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General Pathology > HIGHLIGHTS > Flashcards

HIGHLIGHTS Flashcards

1
Q

Diagnostic pathology

A

an AUTOPSY (syn: necropsy) may be performed to determine the cause of death in an individual or in a group of animals or to explain decreased production

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2
Q

Forensic pathology

A

the purpose of an autopsy is to determine the nature of death from a legal perspective

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3
Q

Surgical pathology

A

(histologic examination of surgically excised tissue specimens) not only facilitates diagnosis and prognosis for a living animal but also can be the basis for therapy

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4
Q

Experimental pathology

A

Contributes from the design to the endpoint of an investigation with the goal of correlating morphologic changes with clinical, functional, and biochemical parameters to elucidate the mechanisms of disease

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5
Q

Comparative pathology

A

compares specific human pathologies with those seen in natural animal models

(tuberculosis, anthrax, erysipelas etc.)

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6
Q

Disease - What do we examine in PATHOLOGY

A

2., Morphological changes

(→ Pathology)
→ Morphological examinations

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7
Q

Most important Method to recognize/investigate the disease:

A

1., Autopsy

In the vast majority of the cases complementary investigations are necessary!

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8
Q

What is Post-mortem and ante-mortem investigations

A

(excision, fine needle aspirate, biopsy samples from living animals)

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9
Q

What is Pathogenesis

A

(how does the disease proceed)

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10
Q

What is

General pathology:

A

Study of the reaction of cells or tissues to injury with a focus on the mechanisms of that response.

Basic changes:

– Circulatory disturbances – Regressive changes
– Proliferative changes
– Inflammations

– Tumors
– Developmental anomalies

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11
Q

What is Special pathology/systemic pathology:

A
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12
Q

Characteristic changes caused by well defined diseases, grouped according to organ systems

A
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13
Q

What are the Groups according to different characteristics

A

Localisation, extension

– general, organ and systemic diseases

Aetiology:
– Infectious (morbidity, mortality, lethality)

• Spreading: endemic, epidemic, pandemic

• Agent: bacterial, viral, fungal, parasitic – Noninfectious

Appearance: continous, periodic, paroxysmal

Duration: fulminant, peracute, acute, subacute, chronic

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14
Q
A

Rupture large intestines - Horse

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15
Q

Staining

A

Ziehl-Neelsen Staining

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16
Q

Staining

A

Perls Staining

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17
Q
A

Immunohistochemistry (IF, IPO), in situ hybridisation

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18
Q

Special staining

A

MAC-387

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19
Q

Type of lesion

A

Trichoblastoma, basalioma

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20
Q
A

Foot and mouth disease in Cattle, Pig and Human

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21
Q

Sanatio

A

Recovery/Healing

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22
Q

• Recreatio

A

Mild degree of functional changes, reversible morphological alterations → revivification (recreatio)

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23
Q

• Restitutio
– ad intergrum – cum defectu

A

Complete recovery following more profound tissue alterations, lost cells are replaced by corresponding tissues → regeneration (regeneratio, restitutio ad integrum/ cum defectu)

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24
Q

• Regeneratio

A

Complete recovery following more profound tissue alterations, lost cells are replaced by corresponding tissues → regeneration (regeneratio, restitutio ad integrum/ cum defectu)

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25
Q

• Reparatio

A
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26
Q

• Demarcatio

A
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27
Q

• Organizatio

A
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28
Q
A

Demarcation (abscesses in the lung, horse)

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29
Q

What is this an example of

A

Callus formation

Permanent morphological or structural changes (restitutio cum defectu) → locus minoris resistentiae

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30
Q

What is clinical death

A

Clinical death

(no breathing, no heartbeat, but tissues and organs survive for a while → resuscitation, grafts, transplantation, culturing) → pathological agony („intermediate life”) → pathological or absolute death

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31
Q

When is the recognition of death

A

Recognition of death:

no heartbeat, no responses to sensory or sensitive stimuli, no reflexes (pupils → „brain death”)

→ when post mortem changes start: obvious

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32
Q

What are the postmortem changes?

