Pathology Vocab

Etiology

Disease causes

(not always diagnosis because those can have multiple causes)

Pathogenesis

Disease Mechanism

Morphology

Structural and appearance changes that occur because of pathogenesis

Function

Clinical symptoms and signs that occur because of pathogenesis

Gross Lesions

Structural abnormalities that are visible to the naked eye

Pathognomonic Lesions

Lesions that’s appearance gives us clues at to the disease cause

Histological Lesions

Structural or architectural changes that are only detectable under a microscope

Biopsies

Tissue samples collected surgically or in postmortem

Cytology

Collection of cells to be smeared or blotted on a slide to be looked at under a microscope

Algor Mortis

Cooling of the body

Rigor Mortis

Stiffening of the body

Hypostatic Congestion (Liver Mortis)

Pooling of fluids due to gravity and position of the body

Results in reddish staining

Anti Mortem

Before Death

Thrombi

Anti mortem blood clots

rough granular, don’t separate, don’t form to the vessel

Post Mortem Clots

Smooth, separates into red and white layers, conforms to shape of the vessel

Autolysis

Breakdown of cells and tissues by bodies enzymes

Putrefaction

Breakdown by bacteria that invade from environment or from gut

Hemoglobin Staining

Red staining everywhere in the body (unlike hypostatic congestion)

Anoxia

The total Lack of oxygen

Hypoxia

Partial lack of oxygen

Hydropic Degeneration

Acute cell swelling (usually due to lack of Na/K pump function)

Apoptosis

Programmed Cell Death (controlled)

Friable

tissue that tears or ruptures easily when touched

Pyknosis

A shrunken dark staining of the nucleus

Karyorrhexis

Fragmentation of the nucleus

Karyolysis

Fading of the nucleus as it loses affinity for hematoxylin

Coagulative Necrosis

Denaturing of cytoplasmic proteins causing cellular detail to be lost but architectural detail is maintained (we can recognize the type of tissue)

Common in kidneys, liver, heart, skeletal muscle

Caseous Necrosis

Cellular and architectural detail of tissue is lost usually due to bacteria

Looks like a soft cheese

Liquefactive Necrosis

Cellular and architectural detail is lost leaving a liquid mass

Common in CNS

Gangrenous Necrosis

Always in extremities

Dry Gangrene

caused by loss of blood supply to the extremity

Example: frostbite caused by extreme vasoconstriction

Wet (moist) Gangrene

Dry gangrene + bacterial infection which cant be fought off without blood

Gas Gangrene

Special moist gangrene caused by bacteria that produce gas usually from gut

Fat Necrosis

Death of fat cells

Enzymatic Fat Necrosis

Enzymatic(lipase) death of fat cells usually around pancreas when there is damage

Traumatic Fat Necrosis

Occurs after trauma or due to chronic pressure of subcutaneous adipose tissue (like recumbent cow)

Nutritional Steatitis (yellow fat disease)

Caused by diets with high polyunsaturated fatty acids and low vitamin E

Common in cats or mink on fish only diets

Idiopathic

Relates to diseases where the cause is unknown

Sequelae

outcome

Sequestra

Encapsulation of necrotic tissue without liquefaction

Erosion

Loss of epithelial cell only

Ulceration

loss of epithelial cells with basement membrane involvement and exposure of connective tissue

Common in luminal organs

Atrophy

Decrease in size

Hypertrophy

Increase in size

Hyperplasia

Increase in number

Metaplasia

one cell changes into a different cell

Dysplasia

Lack of normal histological Architecture

Hypoplasia

Incomplete growth of an organ

Aplasia

Absence of a tissue (extreme form of hypoplasia)

Atresia

Absence of a lumen

Extravascular Hemolysis

Destruction of hemoglobin in the spleen (controlled)

Intravascular Hemolysis

Destruction of hemoglobin in the vessels (bad)

Hemoglobinemia

Red plasma due to increased free hemoglobin in blood

Hemoglobinuria

Red urine due to increased hemoglobin being filtered out of blood.

