrogen, androgens)

Regulated by ACTH

Front 129

Types of Canine Hyperadrenocorticism (and what causes them)

Back 129

Pituitary Dependant (85% of cases)

-Excess ACTH secretion

-Pars distalis adenoma

Adrenal Dependent (15% of cases)

-Excess cortisol secretion

-50:50 benign vs malignant

Iatrogenic

Front 130

Is hyperadrenocorticism common in cats?

Back 130

NO

Front 131

Most common clinical manifestations of canine hyperadrenocorticism (or Cushing's disease)

Back 131

PU/PD

Alopecia

Pendulous abdomen

Hepatomegaly

Polyphagia

Panting

Muscle weakness

*NOTE: complaints of illness are ABSENT!!

Front 132

Adrenal hypo function: when do we see clinical signs?

Back 132

When 85-90% of adrenal tissue is lost

Front 133

Hypoadrenocorticism most commonly results in?

Back 133

Cortisol & Aldosterone deficiency

Front 134

Suspected cause of hypoadrenocorticism

Back 134

Immune mediated mechanism

Front 135

Functions of cortisol

Back 135

Stress hormone

Glucose metabolism (hepatic gluconeogenesis, glycogenesis)

Vascular tone

Front 136

Absence of cortisol results in?

Back 136

Anorexia, lethargy, GI signs, possibly hypoglycemia

Front 137

Aldosterone is the principal cell of??

-Functions of aldosterone

Back 137

*Principal cell of distal tubule & collecting duct

-Tubular reabsorption of sodium

-Promotion of potassium secretion

Front 138

Absence of aldosterone results in?

Back 138

Hyperkalemia

Hyponatremia

Front 139

Clinical signs of 'acute crisis' adrenohypocorticism

Back 139

Weak pulses, bradycardia, prolonged CRT, mental depression, maybe GI signs

Front 140

Clinical signs of 'chronic' hypoadrenocorticism

Back 140

Ain't doing right*, weight loss, intermittent or chronic GI signs, intermittent or chronic lethargy

Front 141

Diagnostic tests for hypoadrenocorticism

Back 141

Serum Biochemistry (electrolytes)

-check for hyponatremia, hyperkalemia

-hypoglycemic

Complete Blood Count

-absence of stress leukogram in clinical ill patient

-cortisol (important role in movement of WBCs)

Front 142

Definitive diagnosis for hypoadrenocorticism

(include steps for test)

Back 142

ACTH Stimulation Test

1) Assess basal cortisol concentrations

2) Administer synthetic ACTH

3) Measure cortisol post-stimulation

Front 143

ACTH Stimulation Test results and what they mean

Back 143

Resting: <27 nmol/L

Post stimulation: <27 nmol/L

*NO CHANGE

*Addison's Disease

Front 144

Hyperadrenocorticism aka

Back 144

Cushing's Disease

Front 145

Hypoadrenocorticism aka

Back 145

Addison's Disease

Front 146

Hypothalamic-Pituitary-Thyroid Axis:

What does the hypothalamus secrete?

Negative feedback on hypothalamus by?

Back 146

TRH - Thyrotropin Releasing Hormone

fT4 & fT3 negative feedback on hypothalamus

Front 147

Hypothalamic-Pituitary-Thyroid Axis:

What does the anterior pituitary secrete?

Negative feedback on anterior pituitary by?

Back 147

TSH - Thyroid Stimulating Hormone

fT4 & fT3 negative feedback on anterior pituitary

Front 148

Hypothalamic-Pituitary-Thyroid Axis:

What does the thyroid gland secrete?

What happens to secretions?

Back 148

Thyroglobulin --> monoiodotyrosine (MIT) & diiodotyrosine (DIT) --> T3 (triiodothyronine) & T4 (thyroxine)

T4 is converted to T3 in peripheral tissues

T3 is more potent than T4

Front 149

Functions of Thyroid Hormone

Back 149

-Increased metabolic rate

-Increased number & affinity to beta adrenergic receptors

-Catabolism of muscle and fat

-Stimulates normal growth

-Influences normal respiratory centre responses

-Stimulates normal bone turnover

-Lipid metabolism (synthesis, mobilization, degradation)

Front 150

Common disorders of thyroid gland:

1) Canine

2) Feline

Back 150

1) Hypothyroidism

2)Hyperthyroidism

Front 151

Causes of thyroid follicular dysfunction

- Hypofunction/Hypothyroidism

Back 151

Primary

-Immune mediated, non-functional neoplasm

-Destruction of gland/failure to develop

Secondary (RARE)

-Failure of TSH

-Pituitary lesions

Tertiary (RARE/NON-EXISTENT)

-Destructive hypothalamus lesion

Front 152

Causes of thyroid follicular dysfunction

-Hyperfunction/Hyperthyroidism

Back 152

Primary

-Neoplasm/hyperplasia of thyroid follicular epithelium

-Autonomously secretes hormone in excess to body's ability to use/degrade

Front 153

Canine Hypothyroidism

-Causes

Back 153

**PRIMARY**

Lymphocytic thyroiditis (50%)

-progressive destruction (slow)

Idiopathic atrophy (45%)

-functional tissue replaced by adipose/fibrous tissue

Front 154

Common clinical manifestations of canine hypothyroidism

Back 154

Obesity (due to decreased metabolic rate)

Dermatological signs

Lethargy, mental dullness

Front 155

Why do we get dermatological signs in canine hypothyroidism?

Back 155

Hair is in resting phase (telogen) due to lack of thyroid hormone

[Thyroid hormone stimulates growth phase of hair cycle (anagen)]

Front 156

Diagnostics for canine hypothyroidism

Back 156

Total T4 (below reference interval; don't use on its own)

Run concurrent TSH (this will be increased)

Front 157

Most common endocrinopathy in cats?

