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General Pathology final examination > A List > Flashcards

A List Flashcards

1
Q

Cytopempsis meaning

A

Excretion to another place without digestion. Cytopempsis through endothel.

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2
Q

Thesaurismosis meaning

A

Regarding Storage of large amount locally or in other tissues

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3
Q

Cicatrix

A

Scar

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4
Q

Demarcatio

A

surroundendtissuese of necrosis with fibers

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5
Q

FMD and BVD disease

A

Foot and mouth disease, Bovine viral diarrhea

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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

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7
Q

PAMPS
DAMPS

A

pathogen-associated molecular patterns , LPS endotoxins
damage associated molecular patterns: proteins from damage necrotized cells alarmins.

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8
Q

Acute inflammation and chronic inflammation

A

Tell me about
Onset
Cells
Tissue injury
signs
cause
duration
outcome

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9
Q

Rubor

A

Circulatory disturbances classical sign of inflammation - leading to hypermia

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10
Q

Sentinel Cells in vascular changes and exudation in the acute inflammation

A

Kupffer cell, alveolar, splenic, peritoneal, microglial, Langerhans and mast cells.

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11
Q

Neutrophil Eosinophil, Basophil

A

Mast cells- histamine, LT, PG

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12
Q

Monocytes, macrophages
Lymphocytes, plasma cells

A

phagocytosis
immunity

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13
Q

Vasodilatation

A

decreased velocity
increased blood flow locally leading to heart redness

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14
Q

Hemostasis

A

decreased blood flow, can be severe in a few minutes

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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

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16
Q

Erythrocytadiapedesis

A

refers to the process of red blood cells passing through the blood vessel walls and entering the surrounding tissues

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17
Q

BLAD and CLAD what does it mean and what breeeds are specially sensitive

A

Leukocyte adhesion deficiency

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18
Q

explain serous catarrhal and haemorrhagic and ichorous inflammation

A

gotta know it by heart bro.

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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

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20
Q

inflammation crouposa on mucous membranes

A

found on stomach intestines, larynx and trachea, no deep pathological changes, Quickly removed through coughing.

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21
Q

Diphteroid- inflammation on the surface and deeper

A

type of fibrinous inflammation, diphteric crusts and scars (lymph follicles) button ulcers (swine fever)

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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

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23
Q

Croupous pneumonia

A

Congestion
Hepatization
lysis

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24
Q

pigment cells (color)

A

lipochromes -yellow
melanin- brownish black
bile- yellowish

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25
Q

Proangiogenic facctors

A

VEGF
FGF
Angiopoetin

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26
Q

Antiangiogenic factors

A

Angiostatin
Endostatin
Vasostatin

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27
Q

3 steps of carcinogenesis

A

Initiation
Promotion
Progression

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28
Q

Carcinogenesis Chemical and Physical agents

A

Chemical:
polycyclic carbohydrates
aromatic amine and other organic and inorganic chemicals

Physical Agents :
UV, radiation, Radioactivity and Ionising radiation + UV rays

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29
Q

Carcinogenesis

A

Biological agents include fungi, plants, viruses, dna viruses, rna viruses, parasites

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30
Q

Factor released by tumours

A

PIF- Proteolysis inducing factor
LMF- lipid mobolizing factor

increase muscle and adipocyte metabolism leading to cachexia

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31
Q

Whats paraneoplasia and paraneoplastic changes

A

-tumor cachexia
Endocrinopathis
paraneoplastic skin lesions
Hematologic symptoms
Hemostatic changes
Musculoskeletal symptoms
Neurological abnomarlities
amyloidosis dysproteinemia
Pyrexia -fever
Nephropathies

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32
Q

Tumor immunity

A

TSA
TAA
Anti tumor cells:
Cytotoxic lymphocytes T (CD8+)
NK cells
Macrophages
Complement system

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33
Q

Metastasis explaination

A

Migration-adhereing- proliferation- secondary neoplasia and generalization

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34
Q

Different routes of metastasis

A

Hematogenous route
Lymphogenous route
Intracanalicular route
Implantation metastasis
Inoculation metastasis