A
  • Cooling off – algor mortis
  • Pale color – pallor mortis
  • Desiccation – exsiccatio postmortalis
  • Soaking – maceratio postmortalis
  • Stiffness – rigor mortis
  • Postmortem clot – cruor postmortalis
  • PM blood sedimentation – hypostasis postmortalis – Livores mortis
  • Discoloration - imbibition
  • Selfsoftening – autolysis (selfdigestion –
  • autodigestion)
  • Postmortem decomposition – putrefaction
  • Grave wax - adipocere
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33
Q

Name of lesion?

Due to?

Found where?

A

Desiccation - exsiccatio postmortalis

Evaporation

Skin

Mucous membranes

Cornea

+ also in alive animals

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34
Q

Characteristics of this postmortem change

A

- complete dehydration of the tissues

- dry heat and/or air current

  • desert, chimney
  • Function of the putrefactive bacteria is also hampered
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35
Q

Characteristics of this postmortem change

A

Soaking, maceratio

  • Skin, organs filled with fluid
  • Foetuses
    • Aseptic autolysis
  • Carcasses staying in the water
  • Also in living animals
    • flows on the skin!
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36
Q

Rigor mortis

In which type of muscles?

Nystens Rule

A

All 3 types of muslcles

Nystens rule - Direction of rigor mortis

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37
Q
  • Skeletal muscles → rigor mortis timeline
A
  • 2-4 hours the beginning (head is stiff)
  • 5-8 hours becomes general (body)
  • 24-48 hours starts to disappear
  • 48-60 passes off
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38
Q

Rigor mortis in Heart Muscle

Systole or diastole?

Development?

Duration?

A
  • Standstill in diastole – looks like systole
  • Develops fast (30 minutes)
  • Lasts for 1 day
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39
Q

Rigor Mortis Smooth muscles

Onset?

Duration?

A
  • Quick process (10-15 minutes)
  • Lasts for 1 – 4 hours
  • Rigid intestines, arteries, spleen
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40
Q

Onset and duration of RM

Rapid and short

A
  • High environmental and/or inner temperature
  • Prolonged muscular activity
  • Young and elder animals
  • Septicaemia, wasting diseases
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41
Q

Onset and duration of RM

Delayed

A
  • Asphyxial death (notably by carbon monoxide poisoning) = SUFFOCATION
  • Severe hemorrhage, cold surroundings
  • Fails to develop In case of degenerative muscle changes
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42
Q

What is this

Characteristics

A
  • Postmortem clot - Cruor postmortalis
    • Dark red, smooth, fleshy with glistening surface
    • Very similar to Trombocytolysis but it isnt attached to the intima
    • After death blood clots in 15-30 minutes in large vessels, non in smaller ones
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43
Q
A

Blood clot in the heart

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44
Q
A
  • PM blood sedimentation, lividity
    • postmortem hypostasis
    • Effect of gravity on the blood fluid – in 1 hour!
    • Also visible inside the organs
    • livores mortis → PM spots dark purple
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45
Q
A

Sulfhemoglobin imbibition

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46
Q
A

Bile imbibition - From Gall bladder

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47
Q
A

Hemoglobin imbibition

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48
Q
A

Self softening - Autolysis

Autolytic ferments of the cell in the cytoplasm

  • Autodigestio (self digestion)
    • Gastromalatia due to gastric juice
    • Oesophagomalatia
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49
Q

What is happening

A

Postmortem destruction - putrefaction

Decomposition products → Activity of saprogenic bacteria

Suffocation supports the putrefaction → blood remains liquid

Decomposition from Intestine – v. portae – liver

Dissolution into gases, liquids and salts

Ptomaines (neurine, muscarine, putrescin)

Gas production – stomach distension

Under 5 degrees putrefaction stops

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50
Q

Pase of Putrefaction

Rapid VS Slow

A
  • Pace of putrefaction
    • Rapid
      • Obese (retaining the body heat)
      • Warm environmental temperature
      • Hyperemic organs
      • Widespread infection
      • Injuries (portals of entry)
      • Oedematous tissues
    • Slow → Lean and Exsanguination (dehydration)
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51
Q
A

