A List Flashcards
(253 cards)
1
Q
Cytopempsis meaning
A
Excretion to another place without digestion. Cytopempsis through endothel.
2
Q
Thesaurismosis meaning
A
Regarding Storage of large amount locally or in other tissues
3
Q
Cicatrix
A
Scar
4
Q
Demarcatio
A
surroundendtissuese of necrosis with fibers
5
Q
FMD and BVD disease
A
Foot and mouth disease, Bovine viral diarrhea
6
Q
what is a callus and what types are there
A
cartilage bone connection, can be periostal, cortical, compact, endostal
connective tissue callus
osteoid or cartilagionous callus
provisional osteoid calus
permanent osteoid callus
7
Q
PAMPS
DAMPS
A
pathogen-associated molecular patterns , LPS endotoxins
damage associated molecular patterns: proteins from damage necrotized cells alarmins.
8
Q
Acute inflammation and chronic inflammation
A
Tell me about
Onset
Cells
Tissue injury
signs
cause
duration
outcome
9
Q
Rubor
A
Circulatory disturbances classical sign of inflammation - leading to hypermia
10
Q
Sentinel Cells in vascular changes and exudation in the acute inflammation
A
Kupffer cell, alveolar, splenic, peritoneal, microglial, Langerhans and mast cells.
11
Q
Neutrophil Eosinophil, Basophil
A
Mast cells- histamine, LT, PG
12
Q
Monocytes, macrophages
Lymphocytes, plasma cells
A
phagocytosis
immunity
13
Q
Vasodilatation
A
decreased velocity
increased blood flow locally leading to heart redness
14
Q
Hemostasis
A
decreased blood flow, can be severe in a few minutes
15
Q
Exudation and their biochemical mediators
A
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
16
Q
Erythrocytadiapedesis
A
refers to the process of red blood cells passing through the blood vessel walls and entering the surrounding tissues
17
Q
BLAD and CLAD what does it mean and what breeeds are specially sensitive
A
Leukocyte adhesion deficiency
18
Q
explain serous catarrhal and haemorrhagic and ichorous inflammation
A
gotta know it by heart bro.
19
Q
whats a phlegmon
A
A phlegmon is a medical term describing an inflammation of soft tissue that spreads under the skin or inside the body
20
Q
inflammation crouposa on mucous membranes
A
found on stomach intestines, larynx and trachea, no deep pathological changes, Quickly removed through coughing.
21
Q
Diphteroid- inflammation on the surface and deeper
A
type of fibrinous inflammation, diphteric crusts and scars (lymph follicles) button ulcers (swine fever)
22
Q
Fibronogen inflammation found in lung
A
ONLY IN LUNG
fibrinogen exudate in alveolar acini, ducts, micro bronchi
no ventilation
Lymphocytes in fibrinous tissue
edema in surrounding interstitium
23
Q
Croupous pneumonia
A
Congestion
Hepatization
lysis
24
Q
pigment cells (color)
A
lipochromes -yellow
melanin- brownish black
bile- yellowish
25
Proangiogenic facctors
VEGF
FGF
Angiopoetin
26
Antiangiogenic factors
Angiostatin
Endostatin
Vasostatin
27
3 steps of carcinogenesis
Initiation
Promotion
Progression
28
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
29
Carcinogenesis
Biological agents include fungi, plants, viruses, dna viruses, rna viruses, parasites
30
Factor released by tumours
PIF- Proteolysis inducing factor
LMF- lipid mobolizing factor
increase muscle and adipocyte metabolism leading to cachexia
31
Whats paraneoplasia and paraneoplastic changes
-tumor cachexia
Endocrinopathis
paraneoplastic skin lesions
Hematologic symptoms
Hemostatic changes
Musculoskeletal symptoms
Neurological abnomarlities
amyloidosis dysproteinemia
Pyrexia -fever
Nephropathies
32
Tumor immunity
TSA
TAA
Anti tumor cells:
Cytotoxic lymphocytes T (CD8+)
NK cells
Macrophages
Complement system
33
Metastasis explaination
Migration-adhereing- proliferation- secondary neoplasia and generalization
34
Different routes of metastasis
Hematogenous route
Lymphogenous route
Intracanalicular route
Implantation metastasis
Inoculation metastasis
35
Metastatic Cascade
1 invasion of basement membrane and ECM
Intravasation
Extravasation leading to dissemination
Implantation and proliferation
36
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
37
wahts asphyxia
lack of oxygen or suffocation
38
Hypoxemia
lower hemoglobulin saturation in O2, not enough O2 in the air, Hb cant take up O2
39
Hypoxia
O2 tissue supply is decreased
40
Hypercapnia
CO2 in tissue in increased
41
What are pathological signs of suffocation
Dark unclotted blood
petechial hemorrhages
acute lung hyperemia and edema
acute heart dilatation
Acute emphysema
42
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
43
types of starvation
Total starvation
partial starvation and malnutrition
obesity and overfeeding
44
Autointoxication types
Diabetic
retention
hepatic
putrid
abnormal direction of metabolism
enterogenic
resorption
what are each ?
