A List Flashcards
Cytopempsis meaning
Excretion to another place without digestion. Cytopempsis through endothel.
Thesaurismosis meaning
Regarding Storage of large amount locally or in other tissues
Cicatrix
Scar
Demarcatio
surroundendtissuese of necrosis with fibers
FMD and BVD disease
Foot and mouth disease, Bovine viral diarrhea
what is a callus and what types are there
cartilage bone connection, can be periostal, cortical, compact, endostal
connective tissue callus
osteoid or cartilagionous callus
provisional osteoid calus
permanent osteoid callus
PAMPS
DAMPS
pathogen-associated molecular patterns , LPS endotoxins
damage associated molecular patterns: proteins from damage necrotized cells alarmins.
Acute inflammation and chronic inflammation
Tell me about
Onset
Cells
Tissue injury
signs
cause
duration
outcome
Rubor
Circulatory disturbances classical sign of inflammation - leading to hypermia
Sentinel Cells in vascular changes and exudation in the acute inflammation
Kupffer cell, alveolar, splenic, peritoneal, microglial, Langerhans and mast cells.
Neutrophil Eosinophil, Basophil
Mast cells- histamine, LT, PG
Monocytes, macrophages
Lymphocytes, plasma cells
phagocytosis
immunity
Vasodilatation
decreased velocity
increased blood flow locally leading to heart redness
Hemostasis
decreased blood flow, can be severe in a few minutes
Exudation and their biochemical mediators
leads to swelling and pain, the slow escape of liquids from blood vessels through pores or breaks in the cell membranes.
From leucocytes: histamine, 5HT, PG
from plasma , bradykinin leading to swelling and pain
Erythrocytadiapedesis
refers to the process of red blood cells passing through the blood vessel walls and entering the surrounding tissues
BLAD and CLAD what does it mean and what breeeds are specially sensitive
Leukocyte adhesion deficiency
explain serous catarrhal and haemorrhagic and ichorous inflammation
gotta know it by heart bro.
whats a phlegmon
A phlegmon is a medical term describing an inflammation of soft tissue that spreads under the skin or inside the body
inflammation crouposa on mucous membranes
found on stomach intestines, larynx and trachea, no deep pathological changes, Quickly removed through coughing.
Diphteroid- inflammation on the surface and deeper
type of fibrinous inflammation, diphteric crusts and scars (lymph follicles) button ulcers (swine fever)
Fibronogen inflammation found in lung
ONLY IN LUNG
fibrinogen exudate in alveolar acini, ducts, micro bronchi
no ventilation
Lymphocytes in fibrinous tissue
edema in surrounding interstitium
Croupous pneumonia
Congestion
Hepatization
lysis
pigment cells (color)
lipochromes -yellow
melanin- brownish black
bile- yellowish
Proangiogenic facctors
VEGF
FGF
Angiopoetin
Antiangiogenic factors
Angiostatin
Endostatin
Vasostatin
3 steps of carcinogenesis
Initiation
Promotion
Progression
Carcinogenesis Chemical and Physical agents
Chemical:
polycyclic carbohydrates
aromatic amine and other organic and inorganic chemicals
Physical Agents :
UV, radiation, Radioactivity and Ionising radiation + UV rays
Carcinogenesis
Biological agents include fungi, plants, viruses, dna viruses, rna viruses, parasites
Factor released by tumours
PIF- Proteolysis inducing factor
LMF- lipid mobolizing factor
increase muscle and adipocyte metabolism leading to cachexia
Whats paraneoplasia and paraneoplastic changes
-tumor cachexia
Endocrinopathis
paraneoplastic skin lesions
Hematologic symptoms
Hemostatic changes
Musculoskeletal symptoms
Neurological abnomarlities
amyloidosis dysproteinemia
Pyrexia -fever
Nephropathies
Tumor immunity
TSA
TAA
Anti tumor cells:
Cytotoxic lymphocytes T (CD8+)
NK cells
Macrophages
Complement system
Metastasis explaination
Migration-adhereing- proliferation- secondary neoplasia and generalization
Different routes of metastasis
Hematogenous route
Lymphogenous route
Intracanalicular route
Implantation metastasis
Inoculation metastasis
Metastatic Cascade
1 invasion of basement membrane and ECM
Intravasation
Extravasation leading to dissemination
Implantation and proliferation
How do you call the different degress of burn and cold
c. erythematosa (combustio)
c. bullosa
c. escharotica
carbonisatio
congelatio erythematosa
c. bullosa
c. escaharotica
c. gangrenosa
wahts asphyxia
lack of oxygen or suffocation
Hypoxemia
lower hemoglobulin saturation in O2, not enough O2 in the air, Hb cant take up O2
Hypoxia
O2 tissue supply is decreased
Hypercapnia
CO2 in tissue in increased
What are pathological signs of suffocation
Dark unclotted blood
petechial hemorrhages
acute lung hyperemia and edema
acute heart dilatation
Acute emphysema
disturbances in water supply
Exsiccosis and dehydration due to decreased water intake (increased electrolyte conc. and ph shift ) , fluid loss (vomiting diarrhea and perpiration)
Hyperhydration and water toxicosis leading to polyuria leading to electrolyte and mineral loss
types of starvation
Total starvation
partial starvation and malnutrition
obesity and overfeeding
Autointoxication types
Diabetic
retention
hepatic
putrid
abnormal direction of metabolism
enterogenic
resorption
what are each ?