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35
Q

Metastatic Cascade

A

1 invasion of basement membrane and ECM
Intravasation
Extravasation leading to dissemination
Implantation and proliferation

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36
Q

How do you call the different degress of burn and cold

A

c. erythematosa (combustio)
c. bullosa
c. escharotica
carbonisatio

congelatio erythematosa
c. bullosa
c. escaharotica
c. gangrenosa

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37
Q

wahts asphyxia

A

lack of oxygen or suffocation

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38
Q

Hypoxemia

A

lower hemoglobulin saturation in O2, not enough O2 in the air, Hb cant take up O2

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39
Q

Hypoxia

A

O2 tissue supply is decreased

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40
Q

Hypercapnia

A

CO2 in tissue in increased

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41
Q

What are pathological signs of suffocation

A

Dark unclotted blood
petechial hemorrhages
acute lung hyperemia and edema
acute heart dilatation
Acute emphysema

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42
Q

disturbances in water supply

A

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

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43
Q

types of starvation

A

Total starvation
partial starvation and malnutrition
obesity and overfeeding

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44
Q

Autointoxication types

A

Diabetic
retention
hepatic
putrid
abnormal direction of metabolism
enterogenic
resorption

what are each ?

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45
Q

hepatic autointoxication has several causes, list them

A

exposure
viral infections
hyperthyroidism
gilberts syndrome
cholestasis
and decreased liver supply in general

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46
Q

Infection routes of routes of entry

A

Oronasal conjunctival
urogenital
venereal
urinary or genital
omphalogen
transplacental intrauterine
ovogen
latrogenic
locus minoris resistentia

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47
Q

influencing factors of infectious agents causing disease

A

infectivity
pathogenicity
virulence
host specificity
invasiveness
contagiouness
Host defense mechanism

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48
Q

MPS Mononuclear phagocytoc system

A

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.

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49
Q

Cytokines =messenger ?

A

messenger of the immunesystem, local action and systemic leading to fever!
Cytokine storm = oversecretion leading to death

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50
Q

Disorders of the immune system

A

Hypersensitivity; may alter the immune sytem response
type 1-4
autoimmune disease
immunodeficieny syndromes (SCID)

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51
Q

Types of hypersensitivity

A

type 1 - immediate IgE mediated - allergies and anaphylaxis
type 2- cytotoxic
type 3- immune complex
type 4- delayed

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52
Q

Feline immunodeficiency Virus (FIV)

A

decreased = CD4+ alteration in CD4 and CD8+ ratio
decrease = antigen presentation
decreased = Ne adhision and migration
increased IgG

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53
Q

DIsturbances of the water balance of the oragnism (EDEMA)

A

can be intracelluar or extracelluar

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54
Q

Types of water regulation

A

Nervous system
Hormonal regulation
and physical chemical factors

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55
Q

increase water retention - filtration (arterioles)

A

more water meaning water will end in tissues
tissues oncotic pressure increased
capillary hydrostatic pressure increased
vascular permeability

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56
Q

decreased water retention - reabsorption in venules

A

increased plsama oncotic pressure
starvation
increased electrolytes in blood leading kidney failure

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57
Q

Water disturbances

A

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

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58
Q

Types of hydrops

A

Hydrops = hemorrhagic acutus
hydrops adiposus
hydrops chylosus

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59
Q

Types of EDEMA

A

Oe. Stagnationis
Dysoricum
Ex. hypoproteinemia
Oe. lymphangioticum
Oe. Hormonale - myxedema

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60
Q

Dehydration, exsiccation

A

decrease water obviously

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61
Q

water balance problems in cells causes

A

hypoxia
LPS endotoxins
Autoxeamia
Burns, and frostbite
alkalosis, acidosis
Conns disease
Water toxicosis
Hypoproteinemia

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62
Q

Disturbances of water cells

A

Cell swelling
vacuolar degeneration
hydropic degeneration

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63
Q

Disturbances in fat metabolism

A

disturbances of simples fats and compound fats

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64
Q

Disturbances in carbohydrate metabolism

A

Hormonal - insulin, growth hormones, glucagon, GC hormones, Adrenaline
Neural - MO, hypothalamus

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65
Q

Diabetus mellitus type 1 and type 2

A

Type one has decreased insulin production leading to B-cell damage

type 2 - insulin resistance leading to receptor ?