45
hepatic autointoxication has several causes, list them
exposure
viral infections
hyperthyroidism
gilberts syndrome
cholestasis
and decreased liver supply in general
46
Infection routes of routes of entry
Oronasal conjunctival
urogenital
venereal
urinary or genital
omphalogen
transplacental intrauterine
ovogen
latrogenic
locus minoris resistentia
47
influencing factors of infectious agents causing disease
infectivity
pathogenicity
virulence
host specificity
invasiveness
contagiouness
Host defense mechanism
48
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.
49
Cytokines =messenger ?
messenger of the immunesystem, local action and systemic leading to fever!
Cytokine storm = oversecretion leading to death
50
Disorders of the immune system
Hypersensitivity; may alter the immune sytem response
type 1-4
autoimmune disease
immunodeficieny syndromes (SCID)
51
Types of hypersensitivity
type 1 - immediate IgE mediated - allergies and anaphylaxis
type 2- cytotoxic
type 3- immune complex
type 4- delayed
52
Feline immunodeficiency Virus (FIV)
decreased = CD4+ alteration in CD4 and CD8+ ratio
decrease = antigen presentation
decreased = Ne adhision and migration
increased IgG
53
DIsturbances of the water balance of the oragnism (EDEMA)
can be intracelluar or extracelluar
54
Types of water regulation
Nervous system
Hormonal regulation
and physical chemical factors
55
increase water retention - filtration (arterioles)
more water meaning water will end in tissues
tissues oncotic pressure increased
capillary hydrostatic pressure increased
vascular permeability
56
decreased water retention - reabsorption in venules
increased plsama oncotic pressure
starvation
increased electrolytes in blood leading kidney failure
57
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
58
Types of hydrops
Hydrops = hemorrhagic acutus
hydrops adiposus
hydrops chylosus
59
Types of EDEMA
Oe. Stagnationis
Dysoricum
Ex. hypoproteinemia
Oe. lymphangioticum
Oe. Hormonale - myxedema
60
Dehydration, exsiccation
decrease water obviously
61
water balance problems in cells causes
hypoxia
LPS endotoxins
Autoxeamia
Burns, and frostbite
alkalosis, acidosis
Conns disease
Water toxicosis
Hypoproteinemia
62
Disturbances of water cells
Cell swelling
vacuolar degeneration
hydropic degeneration
63
Disturbances in fat metabolism
disturbances of simples fats and compound fats
64
Disturbances in carbohydrate metabolism
Hormonal - insulin, growth hormones, glucagon, GC hormones, Adrenaline
Neural - MO, hypothalamus
65
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 ?
66
Diabetus mellitus consequences
Ketoacidosis
Diabetic coma
Glycogen accumulation in renal tubules
Alopecia
microangiopathia
Neuropathia
Cataracta diabetica
67
Disturbances in keratinization and steps
Prekeratine
Keratohyaline granula
Odlands granula
Digestion of organelles leading to keratinocytes
68
Hyperkeratosis
Local hyperkeratosis
systemic hyperkeratosis
hypokeratosis
parakeratosis
hyper + parakeratosis in the rumen (CATTLE LIVER ABSCESSATION)
Dyskeratosis
69
Pathological calcification
calcitonin
primary calcification
secondary calcification
70
Uricosis and GOUT
Gout in birds
gout in mammals
71
Amyloidosis
starch liek, aggregate of proteins,
localized and atypical amyloidosis
systemic and typical ( can be divided into primary and secondary )
72
pathology of amyloidosis
sigsn in liver splees and kidneyAD
73
APUD amloidosis
amine precursos uptake and decarboxylation amyloidosis
74
Atrophy
size of an organ or cell reduces in cells size or number
75
hypoplasia
failure of normal development (developmental anomaly
76
Forms of atrophy
physiological and pathological
reversible and irreversible
local , regional and complete
Atrophia simplex, degenerative and numerical
77
Causes of atrophy
decreased function
decreased innervation
compression
lack of nutrients
age
endocrine disturbances
drugs
other physical exposures such as radiation
78
Actinomycosis
79
Actinobacillosis
80
Disturbances of cell division
-no mitosis starts
rate?
deviant out of the ordinary leading to tumors
81
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
82
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
83
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
84
What are preneoplastic lesions
Hyperplasia- increased cell number in tissue
Metaplasia - transformation of one differentiated cell into another
Dysplasia - abnormal pattern of tissue growth
85
Neoplasia (Benign Tumor)
grow slowly
localized demarvated and well removable
maturated differentiated cells
no invasion meaning no metastasis
simple mutations
no recediva ( no recurrence)
86
Semimalignant tumors ( borderline tumors
histologically nening bit locally invasive
no metastasis
frequent recidiva ( no recurrence )
papilloma and infiltrative lipoma
87
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.
88
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)
89
functional malignancy
when cancer produces hormones or hormone like substances
90
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.