Hemosederin

Orange brown insoluble pigment resulting from iron released during hemolysis (stores iron for later use)

Hemotoidin

Bright yellow pigment derived from hemosiderin (no Fe) happens after hemorrhage

Hematin

Brown black pigment derived from hemosiderin when the iron reacts with improperly fixed formalin

Bilirubin

Yellow pigment results from heme breakdown

causes jaundice

Pre Hepatic jaundice (hemolytic)

Increased RBC breakdown intra or extravascular

Hepatic Jaundice

Liver damage leading to liver not being able to conjugate and excrete bilirubin

Post hepatic Jaundice

bile duct blockage causing bilirubin to not be excreted

Extra - bile ducts that drain liver

Intra - bile canaliculi between hepatocytes

Exogenous

originating from outside the body

Endogenous

originating from inside the body

Melanin

Brown or black pigment

Melanocytes use tyrosine to form melanin granules

Albinism

No melanin production inherited deficiency of enzyme tyrosinase

Vitiligo

Immune mediated attack to melanocytes or keratinocytes leading to depigmentation

Acquired Hypopigmentation

Caused by hormonal imbalances, loss of melanocytes from trauma or injury, dietary deficiency

Acquired Melanosis

increase in melanin production due to UV light stimulation

Congenital Melanosis

Melanocytes don’t disperse evenly in body causing areas of increased melanin

Melanocytic Neoplasia

Cancer melanoma

Anthracosis

Carbon particles accumulating in lungs or lymph nodes

grey black stippling on surface

Carotenes

Yellow pigmentation caused by carotenoids in leafy green plants

Hyperemia

Increased blood flow to an area

physiological - intestines during digestion

pathological - inflamation

Congestion

Decreased blood flow out of tissues

Localized - specific area

Systemic - spread (heart failure)

hypostatic - gravity

Edema

accumulation of fluid from blood vessels in surrounding tissue

Ischemia

Lack of blood supply to affected tissues

Diapedesis

Loss of RBC through intact capillary walls

Infarction

Death of cells because of a lack of blood supply

Hemorrhage

Bleeding from transected or ruptured blood vessel or from heart

Hemorrhage via Diapedesis

Blood loss through tiny gaps in between endothelial cells

Hemorrhage via Rhexis

bleeding from damaged blood vessels (trauma cuts, rupture)

Petechiae

pin point hemorrhages 1-2mm usually diapedesis

Ecchymoses

larger hemorrhages 2-3mm

Suffusive

Large hemorrhages in irregular areas of affected tissue

Hematoma

Local confined accumulation of blood usually clotted

Shock

Cardiovascular failure when the volume of blood is not enough to distribute to vital organs

Hypovolemic Shock

Shock due to dramatic blood loss

Cardiogenic Shock

Shock to to decrease in cardiac output

Vasculogenic shock

Shock due to widespread vasodilation of widespread damage to capillary beds

Embolus

Abnormal Mass circulating in the blood stream

Inflamation

A complex reaction to stimuli that involves blood vessels and leukocytes

What are the cardinal signs of inflamation?

Redness, Swelling, Heat, Pain, Loss of function

Peracute Inflamation

Earliest signs

If animal die we might not be able to see inflamation anywhere

Acute Inflamation

Initial Rapid response, short in duration min to hours

Subacute Inflamation

Transition between acute and chronic vascular changes will be visible but no gross signs of repair are present

Chronic Inflamation

Long term or reoccurring month to years

Tissue granulation and fibrosis may be present

Granulation Tissue

New Connective tissue and microscopic blood vessels that occur during healing

Important Inflamatory Mediator Released by Mast Cells

Histamine

Vascular Phase of Inflamation

Dilation of blood vessels and increase in vascular permiability

Two ways Vascular permiability is increased

Endothelial cells retraction

Injury of endothelial cells