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66
Q

Diabetus mellitus consequences

A

Ketoacidosis
Diabetic coma
Glycogen accumulation in renal tubules
Alopecia
microangiopathia
Neuropathia
Cataracta diabetica

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67
Q

Disturbances in keratinization and steps

A

Prekeratine
Keratohyaline granula
Odlands granula
Digestion of organelles leading to keratinocytes

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68
Q

Hyperkeratosis

A

Local hyperkeratosis
systemic hyperkeratosis
hypokeratosis
parakeratosis
hyper + parakeratosis in the rumen (CATTLE LIVER ABSCESSATION)
Dyskeratosis

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69
Q

Pathological calcification

A

calcitonin
primary calcification
secondary calcification

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70
Q

Uricosis and GOUT

A

Gout in birds
gout in mammals

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71
Q

Amyloidosis

A

starch liek, aggregate of proteins,

localized and atypical amyloidosis
systemic and typical ( can be divided into primary and secondary )

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72
Q

pathology of amyloidosis

A

sigsn in liver splees and kidneyAD

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73
Q

APUD amloidosis

A

amine precursos uptake and decarboxylation amyloidosis

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74
Q

Atrophy

A

size of an organ or cell reduces in cells size or number

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75
Q

hypoplasia

A

failure of normal development (developmental anomaly

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76
Q

Forms of atrophy

A

physiological and pathological
reversible and irreversible
local , regional and complete

Atrophia simplex, degenerative and numerical

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77
Q

Causes of atrophy

A

decreased function
decreased innervation
compression
lack of nutrients
age
endocrine disturbances
drugs
other physical exposures such as radiation

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78
Q

Actinomycosis

A
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79
Q

Actinobacillosis

A
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80
Q

Disturbances of cell division

A

-no mitosis starts
rate?
deviant out of the ordinary leading to tumors

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81
Q

what are oncogenes

A

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

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82
Q

tumorsuppresing genes

A

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

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83
Q

stability genes

A

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

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84
Q

What are preneoplastic lesions

A

Hyperplasia- increased cell number in tissue
Metaplasia - transformation of one differentiated cell into another
Dysplasia - abnormal pattern of tissue growth

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85
Q

Neoplasia (Benign Tumor)

A

grow slowly
localized demarvated and well removable
maturated differentiated cells
no invasion meaning no metastasis
simple mutations
no recediva ( no recurrence)

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86
Q

Semimalignant tumors ( borderline tumors

A

histologically nening bit locally invasive
no metastasis
frequent recidiva ( no recurrence )
papilloma and infiltrative lipoma

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87
Q

In situ Carcinoma (CIS)

A

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.

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88
Q

Malignant Tumors

A

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)

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89
Q

functional malignancy

A

when cancer produces hormones or hormone like substances

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90
Q

Anaplesia

A

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.

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91
Q

Celluar pleomorphism and nuclear polymorphism

A

Anisocytosis & Anisokaryosis

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92
Q

Differentiate between malignant and benign tumors ?

A

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

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93
Q

Benign Mesenchymla tumors of connective tissues

A

Firboma -collagen fibers
Myxoma -embryonic
Lipoma - adipose tissue
Chondroma- cartilage
Osteoma - bone
Ostechondroma - bone and cartilage

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94
Q

Bening mesenchymal tumors of the muscles

A

Rhabdomyoma - of the skeletal muscle (rare)
Leomyoma - of the smooth muscle
Cardiac Rhabdomyoma - heart muscle (mostly in pigs)

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95
Q

What are bening mesenchymal tumors ? explanation

A

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.