91
Celluar pleomorphism and nuclear polymorphism
Anisocytosis & Anisokaryosis
92
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
93
Benign Mesenchymla tumors of connective tissues
Firboma -collagen fibers
Myxoma -embryonic
Lipoma - adipose tissue
Chondroma- cartilage
Osteoma - bone
Ostechondroma - bone and cartilage
94
Bening mesenchymal tumors of the muscles
Rhabdomyoma - of the skeletal muscle (rare)
Leomyoma - of the smooth muscle
Cardiac Rhabdomyoma - heart muscle (mostly in pigs)
95
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.
96
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.
97
connective tissue types of malignant mesenchymal tumors
- Fibrosarcoma
- Myxosarcoma
- Liposarcoma
- CHondrosarcoma
-Osteosarcoma
98
muscle types of malignant mesenchymal tumors
Rhabdomtosarcoma
Leiomyosarcoma
Cardiac Rhabdosarcoma
99
Benign epithelial tumors
covers the surface of the body, muycosa and glandular tissue
100
Malignant epithelial tumors
Squamous cell carcinoma
Basosquamous carcinoma (mostly in dogs)
Basal cell carcinoma
Adenocarcinoma (of glandular epithelium)
101
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.
102
Tumors of the nervous system
mostly in older animals such as cats and dogs
Primary tumors of the nervous system (CNS)
-Astrocytoma
Oligodendroglioma
Oligoastrocytoma
Medullobastoma
Meningioma
PNS tumors
Schwannoma, Neurinoma
Neurofibroma
Malignanat peripheral nerve sheath tumor
mixed tumors
can be mesenchymal origin only + mesenchymal +epithelial
Canine mammary gland tumor
103
Tumors of the vascular tissues (blood and lymph)
Hemangioma ( newly formed vascular spaces filled with blood) congenital in foal and calf
104
types of hemangioma
Hemangioma simplex, cavernosum, arteriale racemosum, areterio-venosum
105
Lymphangioma
lymphangioma simplex, cavernosus
cystic lymphangioma
106
Lymphangioma-Hemangioma
107
Hemolymphatic tumors in mammals
Malignant lymphomas (b cell, t cell and putativve NK cells
Leukemia and Myeloproliferative disease
Plasmocytic tumors (myeloma, Plasmacytoma
Histiocytoses
108
Viral oncogenesis
BLV, FeLV and lymphomas in dogs
109
TSE and BSE
Transmissible spongiform encelopathy and bovine spongifor.....
110
Shock types
Cardiogenic, Hypovolemic (cold shock) and Distributive shock (hot)
111
Cardiogenic shock types
Myocarditis, infarcts, tamponade, decrease CO, heart failure either acute or chronic
112
Hypovolemic shock
Hemorrhagic (blood loss with decreased BP leading to shock), and non hemorrhagic (dehydration, low fluid and lowe BP)
113
Distributive shock
Either neurogenic(vasomotor damage), or anaphalatic (type 1 hypersensitivity, or septic shock by endotoxins LPS Vaso dilation, leakage and coagulation !!!
114
what is hemopericardium/ cardiac tamponade?
pressure on the heart due to fluid accumulation between heart muscle and pericardium.
115
Hemosiderin as a sign of hemorrhage
yellow brown color (Hb degradation)
116
changes of the vascular endothelium in thrombosis and embolism
Vascula damage and injury caused by virusm gungi, bacteria and parasitic
immune mediated vasculitis
collagen exposure, inflammatory mediators release
117
Blood flow alterations in thrombosis and embolism
Pre stasis, stasis, reduced local flow and local stasis, economy class syndrome
Turbulence (aneurism)
circulatory disturbances, hypovolemia and shock
cardiac effects, congenital or acquired, cardiomyopathy, hypertrophy
118
Blood constituents alteration0 hypercoagulability
platlets count increase with aggregated promoting changes inn blood proportion and a decrease in anti-thromboplastic substances
119
Appearance of thrombosis and embolism depends on what
the underlying cause, location and composition (fibrin, platelets, rbc counts
120
Significance of thrombosis and embolism dpends on:
location, ability yo stop blood flow, perfusion
rate and formation, size
121
types of thrombosis
White, Red, mixed , DIC, Plasma thrombus, hyalin thrombus
122
Thrombi can be categorized into two types regarding vessel size
either mural (large vessels, white, parietal with tail eventually becomes occlusive) or occlusive (small vessels, red)
123
White, pale coagulation thrombus
BV damage- mainly platelets- and white
Vascular damage, trauma , inflammation, bacteria, fungi, parasites
thrmbocyte attachement, adhesion, pseudopodia, aggregation leading to the release of granules
Fibrin accumulation - giving it its grey color
uneven, cauliflower like, greyish mass dry, adherent to intima
124
Red Thrombus
Blood Stasis, unresolved pre-hemostatis, hemostasis
Heart failure- everywhere
right heart failure- lung
hypoalbuminemia- cachexia, liver kidney failure
Stasis- RBC damage
Thrombocyte aggregation
Fast fibrin accumulation
red gelatinous, fills lumen, do not adhere to intima
125
Mixed THrombus
alternate layers shows characteristics or red and white thrombus
126
Hyalin, agglitinative thrombus
hypercoagulalobility- in terminal circulatory bed
caused by hypercoagulobility of blood
increased, platelets, fibrinogen, inflammationmediators
shock and endotoxins
hyalin thrombus - mass of coagulated proteins
127
DIC
Disseminated intravascualt coagulopathy (widespread microthrombus formation)
abnormal coagulation activation
increase in Tissue factor, fibrinogen and clots
decrease in Clotting factor, PC (exhaustion) therefore leading to bleeding
Causes: infection of any kind
neoplasm, inflammation, tissue in injury, toxicosis and shock, vascular stasis, anaesthesia, proteolytic enzymes
128
Plasma thrombus
in lymph vessels
129
outcome of thrombosis
healing, stenosis, obturation,
heart stenosis, organ failure, death, embolism
130
Fate of the thrombus
Fibronolysis- destrys in 2 days
colliquation (liquefaction) by enzymes granulocytes
endothelization
organisation and calcification
recanalization
embolus formation
131
Whats and embolism
solid, free floating mass, foreign body in the blood stream
132
Types of emboli
Thrombo
cells
air or gas bubble
foreign body
turmour
fat droplets
parasites
bacteria or fungi?