Putrefaction

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52
Q
A

EMPHYSEMA POSTMORTALIS HEPATIS

Due to putrefaction

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53
Q
A

Postmortal Tympany (gass accumulation)

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54
Q
A

Sulph-hemoglobin imbibition

Reaction of Hb (hemoglobin) plus H2S (hydrogen-sulphid) greyish-green, paling off on air

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55
Q
A

Sulph-hemoglobin

Reaction of Hb (hemoglobin) plus H2S (hydrogen-sulphid) greyish-green, paling off on air

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56
Q
A

Sulph-hemoglobin

Reaction of Hb (hemoglobin) plus H2S (hydrogen-sulphid) greyish-green, paling off on air

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57
Q
A

Sulph-hemoglobin

Reaction of Hb (hemoglobin) plus H2S (hydrogen-sulphid) greyish-green, paling off on air

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58
Q
A

Pseudomelanosis

  • H2S + Fe (from Hb)
  • Iron-sulphide
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59
Q
A
  • PM Wax - Adipocere
  • Saponification
  • In wet, clayey soil
  • Fatty acids and Ca++
  • Form soaps, impregnate soft organs
  • Sweetish odour
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60
Q

What are the causes of cellular damage?

A
  • External causes
    • Physical
      • Mechanical effects
      • High and low temperature
      • Electricity
      • Radiant energy
      • Climate and weather
    • Chemical → Intoxications
    • Biological → Viruses, bacteria, fungi, protozoa
    • Inadequate supplements (malnutrition)
  • Internal causes
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61
Q
A

Luxation

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62
Q
A

bite (vulnus. morsum)

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63
Q
A

gun-shot (vulnus. sclopetarium)

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64
Q
A

Bleeding in the brain tissue

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65
Q
A

Rupture

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66
Q
A

Tituration

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67
Q

Sequelae of traumatic effects

• Local effects

A

– Lesions
– Tissue damage

– Port of entry!

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68
Q

Sequelae of traumatic effects

• General effects

A

– General effect of a local infection

• tetanus, gas-phlegmone

– Loss of blood

• Bleeding out

– Functional disturbances

• fractures, luxations

– Embolism

• fat, bone marrow

– Traumatic shock

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69
Q
A

Bleeding, Haemothorax

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70
Q
A

Loss of function

disruption of the Achilles tendon

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71
Q

Lesions in the tissues

Microscopical or Macroscopical

A

Macroscopic

– Ruptures (ruptura)

– Fractures (fractura)

– Luxation (luxatio)
– Fissure

– Concussion (commotio)

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72
Q

Lesions in the tissue leading to Locus minoris resistenciae

A

– Ruptures (ruptura)

– Fractures (fractura)

– Luxation (luxatio)

Locus minoris resistenciae

  • sick animals
  • bad condition
  • dietetical problems
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73
Q

Lesions in the tissue

Where can you find Concussions

A

– Concussion (commotio)
– brain, spinal cord, bone marrow

– bony capsule!!!

– not always seen with naked eyes

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74
Q

Fractures

What do we have?

Special form of fraction

A
  • open (fr. aperta) or covered (fr. optecta)
  • special appaerance

– Infraction - bone fracture marked by a small line that shows up in X-ray examination

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75
Q

What can be seen

A

Dislocation of the broken ends

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76
Q

Which reaction can be seen?

What does it mean?

A

Vital reaction

Happened in real life

Edges of the wound
– Hemorrhages at the surrounding tissues – After soaking it disappears!