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96
Q

Malignant mesenchymal tumors (sarcoma)

A

Sarcoma is a type of cancer that arise from the mesenchymal tissues such as connective tissue, bone , cartilage and blood vessels.

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97
Q

connective tissue types of malignant mesenchymal tumors

A
  • Fibrosarcoma
  • Myxosarcoma
  • Liposarcoma
  • CHondrosarcoma
    -Osteosarcoma
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98
Q

muscle types of malignant mesenchymal tumors

A

Rhabdomtosarcoma
Leiomyosarcoma
Cardiac Rhabdosarcoma

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99
Q

Benign epithelial tumors

A

covers the surface of the body, muycosa and glandular tissue

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100
Q

Malignant epithelial tumors

A

Squamous cell carcinoma
Basosquamous carcinoma (mostly in dogs)
Basal cell carcinoma
Adenocarcinoma (of glandular epithelium)

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101
Q

Melanocytic tumors

A

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.

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102
Q

Tumors of the nervous system

A

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
Q

Tumors of the vascular tissues (blood and lymph)

A

Hemangioma ( newly formed vascular spaces filled with blood) congenital in foal and calf

104
Q

types of hemangioma

A

Hemangioma simplex, cavernosum, arteriale racemosum, areterio-venosum

105
Q

Lymphangioma

A

lymphangioma simplex, cavernosus
cystic lymphangioma

106
Q

Lymphangioma-Hemangioma

A
107
Q

Hemolymphatic tumors in mammals

A

Malignant lymphomas (b cell, t cell and putativve NK cells
Leukemia and Myeloproliferative disease
Plasmocytic tumors (myeloma, Plasmacytoma
Histiocytoses

108
Q

Viral oncogenesis

A

BLV, FeLV and lymphomas in dogs

109
Q

TSE and BSE

A

Transmissible spongiform encelopathy and bovine spongifor…..

110
Q

Shock types

A

Cardiogenic, Hypovolemic (cold shock) and Distributive shock (hot)

111
Q

Cardiogenic shock types

A

Myocarditis, infarcts, tamponade, decrease CO, heart failure either acute or chronic

112
Q

Hypovolemic shock

A

Hemorrhagic (blood loss with decreased BP leading to shock), and non hemorrhagic (dehydration, low fluid and lowe BP)

113
Q

Distributive shock

A

Either neurogenic(vasomotor damage), or anaphalatic (type 1 hypersensitivity, or septic shock by endotoxins LPS Vaso dilation, leakage and coagulation !!!

114
Q

what is hemopericardium/ cardiac tamponade?

A

pressure on the heart due to fluid accumulation between heart muscle and pericardium.

115
Q

Hemosiderin as a sign of hemorrhage

A

yellow brown color (Hb degradation)

116
Q

changes of the vascular endothelium in thrombosis and embolism

A

Vascula damage and injury caused by virusm gungi, bacteria and parasitic
immune mediated vasculitis
collagen exposure, inflammatory mediators release

117
Q

Blood flow alterations in thrombosis and embolism

A

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
Q

Blood constituents alteration0 hypercoagulability

A

platlets count increase with aggregated promoting changes inn blood proportion and a decrease in anti-thromboplastic substances

119
Q

Appearance of thrombosis and embolism depends on what

A

the underlying cause, location and composition (fibrin, platelets, rbc counts

120
Q

Significance of thrombosis and embolism dpends on:

A

location, ability yo stop blood flow, perfusion
rate and formation, size

121
Q

types of thrombosis

A

White, Red, mixed , DIC, Plasma thrombus, hyalin thrombus

122
Q

Thrombi can be categorized into two types regarding vessel size

A

either mural (large vessels, white, parietal with tail eventually becomes occlusive) or occlusive (small vessels, red)

123
Q

White, pale coagulation thrombus

A

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
Q

Red Thrombus

A

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
Q

Mixed THrombus

A

alternate layers shows characteristics or red and white thrombus

126
Q

Hyalin, agglitinative thrombus

A

hypercoagulalobility- in terminal circulatory bed

caused by hypercoagulobility of blood
increased, platelets, fibrinogen, inflammationmediators
shock and endotoxins
hyalin thrombus - mass of coagulated proteins