tissue fragments
133
Emboli causes
trauma, sudden movement
forced abdominal pressure
coughing
inflammation
malignant tumor
Iatrogenic (puncture)
134
direction of blood embolism
according to blood stream
paradox: through foramen ovale
retrograde: backwards. kinda rare
135
outcome of embolism
removal of organizastion
compensation by anastomes
local infarct
metastasis of pathogens- spreading
sudden death, lung brain
136
Necrosis and Apoptosis difference
pathological cell death and programmed cell death with limited cell death
137
Necrosis
passive cell death, enzynatic degradation,
138
Necrosis causes can either be .....
external or internal
139
External Necrosis
mechanical trauma
thermal
Chemical
Toxins
Pathogens
140
internal necrosis
Hypoxia
Trophoneurotic disorder
Pancreatic enzymes
141
microscopic histiopathy
detached ribosomes
swollen michrochondia
fragmented membranes
decreased chromatin density (clumped chromatin
142
Katyo....... ?
nucleus changes during necrosis
membrane hyperchromatosis- thicker nucleus membrane
karyopycnosis-smaller nucleus
karyorrhexis - fragmented nucleus
Karyolysis - no nucleus (lysis)
143
cytoplasm changes during necrosis
decresed glycogen, increased eosinophil and cytoplasmosis
144
Types of necrosis
Coagulative, colliquation, zenker, caseous, lipo, blackleg disesase
145
Coagulation Necrosis
protein coagulation happens in livcer kidney spleen
caused by bacterial toxins
sharp edges, elevated surface, white ischemic infarct, dark red - hemorrhagic infract
dry friable
146
colliquation necrosis
liquefactive follows coagulation necrosis
cause of enzymatic, too much protein, prancreatitis
pulpy and smeary necrotic area
147
Zenker Necrosis
Striated muscle degenaration, muscles heart
caused by vitamin e and selenium deficiency, white muscle disease
circulation disorders, neuro or vasconstriction, hyperemia
physical: burn, frost, trauma
pale, dry and cooked like muscles (white muscle disease )
148
Caseous Necrosis
fatty infiltration of soft tissues
mostly happens due to bacteria, TB, PTB
onion like layers in lymph and fat infiltration
149
Lipo Necrosis,
lipid and lipochromes subcuteaneus fatty tissue.
150
Blackleg Disease
Clostridium Chauvoei
151
What are consequences of necrosis
regenration, calcification, sequestration, Cicatrix, lysis, desquamation erosion and ulceration.
abscesses, septicemia and autointoxication
152
what is cell replacement
lost cells or tissues are placed by other of the same kind mitosis
153
regenration post injury or during the healing of tissue lesions
Rescuscition
Resorption and removal
Replacement
154
What increases regeneration ability of the organism
External stimuli- such as x ray
biogen stimulants wound hormones (grwoth hormones)
embryonic tissue extract
necrotic, injured tissues substances
155
decreases regenration ability of organism
differentiation
age and condition
decreased metabolism
decrease blood supply and innervation
chalones (controls the cell death and cell regeneration of the epidermis
156
types of regenration
Perfect
Imperfect: Hypotypia, Heteromophis, Hyperregenartion, Organisation , Hypertrophia and Accomodatio
157
Removal of necrotic tissues steps
preparation
resorption
removal
158
Preparation of the removal of necrotic tissue
preparation of cells and tissue for removal, with enzymes and cells around and in tissue
Coagulation necrosis uses neutrophils and heterophil
Colliquative necrosis uses partly lytic enzymes, partly pathogen (bacteria and fungi)
and party organ features (brain, microglia and oligodendrocytes
159
Resorption of necrosis
Uses fluids and solution, osmosis and diffusion
colloid use pinocytosis
Corpuscles cellular, tissue fragments, phagocytosis helped cytosomes
involved cells in resoprtion are
granulocytes
histiocytes
Oligodendrocytes, microgliocytes
Lymphocytes
160
Removal -remotio of resorbed materials
Digestion by cytosomes(phagolysosome
Excretion,, via blood vessels and lymph leads to spleen to be destroyed
excretion to another place- cytopempsis through endothel
Storage- thesaurismosis, locally or other tissue
161
Cytopempsin
it is transcytosis, transcelluar transport
162
what is organisation
replacment by collagen fibrious connective tissue
tissue loss excessive
resorption, and removal not satisfactory
163
Process of organisation
angiofibriblast tissue production
infiltraion of granulocytes, histiocytes, and giant cells
histolysis resorption and removal
angiogenesis, fibroblast and differentiation
maturation of granualtion tissue
164
Cicatrix
scar
brain- glia cicatrix
bone fracture - callus
165
organisation is .....