Back 157

Feline hyperthyroidism

Front 158

Aetiologies of feline hyperthyroidism?

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Adenoma (90-95%)

-70% bilateral, 30% unilateral

Adenocarcinoma (2-5%)

Functional ectopic tissue (rare)

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Clinical manifestations of feline hyperthyroidism

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Weight loss

Palpable thyroid

Polyphagia

Hyperactivity

Tachycardia

PU/PD

Vomiting

Cardiac murmur

Diarrhea

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Why do we see PU/PD in feline hyperthyroidism?

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Increased renal blood flow

Thyroid has direct effect on thirst centre

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Why do we see tachycardia in feline hyperthyroidism?

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Increased adrenergic receptors and sensitivity in heart

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Diagnosis of feline hyperthyroidism

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Consistent clinical signs

Thyroid hormone analysis (elevated!)

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Low dose dexamethasone suppression test:

-What does it screen for?

-Theory of results?

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Presence of hyperadrenocorticism

Normally, glucocorticoids have negative feedback to pituitary-adrenal axis and ACTH release. Exogenous steroids will thus reduce cortisol levels in a normal patient. If cortisol not suppressed in 8 hours, then animal has hyperadrenocorticism

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What is a Stress Leukogram

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Test that looks at cortisol by examining WBCs in circulation:

-Lymphopenia (decreased lymphocytes)

-Neutrophilia (increased neutrophils)

-Monocytosis (increased monocytes)

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Why do we have hyperkalemia and hyponatremia in Addison's disease?

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Lack of aldosterone, which is important for Na reabsorption and Na/K ATPase function

Tubular lumen does not maintain negativity and thus, K is not excreted as much

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Diseases with weight loss AND polyphagia

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1. Hyperthyroidism2. Exocrine Pancreatic Insufficiency (EPI)3. Diabetes

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What is the cornea and what does it do?

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Avascular, transparent layer that is found in anterior fifth of fibrous tunic

-Supports intraocular contents, refraction of light and transmission of light

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What is the sclera?

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Opaque, vascular remainder of the fibrous tunic

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Iris is composed of? What does it do?

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Dilator muscle - radial smooth muscle (sympathetic)

Sphincter muscle - ring of smooth muscle at pupillary margin (parasympathetic)

Affects pupil size, shape and reaction to light

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Term for pupils that are of unequal size or asymmetric??

More specific: Dilated? Constricted?

Most common cause? other cause?

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Anisocoria

Mydrasis (dilated)

Miosis (constricted)

Ocular cause most common, also neurologic

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What is the lens and what does it do?

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It is a refractive structure, suspended in the globe by zonular ligaments

Focuses images on the retina

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Which structure refracts light more: the cornea or the lens?

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CORNEA!

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What is a cataract?

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Opacity to the lens

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What is the vitreous of the eye? What does it do?

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Largest structure in the eye that is transparent and made up of jelly-like material

Transmits light, maintains normal shape of the eye and supports the retina

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What is the choroid of the eye? What does it do?

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Layer of vasculature under the retina

Main source of nutrition for the retina

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Tapedum lucidum is part of? What is it?

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Choroid

Reflective layer that restimulates photoreceptors

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2 important layers of the retina?

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Retinal pigmented epithelium

Neurosensory retina (all the other 9 layers)

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What does the retina do?

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Phototransduction

Process by which the light is converted into a neuronal signal via rods and cones

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Types of Retinal Vascular Patterns

(where are blood vessels located in eye)

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Holangiotic - whole eye (ruminants, pigs, carnivores)

Paurangiotic - minute vessels around optic nerve head (horses, guinea pigs)

Merangiotic - vessels eminate as broad horizontal bands from optic nerve head (rabbits)

Anangiotic - avascular (birds, do have vascularized pecten though)

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What is the fundus? How can we examine it?

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Internal structures of the eye including the retina, optic disc and choroid

Opthalmoscopy!

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Proportion of ipsilateral nerve fibres in:

1. Horses

2. Dogs

3. Cats

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1. 15% ipsilateral

2. 25% ipsilateral

3. 33% ipsilateral

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Visual pathway:

Why is partial crossover important?

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Allows for both hemispheres to continue receiving input if there is 100% destruction of one retina/optic nerve

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1. Retina

2. Optic Nerve

3. Optic Chiasm

4. Optic Tract

5. Lateral Geniculate Nucleus (LGN)

6. Optic Radiations

7. Occipital Cortex

8. Pretectal & Oculomotor Nerve Nuclei

9. Oculomotor Nerve

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Visual Pathway

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Axons of ganglion cells converge at optic disc to form optic nerve - retinotopic arrangement of axons - optic nerve exits orbit - optic chiasm - optic tracts - 20% to brainstem nuclei, 80% go to LGN and then visual cortex in occipital lobe

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The dazzle reflex is a _____________ reflex and requires?

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Subcortical

Intact retina, optic nerve, optic tract and midbrain (does NOT require occipital cortex)

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Menace response is?

What does it involve?

What does it require?

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NOT A REFLEX

Involves cerebral cortical integration & interpretation

Requires intact retina, visual pathways, visual cortex and CN VII

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What is an electroretinogram?

What does it not assess?

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Test to assess retinal activity (specifically outer retina)

Doesn't assess ganglion cells or optic nerve

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Terms for

1. Right eye

2. Left eye

3. Both eyes

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1. OD - Oculus dexter2. OS - Oculus sinister3. OU - Oculus uterque