127
Q

DIC

A

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
Q

Plasma thrombus

A

in lymph vessels

129
Q

outcome of thrombosis

A

healing, stenosis, obturation,
heart stenosis, organ failure, death, embolism

130
Q

Fate of the thrombus

A

Fibronolysis- destrys in 2 days
colliquation (liquefaction) by enzymes granulocytes
endothelization
organisation and calcification
recanalization
embolus formation

131
Q

Whats and embolism

A

solid, free floating mass, foreign body in the blood stream

132
Q

Types of emboli

A

Thrombo
cells
air or gas bubble
foreign body
turmour
fat droplets
parasites
bacteria or fungi?
tissue fragments

133
Q

Emboli causes

A

trauma, sudden movement
forced abdominal pressure
coughing
inflammation
malignant tumor
Iatrogenic (puncture)

134
Q

direction of blood embolism

A

according to blood stream
paradox: through foramen ovale
retrograde: backwards. kinda rare

135
Q

outcome of embolism

A

removal of organizastion
compensation by anastomes
local infarct
metastasis of pathogens- spreading
sudden death, lung brain

136
Q

Necrosis and Apoptosis difference

A

pathological cell death and programmed cell death with limited cell death

137
Q

Necrosis

A

passive cell death, enzynatic degradation,

138
Q

Necrosis causes can either be …..

A

external or internal

139
Q

External Necrosis

A

mechanical trauma
thermal
Chemical
Toxins
Pathogens

140
Q

internal necrosis

A

Hypoxia
Trophoneurotic disorder
Pancreatic enzymes

141
Q

microscopic histiopathy

A

detached ribosomes
swollen michrochondia
fragmented membranes
decreased chromatin density (clumped chromatin

142
Q

Katyo……. ?

A

nucleus changes during necrosis

membrane hyperchromatosis- thicker nucleus membrane
karyopycnosis-smaller nucleus
karyorrhexis - fragmented nucleus
Karyolysis - no nucleus (lysis)

143
Q

cytoplasm changes during necrosis

A

decresed glycogen, increased eosinophil and cytoplasmosis

144
Q

Types of necrosis

A

Coagulative, colliquation, zenker, caseous, lipo, blackleg disesase

145
Q

Coagulation Necrosis

A

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
Q

colliquation necrosis

A

liquefactive follows coagulation necrosis

cause of enzymatic, too much protein, prancreatitis

pulpy and smeary necrotic area

147
Q

Zenker Necrosis

A

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
Q

Caseous Necrosis

A

fatty infiltration of soft tissues
mostly happens due to bacteria, TB, PTB

onion like layers in lymph and fat infiltration

149
Q

Lipo Necrosis,

A

lipid and lipochromes subcuteaneus fatty tissue.

150
Q

Blackleg Disease

A

Clostridium Chauvoei

151
Q

What are consequences of necrosis

A

regenration, calcification, sequestration, Cicatrix, lysis, desquamation erosion and ulceration.
abscesses, septicemia and autointoxication

152
Q

what is cell replacement

A

lost cells or tissues are placed by other of the same kind mitosis

153
Q

regenration post injury or during the healing of tissue lesions

A

Rescuscition
Resorption and removal
Replacement

154
Q

What increases regeneration ability of the organism

A

External stimuli- such as x ray
biogen stimulants wound hormones (grwoth hormones)
embryonic tissue extract
necrotic, injured tissues substances

155
Q

decreases regenration ability of organism

A

differentiation
age and condition
decreased metabolism
decrease blood supply and innervation
chalones (controls the cell death and cell regeneration of the epidermis

156
Q

types of regenration

A

Perfect
Imperfect: Hypotypia, Heteromophis, Hyperregenartion, Organisation , Hypertrophia and Accomodatio