resorption=removal=replacement of callagen fibrous tissue
166
What is demarcation
Ct encircles the area
same as organisation but the connective tissue encircles the are and does not fill the cavity
possible for secondary calcification
167
Regeneration of epithelial tissue. what types of mucous membranes
stratified squamous epithel: includes esiphagus, nostrols and oral cavity
columnar epithelium: stomach intestines and uterus
glandualr pithelium: found in liver kidney pancrease and thyroid gland
168
Regen of skin and mucous membranes
seperated into
destruction of upper layers only
destruction of stratum germinativum (ulceration)
and regenration of glandular epithelium
169
Destroyed upper layer only
abrasion and erosion
quick regenration, cells of the str. germinativum proliferate quickly and fill gap
irregular epihtelial papilla complete the epithilization
healing from BVD and FMD
170
Destroyed ustratum germinativum (stra. basale)
ulceration
gap is filled with serum blood and tissue debris
angio fibroblast tissue infiltrated by mobile cells
slow proliferation of epithelial cells
epithelial cells migration (1 layer to be stratified
Complete epithelization
171
regen. of glandular epithe
Liver is good at regen
endocrine galnds (thyroid, parathyroid, pituitary, pancreas (good regen)
Gonads ahve alsmost no regen
Intact basement membrane is the connective tissue framwork
livers and kidney ... tubular regenration
Basement membrane destroyed
no integration structure, hypotypia and heteromorphosis
fibrous scarring, regenerative nodules leading to cirrhosis
172
Regen of muscles and neura tissue
Isomorph (skeletal muscles
Partial regen=segemental= zenker necrosis (sarcolema and stem cells need to be intact
Heteromorph (smooth and heart muscles
CNS has no neural regenration
PNS possible regen, evena fter transection (myelin and axon)
173
Injury evaluation of PNS regenration
injury can be swollen, thickened, myelin sheath, irregular caricose, fragmented, fatty debris: stain
1st Marchi's
later: sudan red, Sudan black and scarlet red
174
Degeneration of PNS
Proximal (centipedal) part survives
Distal part (centrifugal - necrosis degenration)
wallerian degeneration: breakdonw of 1-2 ranvier nodes
175
Criteria for schwann cells
nucleus must be intact
neurlemma must be present (absent in CNS !!!)
2 cut ends must be max 3mm away from the same line
176
Regenartion Phase
Resoprtion, Removal
Schwann cell proliferation Buengners bands
Stumps (2 ends ) connection
Axonal regenration
177
Regenration of connective tissureand blood vessel, wound healing
what are the function of ct?
supportive
transport immunity in blood
storage of nutrients
178
Collagen Fibrous CT and Blood VEssels regenration
Almost unlimited with good regenrative capcaity
Multipotent cells of adventitia =Rouget cells+scattered undifferentiated cells
1.angiofibriblast tissue
=fibroblast, ni fibers
eloganted, stellate shape, large number of new vessels
2. maturation
fibroblast -fibrocytes elongated and dark nucleus
tropocollagen leading to thickening !!! (5-7days)
blood vessels
What does Vitamin C have to do with this ? (deficiecy leads to fibroblast degenration
179
types of regen of connective tissue
1 angiofibroblast tissue
Maturation
2 Elastic Fibrous
3 Cartilaginous
4 Bone regenration
180
steps of regenration in bone
Hematoma
connective tissue callus
OSteoid or cartilagionous callus
Provisional osteoid calus
Permanent osteoid callus
181
Elastic fibrous regenration
similar as collagen fibrous ct but longer around 4 weeks
elasticity will not reach original one
182
Cartilaginous tissue regen
very limited
happens from perichondrium (layers surrounding cartilage in body
young proliferating mesenchymal cells- mature chondroblasts
intracelluar matrix secretion and fiber production
chondroblast -chrondrocytes
hyalinization
183
Bon regen is either ....
primary or secondary
primary
broken ends but not seperated, no clot formed!
contact healing: osteoblasts proliferate from BC of cortical part of bone, fast and no callus
Fissure healing: following intramedullary pinning (fixation)
osteoblasts proliferate from periosteal an endosteal blood no callus
secondary
regeneration when the twon ends are seperated
osteoblasts proliferate from BV, angiogen callus is formed
Osteoblast behave like fibroblast create union and form scar tissue, unsatisfactory end result.