hepatic autointoxication has several causes, list them
exposure
viral infections
hyperthyroidism
gilberts syndrome
cholestasis
and decreased liver supply in general
Infection routes of routes of entry
Oronasal conjunctival
urogenital
venereal
urinary or genital
omphalogen
transplacental intrauterine
ovogen
latrogenic
locus minoris resistentia
influencing factors of infectious agents causing disease
infectivity
pathogenicity
virulence
host specificity
invasiveness
contagiouness
Host defense mechanism
MPS Mononuclear phagocytoc system
The Mononuclear Phagocytic System (MPS), also known as the reticuloendothelial system (RES), is a part of the immune system composed of specialized cells that are involved in the detection, engulfment, and destruction of foreign particles, pathogens, and cellular debris. It consists primarily of monocytes, macrophages, and dendritic cells distributed throughout various tissues and organs in the body.
Cytokines =messenger ?
messenger of the immunesystem, local action and systemic leading to fever!
Cytokine storm = oversecretion leading to death
Disorders of the immune system
Hypersensitivity; may alter the immune sytem response
type 1-4
autoimmune disease
immunodeficieny syndromes (SCID)
Types of hypersensitivity
type 1 - immediate IgE mediated - allergies and anaphylaxis
type 2- cytotoxic
type 3- immune complex
type 4- delayed
Feline immunodeficiency Virus (FIV)
decreased = CD4+ alteration in CD4 and CD8+ ratio
decrease = antigen presentation
decreased = Ne adhision and migration
increased IgG
DIsturbances of the water balance of the oragnism (EDEMA)
can be intracelluar or extracelluar
Types of water regulation
Nervous system
Hormonal regulation
and physical chemical factors
increase water retention - filtration (arterioles)
more water meaning water will end in tissues
tissues oncotic pressure increased
capillary hydrostatic pressure increased
vascular permeability
decreased water retention - reabsorption in venules
increased plsama oncotic pressure
starvation
increased electrolytes in blood leading kidney failure
Water disturbances
hyperhydria = increased water
anasarca= excess water in skin subcutis all over the day
hydrops= fluid accumulation in interstices or serous cavities
Fluid can be transudate modified transudate exudate
EDEMA
Types of hydrops
Hydrops = hemorrhagic acutus
hydrops adiposus
hydrops chylosus
Types of EDEMA
Oe. Stagnationis
Dysoricum
Ex. hypoproteinemia
Oe. lymphangioticum
Oe. Hormonale - myxedema
Dehydration, exsiccation
decrease water obviously
water balance problems in cells causes
hypoxia
LPS endotoxins
Autoxeamia
Burns, and frostbite
alkalosis, acidosis
Conns disease
Water toxicosis
Hypoproteinemia
Disturbances of water cells
Cell swelling
vacuolar degeneration
hydropic degeneration
Disturbances in fat metabolism
disturbances of simples fats and compound fats
Disturbances in carbohydrate metabolism
Hormonal - insulin, growth hormones, glucagon, GC hormones, Adrenaline
Neural - MO, hypothalamus
Diabetus mellitus type 1 and type 2
Type one has decreased insulin production leading to B-cell damage
type 2 - insulin resistance leading to receptor ?
Diabetus mellitus consequences
Ketoacidosis
Diabetic coma
Glycogen accumulation in renal tubules
Alopecia
microangiopathia
Neuropathia
Cataracta diabetica
Disturbances in keratinization and steps
Prekeratine
Keratohyaline granula
Odlands granula
Digestion of organelles leading to keratinocytes
Hyperkeratosis
Local hyperkeratosis
systemic hyperkeratosis
hypokeratosis
parakeratosis
hyper + parakeratosis in the rumen (CATTLE LIVER ABSCESSATION)
Dyskeratosis
Pathological calcification
calcitonin
primary calcification
secondary calcification
Uricosis and GOUT
Gout in birds
gout in mammals
Amyloidosis
starch liek, aggregate of proteins,
localized and atypical amyloidosis
systemic and typical ( can be divided into primary and secondary )
pathology of amyloidosis
sigsn in liver splees and kidneyAD
APUD amloidosis
amine precursos uptake and decarboxylation amyloidosis
Atrophy
size of an organ or cell reduces in cells size or number
hypoplasia
failure of normal development (developmental anomaly
Forms of atrophy
physiological and pathological
reversible and irreversible
local , regional and complete
Atrophia simplex, degenerative and numerical
Causes of atrophy
decreased function
decreased innervation
compression
lack of nutrients
age
endocrine disturbances
drugs
other physical exposures such as radiation
Actinomycosis
Actinobacillosis
Disturbances of cell division
-no mitosis starts
rate?