157
Q

Removal of necrotic tissues steps

A

preparation
resorption
removal

158
Q

Preparation of the removal of necrotic tissue

A

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
Q

Resorption of necrosis

A

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
Q

Removal -remotio of resorbed materials

A

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
Q

Cytopempsin

A

it is transcytosis, transcelluar transport

162
Q

what is organisation

A

replacment by collagen fibrious connective tissue
tissue loss excessive
resorption, and removal not satisfactory

163
Q

Process of organisation

A

angiofibriblast tissue production
infiltraion of granulocytes, histiocytes, and giant cells
histolysis resorption and removal
angiogenesis, fibroblast and differentiation
maturation of granualtion tissue

164
Q

Cicatrix

A

scar

brain- glia cicatrix
bone fracture - callus

165
Q

organisation is …..

A

resorption=removal=replacement of callagen fibrous tissue

166
Q

What is demarcation

A

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
Q

Regeneration of epithelial tissue. what types of mucous membranes

A

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
Q

Regen of skin and mucous membranes

A

seperated into
destruction of upper layers only
destruction of stratum germinativum (ulceration)
and regenration of glandular epithelium

169
Q

Destroyed upper layer only

A

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
Q

Destroyed ustratum germinativum (stra. basale)

A

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
Q

regen. of glandular epithe

A

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
Q

Regen of muscles and neura tissue

A

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
Q

Injury evaluation of PNS regenration

A

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
Q

Degeneration of PNS

A

Proximal (centipedal) part survives
Distal part (centrifugal - necrosis degenration)
wallerian degeneration: breakdonw of 1-2 ranvier nodes

175
Q

Criteria for schwann cells

A

nucleus must be intact
neurlemma must be present (absent in CNS !!!)
2 cut ends must be max 3mm away from the same line

176
Q

Regenartion Phase

A

Resoprtion, Removal
Schwann cell proliferation Buengners bands
Stumps (2 ends ) connection
Axonal regenration

177
Q

Regenration of connective tissureand blood vessel, wound healing

what are the function of ct?

A

supportive
transport immunity in blood
storage of nutrients

178
Q

Collagen Fibrous CT and Blood VEssels regenration

A

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
Q

types of regen of connective tissue

A

1 angiofibroblast tissue
Maturation
2 Elastic Fibrous
3 Cartilaginous
4 Bone regenration

180
Q

steps of regenration in bone

A

Hematoma
connective tissue callus
OSteoid or cartilagionous callus
Provisional osteoid calus
Permanent osteoid callus

181
Q

Elastic fibrous regenration

A

similar as collagen fibrous ct but longer around 4 weeks
elasticity will not reach original one

182
Q

Cartilaginous tissue regen

A

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
Q

Bon regen is either ….

A

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.

184
Q

Hematopoietic tissue regenration

A

no regenration: hyperplasia!!!
spleen: repair by CT
Bone marrow: hyperplasia: fat Bm leading to red marrow, extra medullar hematopoiesis

185
Q

Wound healing: After Injury what happens Steps?

A

!. Hemostasis (immediately)
2. Inflammation (24-96h)
3. Proliferation (
4.Contration, repithelization
5. Remodeling and maturation

186
Q

types of wound healing

A

First and second intention of wound healing

187
Q

First intention wound healing

A

Sanatio per primam intntionem

when:no nor minimla tissue loss
edges are clear, wound is closed,
no bacterial contamination
eg. cuts, surgical wounds etc.

188
Q

second intention wound healing

A

senatio per secundunm intentionem

When: due to major tissue loss
-granulation tissues filles the gap- epithelization

189
Q

What are the factors influencing wound healing

A

location
status
drugs and chemotherapeutics, GC
Foreign bodies, infections and tumors
Autoimmune disease and obesity

190
Q

Acute inflammation

A

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

191
Q

Steps of acute inflammation

A

Circulatory disturbances
Exudation
Regressive changes
Proliferative Changes

192
Q

Acute inflammation and the recognition of what….