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Hematopoietic tissue regenration
no regenration: hyperplasia!!!
spleen: repair by CT
Bone marrow: hyperplasia: fat Bm leading to red marrow, extra medullar hematopoiesis
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Wound healing: After Injury what happens Steps?
!. Hemostasis (immediately)
2. Inflammation (24-96h)
3. Proliferation (
4.Contration, repithelization
5. Remodeling and maturation
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types of wound healing
First and second intention of wound healing
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First intention wound healing
Sanatio per primam intntionem
when:no nor minimla tissue loss
edges are clear, wound is closed,
no bacterial contamination
eg. cuts, surgical wounds etc.
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second intention wound healing
senatio per secundunm intentionem
When: due to major tissue loss
-granulation tissues filles the gap- epithelization
189
What are the factors influencing wound healing
location
status
drugs and chemotherapeutics, GC
Foreign bodies, infections and tumors
Autoimmune disease and obesity
190
Acute inflammation
Is a non specific, congenital respsone with rapid onset
can be either infection or non- infectious
Promoetd by neutrlization, sequestration, elimination and repai, regenration and wound healing
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Steps of acute inflammation
Circulatory disturbances
Exudation
Regressive changes
Proliferative Changes
192
Acute inflammation and the recognition of what....
PAMPS and DAMPS recognized by TLR and PRR
to minimize destruction and rapid protection before immune response
193
Acute inflammation vs Chronic Inflammation
Talk about:
Onset
Cells (neutrophils/monocytes, macrphages
Tissue injury
tumor, calor, dalor rubor etc?
Sign
Cause
Duration
Outcome
194
explain
Rubor?
Tumour?
Heat?
Dolor
Function leasa
Rubor is the circulatory disturbances, hyperemia
tumour, blood vessel dilatation, hyperamia, exudative, infiltrative adn proliferative proc.
heat: active hyperemia, increased blood flow
Dolor: increase pressure in tissue, nerve endings excitation by vasoactive mediators (bradykinin
funtion leasa: regressive changes
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Cells involved with inflammation
Sentinel cells: kupffer cell(liver), alveolar macrophages (lungs), splenic macrophages (spleen), peritoneal macrophages, microglial cells (NS), langerhans cells (endothelium), mast cells (blood)
Neutrophil, Eosinophil, Basophil: Mast cells, histamine, LT,PG
Monocytes, macrophages- phagocytosis
(lymphocytes, plasma cells) - immunity
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Vascular Changes (inflammation)
Hemodynamic changes: heat and redness
Vasodilation : decrease in blood velocity and increase blood flow locally leading to heat and redness
induced by release of inflammatory mediators
Histamine, 5HT release (leukotriens)
NO, PG release
from plasma some coagulation factos, kinin, fibrinolysis
Hemostasis: decrease blood flow, induced by vaso D and increase in viscosity and RB.
Blood flow decrease - neutrophils accumulation- margination
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EXudation (inflammation)
Permability changes, swelling and pain
vascular leakage
increased permability
increased intestinal hydrstatic pressure and endothelial dysfunction
biochemical mediators
histamin, 5ht, pg and leukotriens
bradykinin leading to swelling and pain.
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infiltrative processes during inflammation
margination, rolling and adhesion
leukodiapedesis
Chemotactic Migration
Leukocyte activation - phagocytosis
Ic degradation
Apoptosis of neutrophils
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Nargination, Rolling and Adhesion
Margination: of leucocztes )neutrophils, dexreases blood flow and leads to vasodilation
Rolling: selectins (E-,P-)
adhesion ( integrins (b1,b2) immunoglibulins (ICAM, VCAM) stronger adhesion
200
Leukodiapedesis
transmigration across endothelium, neutrophils mainyl during 24-48 then monocytes and macrophages
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Chemotactic migration
in intestinal tissues, towards injury or pathogen
exogenous (bacterial products)
endogenous (complement C5a) cytokines (IL1, TNFalpha, leukotriens
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Leukocyte Activation- phagocytosis
Recognition: attachement- ingestionhelping opsonization Fc, C3b
Engulfment: phagocytic vacuole formation
Killing, degradation
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IC degradation
O2 dependant - oxidative burst - ROOS
O2 independant: Granule release- proteolytic enzymes, defensins, lysozyme cationic proteins
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Apoptosis of Neutrophils
Ingestion by macrophages
205
Leukocyte adhesion deficiency
BLAD and CLAD
BLAD:Holstein- gingivitis, teeth loss, ulcers, abscesses, pneumonia, death
CLad: irish settlers
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erythrocytadiapedesis
talks about rbc leaving the blood vessels and entering the surroudning tissue
207
Proliferative changes of inflammation, when they happen
appears during acute phase, increases inflammation.