deviant out of the ordinary leading to tumors
what are oncogenes
genes that have the ability to casue cancer
coding for oncoproteins
oncogene alleles are dominant with only one mutating already gaining function
overexpression leads to tumor
tumorsuppresing genes
regulate cell division and replication- avoids proliferation of genes with mutation
tumor suppressed genes may be mutated where it looses it function and leads to the loos of function and than to tumor
stability genes
DNA repair and indirect tumor supressing genes
mutation or inactivation of stability genes can lead to the mutation of other genes -meaning it leads to tumor formation
Mutation is often inheritated
What are preneoplastic lesions
Hyperplasia- increased cell number in tissue
Metaplasia - transformation of one differentiated cell into another
Dysplasia - abnormal pattern of tissue growth
Neoplasia (Benign Tumor)
grow slowly
localized demarvated and well removable
maturated differentiated cells
no invasion meaning no metastasis
simple mutations
no recediva ( no recurrence)
Semimalignant tumors ( borderline tumors
histologically nening bit locally invasive
no metastasis
frequent recidiva ( no recurrence )
papilloma and infiltrative lipoma
In situ Carcinoma (CIS)
not yet invavaded other surroudning tissue, pre invasive phase
disorientated atypic cells and dysplasia.
don’t forget Bowens disease (CIS of the skin superficial gastric tumors ontraductual mammary gland tumor.
Malignant Tumors
grow quickly- central necrosis hypoxia and anoxia
no capsule, atypical structure poorly differentiated inmature
invasion of surrounding tissue (metastasis
RECEDIVA ( definitely comes back to fuck you in the ass)
functional malignancy
when cancer produces hormones or hormone like substances
Anaplesia
Anaplasia is a term used in pathology to describe the loss of differentiation and organization of cells in a tumor or neoplasm. It refers to a state of dedifferentiation where cells become more primitive and exhibit features characteristic of undifferentiated or embryonic cells. Anaplastic cells often have abnormal nuclei, prominent nucleoli, and increased nuclear-to-cytoplasmic ratio.
Celluar pleomorphism and nuclear polymorphism
Anisocytosis & Anisokaryosis
Differentiate between malignant and benign tumors ?
Benign (typical)
-differentiated cells
grows slowly
localized demarcated
well removable
no metastasis and no recurrence
Malignant (atypical)
undifferentiated immature cells
grow quickly
infiltrative destructive
Foci not demarcated Pleomophism
Metastasis
Benign Mesenchymla tumors of connective tissues
Firboma -collagen fibers
Myxoma -embryonic
Lipoma - adipose tissue
Chondroma- cartilage
Osteoma - bone
Ostechondroma - bone and cartilage
Bening mesenchymal tumors of the muscles
Rhabdomyoma - of the skeletal muscle (rare)
Leomyoma - of the smooth muscle
Cardiac Rhabdomyoma - heart muscle (mostly in pigs)
What are bening mesenchymal tumors ? explanation
Benign mesenchymal tumors are growths that originate from mesenchymal tissues and are non-cancerous in nature. Mesenchymal tissues give rise to a variety of connective tissues in the body, including bone, cartilage, muscle, fat, and blood vessels. Therefore, benign mesenchymal tumors can arise from any of these tissues and can occur in various locations throughout the body.
Malignant mesenchymal tumors (sarcoma)
Sarcoma is a type of cancer that arise from the mesenchymal tissues such as connective tissue, bone , cartilage and blood vessels.
connective tissue types of malignant mesenchymal tumors
- Fibrosarcoma
- Myxosarcoma
- Liposarcoma
- CHondrosarcoma
-Osteosarcoma
muscle types of malignant mesenchymal tumors
Rhabdomtosarcoma
Leiomyosarcoma
Cardiac Rhabdosarcoma
Benign epithelial tumors
covers the surface of the body, muycosa and glandular tissue
Malignant epithelial tumors
Squamous cell carcinoma
Basosquamous carcinoma (mostly in dogs)
Basal cell carcinoma
Adenocarcinoma (of glandular epithelium)
Melanocytic tumors
Melanocytic tumors are growths that arise from melanocytes, the pigment-producing cells found in the skin and other parts of the body. These tumors can be benign (non-cancerous) or malignant (cancerous). The most common type of melanocytic tumor is melanoma, a malignant tumor that arises from melanocytes and is known for its potential to metastasize and spread to other parts of the body.