A

PAMPS and DAMPS recognized by TLR and PRR

to minimize destruction and rapid protection before immune response

193
Q

Acute inflammation vs Chronic Inflammation

A

Talk about:
Onset
Cells (neutrophils/monocytes, macrphages

Tissue injury
tumor, calor, dalor rubor etc?
Sign
Cause
Duration
Outcome

194
Q

explain

Rubor?
Tumour?
Heat?
Dolor
Function leasa

A

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

195
Q

Cells involved with inflammation

A

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

196
Q

Vascular Changes (inflammation)

A

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

197
Q

EXudation (inflammation)

A

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.

198
Q

infiltrative processes during inflammation

A

margination, rolling and adhesion

leukodiapedesis

Chemotactic Migration

Leukocyte activation - phagocytosis

Ic degradation

Apoptosis of neutrophils

199
Q

Nargination, Rolling and Adhesion

A

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
Q

Leukodiapedesis

A

transmigration across endothelium, neutrophils mainyl during 24-48 then monocytes and macrophages

201
Q

Chemotactic migration

A

in intestinal tissues, towards injury or pathogen

exogenous (bacterial products)
endogenous (complement C5a) cytokines (IL1, TNFalpha, leukotriens

202
Q

Leukocyte Activation- phagocytosis

A

Recognition: attachement- ingestionhelping opsonization Fc, C3b

Engulfment: phagocytic vacuole formation

Killing, degradation

203
Q

IC degradation

A

O2 dependant - oxidative burst - ROOS
O2 independant: Granule release- proteolytic enzymes, defensins, lysozyme cationic proteins

204
Q

Apoptosis of Neutrophils

A

Ingestion by macrophages

205
Q

Leukocyte adhesion deficiency

A

BLAD and CLAD

BLAD:Holstein- gingivitis, teeth loss, ulcers, abscesses, pneumonia, death

CLad: irish settlers

206
Q

erythrocytadiapedesis

A

talks about rbc leaving the blood vessels and entering the surroudning tissue

207
Q

Proliferative changes of inflammation, when they happen

A

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

208
Q

Long lasting (chronic inflmmation)

A

plasma cells proliferated
angio-fibroblast tissue- multiplication of CT, collagen fibers- fibrosis, sclerosis

209
Q

Progression of chronic inflammation

A

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
  2. Autoimmune
210
Q

Characteristics of proliferative process during inflammation

A

1.continous cell migration
2.Fibroblast and collagen increased
3.Re-capillarization regeneration reparation

211
Q

Influencing factors of proliferative processes during inflammation

A

ACTH, glucorticoids: supress inflammation
GC: inhibits cell proliferation

STH mineralcorticoids increased inflammation
STH: increased cell proliferation

212
Q

Serous Inflammation

A

=inflammatory edema is the mildest form of inflammation

Conten: ALbumin, fibrinogen, glubulins, lipids, cells, enzymes, ion, mediators

213
Q

Serous inflammation

A

serous membrane, subcutis, submucosa, parenchymal organs

214
Q

Serous inflammation, exudate

A

is clear, transparent , yellowish and sometimes opalescent, turbid and coagulated

215
Q

Serous inflammation, CHronic

A

thickening, fibrin threads

216
Q

Serous inflammation where to find it ?
serous membranes

A

on serous membranes:
pleuritis, peritonitis, pericarditis
high amount of fluids, petechia, hemorrhages

217
Q

serous inflammation on skin (subcutis)

A

primary: allergodermatitis, autoimmune dermatitis, photosensibilization

Secondary: abscesses infectious (FMD, pox), physical( burns frostbites
-vascular injection
-red swollen
-spreads to subcutis- dough like consistency