mainly histocytes, pushed together, epithelial like arrangement= epitheloid cells
giant cells
later: lymphoid cells+monocyte
sometimes: epithelial cells, alveolar epithelial cells, CNS: glial cells proliferation
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Long lasting (chronic inflmmation)
plasma cells proliferated
angio-fibroblast tissue- multiplication of CT, collagen fibers- fibrosis, sclerosis
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Progression of chronic inflammation
several months to years
1. fail of acute inflammation response
2.Repeated acute inflammation
3.Persistent infections (mycobacterium - TB
4.Prolonged exposure to toxic, silica and silicosis
5. Autoimmune
210
Characteristics of proliferative process during inflammation
1.continous cell migration
2.Fibroblast and collagen increased
3.Re-capillarization regeneration reparation
211
Influencing factors of proliferative processes during inflammation
ACTH, glucorticoids: supress inflammation
GC: inhibits cell proliferation
STH mineralcorticoids increased inflammation
STH: increased cell proliferation
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Serous Inflammation
=inflammatory edema is the mildest form of inflammation
Conten: ALbumin, fibrinogen, glubulins, lipids, cells, enzymes, ion, mediators
213
Serous inflammation
serous membrane, subcutis, submucosa, parenchymal organs
214
Serous inflammation, exudate
is clear, transparent , yellowish and sometimes opalescent, turbid and coagulated
215
Serous inflammation, CHronic
thickening, fibrin threads
216
Serous inflammation where to find it ?
serous membranes
on serous membranes:
pleuritis, peritonitis, pericarditis
high amount of fluids, petechia, hemorrhages
217
serous inflammation on skin (subcutis)
primary: allergodermatitis, autoimmune dermatitis, photosensibilization
Secondary: abscesses infectious (FMD, pox), physical( burns frostbites
-vascular injection
-red swollen
-spreads to subcutis- dough like consistency
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serous inflammation on submucosa
Thick, jelly fish lke plasma
219
serous inflammation on organs
lung: common, alveolar dcuts filled with exudate
desquamatio of alveolar epithelium
More heavy solid, turbid fluid
Liver: serous hepatitis
exudate accumulates in Disse space
Enlarged, swollen, fragile, granular
moist cut surface
perhepatitis- edema in dog
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Catarrhal inflammation
happens in presence of goblets cells, mucous membranes, respiratory tract, GIT
swollen, red
cut sruface: sero-mucus exudate, contains mucin
catarrhal: serous or purulent inflammation!, desquamative+ detached epithelial cells
221
Hemorrhagic Inflammation
Erythrocyto diapedesis: RBC extravasation
Forms: sero-hemorrhagic, sero-purulent-hemorrhagic
happens in GIT, airways, organs
causes: severe circulatory disturbances, capillary damage, toxicosis, infectious
Petechiae
Reddish organ
hemorrhagic infiltration of lymph -nodes
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Ichorus inflammation
Most severe exudate inflammation
leading to putrid. putrefecation
happens in cavitis, mucous membranes, organs
cattle: traumatic reticuloperitonitis, putrid metritis
necrosis- putrfecationand protelytic bacteria
large amount of exudate- thinner than pus, smells, turbid, greenish
can be either primary, secondary
223
Suppurative inflammation/ purulent inflammation causes
Pyogenic bacteria
Chemicals
Necrotic tissue
224
Suppurative inflammation/ purulent inflammation localization
on mucous membranes
serous membranes: pyopericardium, pyothorax, pyoarthros
organs: phlegmone, microabscess, abscess
225
Purulent exudate
pus, pyon, process= suppuratio
Rich in cells, neutrophils, lymphocytes, histiocytes, RBC, monocytes
Color: greyish, white yellowish sour cream like, viscous, turbid, greenish
consistency: watery, dense, dry
226
Purulent inflammation on mucous membranes
acute, superficial- purulent catarrh
due to drainage: anatomical orifices, pyorrhea- healing
if it accumulates:
empyema- pyometra chronic purulent inflammation
227
Purulent inflammation on serous membranes
circulatory disturbances- vascular injection hemorrhages- exudation, infiltration, if accumulates leading to empyema
Thorax:pyothorax
Joint: Pyoarthros
Pericardium: Pyopericardium
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Purulent inflammation inside the organs
1. Phlegmon(inflammation of soft tissue that spreads under the skin or inside the body
exudation+infiltration: failed dermatication
2. Microabscesses, Abscesses
there is demarcation, pus filled cavities
no spreading
229
Purulent inflammation in the skin
in epithelial layer, tiny intradermal abscesses=pustula
230
Greasy pig disease
impetigo- Staphylococcus hyicus (pus filled vesicles)
231
Fibrinous inflammation
- rich in fibrinogen exudate
Cattle, swin, sheep, duck, goose very high fibrin content in the blood
Fibrinogen -to- fibrin -to- precipitation -to- fibrin srtands -to- leading to pseudomembranaceae
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Fibrinous inflammation
appearance, localization, outcome
Appearance is fibrin strands, gel-like: exudate +fibrin
Thick casts- pseudomembranes
Localization
-serous membranes
- mucous membranes
-inside organs > lung only
Outcome: fibrinolyisis, organisation
233
Fibrinous inflammation on Serous membranes
Serous membranes
cloudy precipitation
larger flakes, fibrin strands
sero fibrnous, dry fibronous
Outcome:
absorption, proteolytic enzymes
organizastion (5-6 days), granulation tissue- villous growth
adhesion=synechia
extensive thickening= macula tendinea
CT ligaments= adhesio ligamentosa
234
Fibrinous inflammation on mucous membranes
Croupous
1.Croupous- infl. Crouposa: surface
-loose fibrin
-on stomach larynx, intestines, trachea
fast regenration
Ne loosen adhesion, quick removal (coughing passage)
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Fibrinous inflammation on mucous membranes
Diphteroid
2. inflammation, diphteroides: surface+deeper
-diffuse: uneven dull friable+ necrosis
Circumscribed -diphteric , crusts and scars (lymph follicles), button ulcers (swine fever)
superficial coagulative necrosis- healing/ profound- organisation
236
Fibrinous inflammation in the organs
LUNG
-Fibrinogen rich exudate precipitate , in alveolar acini, ducts, microbronchi
fibrin accumulates, no ventilation
detached alveolar epithelial cells, lymphocytes in fibrinous tissue
edema insurrounding interstitium
237
Croupous pneumonia
1. Congestion: hypermia, fibrinogen
2. Hepatization: Ne- red, grey, yellow
3. Lysis- healing
outcome:?
