Foundations - Exam 3

Intervertebral spaces on the periphery of the x-ray will show up

as narrow so if you want to see a certain point of the spine have it in the center on the shot

What is this called

Block vertebra

What is this called?

dorsal hemivertebra

What is this called?

Ventral wedge shape

What is this called?

Lateral hemivertebra

What is this called?

Lateral wedge shape

What is this called?

Dorsolateral hemivertebra

What is this called

Butterfly vertebra

What is this called

Hemivertebra

What is this called?

Butterfly vertebra

What is this called?

Spina Bifida

What is this called

block vertebra

What is this called

Transitional vertebra

Spondylosis deformans - definiton

bone proliferation associated with vertebral endplates on ventral and lateral contours (osteophytes of vertebra)
Also a degenerative process

Spondylosis deformans - signalment

almost all older dogs and some cats

What is this

Spondylosis deformans

Atlantoaxial Instability - definition and signlament

Increased movement between C2 and C1
can be due to c2 agenesis, hypoplasia, fragmentation, malangulation, or absence of ligament support or truama that causes fx of the dens

mini/toy breeds but also in larger dogs

What is this?

Atlantoaxial instability

Changes in morphology and biomechanics of the intervertebral disc may result in

Portusion of the nucleus pulposus into the annulus fibrosus, but without annular rupture
extrusion of the nucleus through a ruptured annulus, into the spinal canal

Intervertebral disc extrusion

Acute extrusion of the nucleus pulposus through the ruptured annulus fibrosus, more common in chondrodystrophic breeds
AKA hansen type I

What is this

Intervertebral disc extrusion

Intervertebral disc protrusion

Dorsal buldge or protrusion of the nucleus that gradually passes through into the annulus fibrosus without annular rupture
usually more chornic
aka hansen type II

hypertrophy

Cells are gigger

Atrophy

Cells are smaller than normal

Hyperplasia

Too maby cells

Metaplasia

orderly replacement of one mature epithelial type by another

Acquired dysregulated growth

Atrophy, hyperplasia, hypertrophy, metaplasia, dysplasia

Developmental distrubances of growth

Hypoplasia, aplasia, agenesis

Begnin neoplasia

Locallized and non invasive (basmement membrane intact)

Control, organized, and reversible nonneoplastic disturbances of growht

protooncogenes
hypertrophy, hyperplasia, metaplasia

dysplasia

abnormal changes to the cells that may regress but after additional mutations and clonal selection can become neoplasia

What non-neoplastic disturbances?

Hyperplasia

What non-neoplastic distrubance of growth

hypertrophy

Labile cells and what non-neoplastic distrubance of growth will they undergo

retain the ability to divide throughout their life spans and are epithelial origin
these will undergo hyperplasia

Stable (quiescent) cells and what non-neoplastic distrubance do they undergo

Lose the ability for significant cell division (muscle, chondrocytes, osteocytes)
hypertrophy

Permanent cells

lose the ability for cell diiison, when damaged they die and don’t come back
CNS

is it hypertrophy or hyperplasia

hypertrophy becuase the muscle is sticking out and that undergoes hypertrophy

What is your diagnosis

hyperplasia

Diagnosis, etiology, pathogeneis, reversible or irreversible

swiney shoulder
damage to the suprscapular never that leads to decrease muscle stimulaiton and leads to muscle atrophy
reversible except if it is denervation

What distrubance of growth and is it reversible or not?

metaplasia and it is reversibleq

Agenesis

no formaiton at all

Aplasia

formation of something unrecognizable

Hypoplasia

formation of orgna or structure jsut small (never reached full size)

what’s your diagnosis

Renal agenesis

What is your diagnosis

Cerebellar aplasia

Ectopic tissue

normal tissue or organ in abnormal place

Hamartoma

too much of a tissue in a normal place

Choristoma

Normal tissue in abnormal place

Supernumerary

More than the correct number

Coloboma

defect in ocular tissue

Neoplasia

an abnormal tissue mass whose growth exceeds and is uncoordinated with that o adjacent normal tissue and persists after cessation of the stimuli that provoked it

cancer refers to only

malignant neoplasma
is the same thing as malignant tumor

Bening neoplasm

a neoplasm that grows without invading adjacent tissue of spread to distnat sites
usually well-circumscribed due to the lack of invasion of surrounding tissues

Malignant neoplasm

a neoplasm that invades the surrounding normal tissue
usually spreads to distant sites given sufficiet time
usually is not well circumscribed

Benign tumor - cell ize, nucleoli, mitose, N:C ratio, effect on host

cell size - uniform
nucleoli - normal
mitoses - few
N:C ratio - low
effect on host - does not metastasize