218
Q

serous inflammation on submucosa

A

Thick, jelly fish lke plasma

219
Q

serous inflammation on organs

A

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

220
Q

Catarrhal inflammation

A

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
Q

Hemorrhagic Inflammation

A

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

222
Q

Ichorus inflammation

A

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
Q

Suppurative inflammation/ purulent inflammation causes

A

Pyogenic bacteria
Chemicals
Necrotic tissue

224
Q

Suppurative inflammation/ purulent inflammation localization

A

on mucous membranes

serous membranes: pyopericardium, pyothorax, pyoarthros

organs: phlegmone, microabscess, abscess

225
Q

Purulent exudate

A

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
Q

Purulent inflammation on mucous membranes

A

acute, superficial- purulent catarrh

due to drainage: anatomical orifices, pyorrhea- healing

if it accumulates:
empyema- pyometra chronic purulent inflammation

227
Q

Purulent inflammation on serous membranes

A

circulatory disturbances- vascular injection hemorrhages- exudation, infiltration, if accumulates leading to empyema

Thorax:pyothorax
Joint: Pyoarthros
Pericardium: Pyopericardium

228
Q

Purulent inflammation inside the organs

A
  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
Q

Purulent inflammation in the skin

A

in epithelial layer, tiny intradermal abscesses=pustula

230
Q

Greasy pig disease

A

impetigo- Staphylococcus hyicus (pus filled vesicles)

231
Q

Fibrinous inflammation

A
  • 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

232
Q

Fibrinous inflammation
appearance, localization, outcome

A

Appearance is fibrin strands, gel-like: exudate +fibrin
Thick casts- pseudomembranes

Localization
-serous membranes
- mucous membranes
-inside organs > lung only

Outcome: fibrinolyisis, organisation

233
Q

Fibrinous inflammation on Serous membranes

A

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
Q

Fibrinous inflammation on mucous membranes

Croupous

A

1.Croupous- infl. Crouposa: surface
-loose fibrin
-on stomach larynx, intestines, trachea
fast regenration
Ne loosen adhesion, quick removal (coughing passage)

235
Q

Fibrinous inflammation on mucous membranes

Diphteroid

A
  1. 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
Q

Fibrinous inflammation in the organs

A

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
Q

Croupous pneumonia

A
  1. Congestion: hypermia, fibrinogen
  2. Hepatization: Ne- red, grey, yellow
  3. Lysis- healing

outcome:?

238
Q

Tuberculosis

A

Specific lesion: tuberculosis
small granulomas: tuberculum

Mostly cause by Mycobacterium by inhalation
m. tuberculum
m. bovis
m. avium

239
Q

what is a tuberculum

A

=localized are of inflammation associated with granuloma formation
- epitheloid cells (aligned histiocytes) +lymphocytes+ langerhans giant cells

240
Q

Formation of tuberculum

A

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
Q

Time points of tuberculosis in cattle

A

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
Q

The celluar pathogenesis of tuberculom

A

=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
Q

hitologi of tubercle

A

central coagulative caseous necrosis
-Vascularized- drug sensitive!!!
keratinized and calcified - x-ray
Surrounding macrophages
Capsule

244
Q

morphology of tuberculum

A

pinhead size, greyish whitish, cheese like necrosis
central calcification
granulation of surrounding tissue
cold abscess
caverns?
ulcers
fibrotic tubercle
Miliary tuberculosisTub

245
Q

Tuberculum in birds

A

Central necrotic areaaa
foreign body giant cells
histiocytes
lymphocytes
CT
palissade formation

246
Q

Predominantly Proliferative Tuberculosis

A

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
Q

PREDOMINANTLY EXUDATIVE TUBERCULOSIS

A

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
Q

forms of tuberculosis

A

P: predominantly proliferative
E: predominantly exudative
T: Tubercle formation

Morphology and pathogenesis depend on many factors

249
Q

Bacillus and host species of tuberculosis pain

A

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
Q

Characteristics of infected tissues of tuberculosis

A

LUNG
very sensitive, main site for tubercles
Pharynx, fore stomach, percardium
UDDER
SKIN, skeltal muscle
Thyroid, parotid gland

251
Q

Individual, innate, non-specific reactivity of the host Tuberculosis

A

In sensitive animals → exudative
In more resistant animals → proliferative
Hu : AIDS patients → sensitive ++

252
Q

Amount of bacteria determining type of tuberculosis

A

Large amount → exudative
Small amount → proliferative

253
Q
A

General Pathology final examination (2 decks)

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