238
Tuberculosis
Specific lesion: tuberculosis
small granulomas: tuberculum
Mostly cause by Mycobacterium by inhalation
m. tuberculum
m. bovis
m. avium
239
what is a tuberculum
=localized are of inflammation associated with granuloma formation
- epitheloid cells (aligned histiocytes) +lymphocytes+ langerhans giant cells
240
Formation of tuberculum
can either be exudative or proliferative
exudative:
exudation-infiltration-necrosis- macrophage surrounding
proliferative
proliferation-macrophage surrounding- necrosis
Both cases results in:
Central necrosis surrounded by lymphocytes
241
Time points of tuberculosis in cattle
7 days- early lesions, bacteria in intra alveola macrophages, giant cells, neurophils
14- days neutrophils aggregate in central part of tubercle surrounded by epithelial cells
21 days- central caseous necrosis
35 days- beginning of mineralization
242
The celluar pathogenesis of tuberculom
=type 4 hypersensitivity- cell-mediated immune response.
early phase
-phagocyte, lysosome APC
-IL12-
sensitization phase
Th1 (response)
CD4+Th1 -----IL2
(TH17, IL17)
effector phase
TNF alpha, IL1
try to explain that shit with video I guess
243
hitologi of tubercle
central coagulative caseous necrosis
-Vascularized- drug sensitive!!!
keratinized and calcified - x-ray
Surrounding macrophages
Capsule
244
morphology of tuberculum
pinhead size, greyish whitish, cheese like necrosis
central calcification
granulation of surrounding tissue
cold abscess
caverns?
ulcers
fibrotic tubercle
Miliary tuberculosisTub
245
Tuberculum in birds
Central necrotic areaaa
foreign body giant cells
histiocytes
lymphocytes
CT
palissade formation
246
Predominantly Proliferative Tuberculosis
host has the advantage
e.g M. avium subsp hominissuis in dogs
➢ No Th1 response → no tuberculum
➢ Granulation tissue proliferates + scattered CT cells + histiocytes and giants cells in foci
→ tuberculous granulation tissue
➢ If only histiocytes and giants cells proliferate → great cell granulation
→ no tuberculum formation, no necrosis, no calcification
→ larger tumor-like (fibrosarcoma) lesions
greyish, homogenous, infiltrative lesion, no demarcation
247
PREDOMINANTLY EXUDATIVE TUBERCULOSIS
Response by basic procedure of inflammation, no cellular response
→ exudation : fibrinogen rich exudate → coagulation, necrosis → caseation → demarcation
→ tuberculous demarcation tissues
In organs with loosen structure : lungs, udder, lnn, uterus, kidneys
248
forms of tuberculosis
P: predominantly proliferative
E: predominantly exudative
T: Tubercle formation
Morphology and pathogenesis depend on many factors
249
Bacillus and host species of tuberculosis pain
PIGS
P= M. avium
T=M. bovis
E= ...
CATTLE
P= M.Bovis, M. tuberculosis, M.avium
E=M.Bovis
T=M.Bovis
HORSE+ CAR.
P= M.Bovis, M. tuberculosis, M.avium
E=...
T=...
Poultry
P=...
E=...
T=M. avium!
250
Characteristics of infected tissues of tuberculosis
LUNG
very sensitive, main site for tubercles
Pharynx, fore stomach, percardium
UDDER
SKIN, skeltal muscle
Thyroid, parotid gland
251
Individual, innate, non-specific reactivity of the host Tuberculosis
In sensitive animals → exudative
In more resistant animals → proliferative
Hu : AIDS patients → sensitive ++
252
Amount of bacteria determining type of tuberculosis
Large amount → exudative
Small amount → proliferative
253