Malignant tumor - cell size, nucleoli, mitoses, N:C ratio, effect on host

pleomorphic large/multiple, numerous, high, may metastasize

Anaplastic cells

have lost many of the cellular characterisitcs of normal, differentiated cells
no longer resemble normal cells
irreversible cellular changes
malignant cells often exhibit varying deggres of anaplasia

papiloma

bening epithelial tumor with differnt types of epithelia

Adenoma

bening epithelial tumor
can be solid or cystic (serous/mucous)

Carcinoma

malignant epithelial tumor
Squamous cell carcinoma or adenocarcinoma (glandular epithelium or solid organ)

Mesenchyla bening tumors

lipoma, leiomyoma, hemangioma

Sarcoma

malignant mesenchymal tumor
Matrix (fibrosarcoma, chondrosarcoma, osteoscaroma)
no matrix (spindle cell sarcoma, round cell sarcoma, giant cell sarcoma)

Round cell neoplasia

neoplasia of inflammatory cells
lymphocytes, plasma cells, marcophages (hstiocytes)

Are benign and maligant tumors reversible or irreversible

irreversible

teratoma

neoplasm of germ cells

seminoma

neoplasm of seminiferous epithelium

melanoma/melanocytoma

neoplasm of melanocytes

Leukemia

neoplasm of blood cells

lymphoma

malignant neoplasm of lymphocytes in tissue

neoplasm of squamous epithelium - benign and malignant

Bening - squamous papiloma
sqauous cell arcinoma

Neoplasm of endothelial cells bening and malignant

Hemangioma
hemangiosarcoma

Neoplasm of mammary glands bening and malignat

mammary adeoma
mamary adenocarciinoma

Neoplams of bone - bening and malignant

Osteoma
osteosarcoma

Neoplasm of hepatocytes - beining and malignant

heptaoma, hepatic ademoma
Hepatic carcinoma, adenocarcinoma

Neoplasm of thyroid gland - being

thyroid gland adenoma

Neoplasm of neutrophils only in blood vascular systems

myeloid leukemia - any wbc
nuetrophilic leukemia

Rhabdomyoma - on test

a bening neoplasm of striated both cardiac and skeletal muscle

hemangiosarcoma

a maligant neoplasm of endothelial cells lining blood vessels

Non-natrually produced toxicants (5)

pesticides, pharmaceuticals, food aditives, solvenet, enrvironmental contaminats

Biotxisn (4)

plants - phytotoxins
fungal - myotoxins
bacterial - exotoxins
animals/insects - venoms

Top 10 veterinay posions

1) human over the counter meds
2) Human food/drinks
3) Human presecreption meds
4) chocolate
5) vet products nad medications
6) plants and fungi
7) Rodenticides
8) hosehold products
9) insecticides
10) recreational durgs (thc decreasing, hallucinogneics/psychedelics increasing)

Most common species for posion control calls

dogs 86% cats 11%
more common in dogs under 4 years

Toxicants exposures are most common during what months

may-august with a spike in december

top 3 toxicants causing death

organophsphate insecticide, ethylene lgycol, rodenticides

Toxicology - target (site)

where a toxicant produces its effect, locatoin
target site - molecular or subcellular organelle

Toxicosis

illness or disease state

toxicity

the amount that produces the advere effect

Toxic

how bad is iti

Toxicosis (charaterisitics)

immediate vs delayed
reversible vs irreversible
local vs multisystemic

relay toxicosis

animal to animal

individyal dose response relation ship characterisitics

graded - spectrum of responses over a range of doses, severity increases with increasing dose

How to determine the population’s dose response

single dose - give dose to a wide range of P and see effets, spectrum of responses, normal distributiona cross population, median response, outliers
single -endpoint - it does the one thing we are looking for or it doesnt (letahlity, min/max dose, 50% response dose, therapeutic indeix, margin of safety)

Threshold

point at which the detoxifcation pathways/ the repair mechanism become saturated/overhwlemed
once corssed adverse response is observed

Threshold dose

therortical dose where the d-r curve approaches the x-axis
no response to the drug

What determine toxicitt

chemical factors (toxicant factors - physical/chem properties or presence of other chemicals/potential interaction), biological factors (host and environmental), exposure factors (route and duration)

antagonism - toxicity chemical factors

exposure to one chemical results in a recution in the effect of the other chemical

Potentiation

exposure to one inactivate chemcial reuslts in the other chemical producing an effect greater than if given alone

Synergism

exposure to one chemical cuases a dramatic increase in the effect of another chemical

Species related factors in toxicology

biotransformaiton (metabolic) pathways, excretion pathways, antatomy/physiology of gi tract/repsiratory tract, target recepotr density/subtypes

Host factors toxicocology related to age

Enzyme expression - developmental differences in detoxification and bioactivation pathways
organ function (ex decreased renal clearance)
presence of protective barriers