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77
Q

High temp as a cause of disease - Categories

A

CAUSED BY: Radiant heat, hot liquid, steam, gas, solid substances (live coal, melted metal)

  • Categorized by the severity of the lesions

​LOCAL EFFECT = COMBUSTIO

  1. • C. erythematosa
  2. • C. bullosa
  3. • C. escharotica
  4. • Carbonization

(1st) (2nd) (3rd) (4th)

partial depth (epidermis) 1+2

complete depth 3+4

GENERAL = HYPERTHERMIA

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78
Q

Appearance of the Burns

A

C. erythematosa (1st degree)

Hyperaemic area, vasodilatation, edema

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79
Q

Appearance of the Burns

A

C. bullosa (2nd degree)

  • Vesication,
  • Denaturation of proteins,
  • Pain
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80
Q

Appearance of the burns

A

C. escharotica (3rd degree)

  • Coagulation necrosis of the tissues
  • Hemostasis
  • Thrombosis
  • Pale
  • Insensible
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81
Q

Appearance of the Burn

A

Carbonization (4th degree)

  • Tissues are charred
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82
Q

Inhalational Burns

A

Inhalation Burns

  • Destruction of airways and lungs
    • The mucous membrane of the nasal and oral cavity, upper respiratory system
    • Gasses soluble in water = form acids or base and cause edema
      • Chloride, sulphur dioxide, ammonia
      • swelling, inflammation
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83
Q
A

Carbonization (4th degree)

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84
Q

General effects of burns

(exept hyperthermia)

A
  • Circulatory disturbance, shock… (immediate)
    • edema (permeability of the blood vessels)
    • pain, hypovolaemia, hyperkalemia, autointoxication
  • Necrosis, enzymatic lysis of proteins – increased local osmotic pressure
  • Hemoconcentration, desiccation
  • Degeneration of parenchymal organs
    • catabolic enzimes continue to work
    • liver, kidney, heart, bone marrow! (anaemia)
  • Hyperkalaemia (potassium released from the cells)
    • 2nd day: oliguria, anuria (degeneration of tubular cells)
    • 3rd day: polyuria (later no water retention ability)
  • Toxaemia
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85
Q

General effects of burn

HYPERTHERMIA

A

Hyperthermia

  • Extremely increased internal temperature of the body
  • Hyperthermia = (failure of physical heat regulation)
    • High (and humid) environmental temperature
    • High own heat production (pyrogens)
    • Heat loss is inhibited
  • Consequences similar to burn consequences
  • Pathologic findings
    • Quickly developing RM, incompletely CLOTTED blood, early PUTREFACTION
    • Hemostasis in internal organs, brain edema, meningeal hyperemia, and hemorrhages in the hypothalamus
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86
Q

HYPERTHERMIA

HEAT STROKE

A
  • Heat stroke (> 43°C)
  • Lesions
    • Heat spasms
      • electrolyte loss (sweating)
    • Heat distress
      • most often seen, collapse
      • failure of cardiovascular compensatory mechanisms after hypovolemia
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87
Q
A

Sunstroke - Insolation

  • Infrared (ultraviolet?) radiation of sunshine
  • Longlasting or strong impact of sunshine
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88
Q

Low temperature as a cause of disease

LOCAL EFFECTS

A
  • Contraction of vessels, local ischaemia
    • Metabolic and waste products (lactic acid, histamin)
    • Irregular vasodilatation! - hemostasis
  • Frostbite (congelatio)
    • Not only at freezing point - wet, windy surroundings
      • Piglet with diarrhea, protruding body parts (ears,tail,testicles)
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89
Q

LESION

A

C. erythematosa (1st)

– bluish-red, swollen

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90
Q

LESION

A

C. bullosa (2nd)

– vesication, edema

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91
Q

LESION

A

C. escharotica (3rd)

– necrosis

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92
Q

LESION

A

C. gangrenosa (4th)

gangrene

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93
Q

Low temperature as a cause of disease

GENERAL effects

(Not hypothermia)

A

• General effects

– Gangrenous lesions, necrosis

• Toxaemia

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94
Q

Hypothermia at which temp?

A

Failure of the heat regulation – around 35oC

27-30 oC: vital functions come to standstill

20-25 oC: death

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95
Q

Hypothermia

  1. Endangered species
  2. Predisposing factors
  3. Factor of great metabolic Activity
A
  1. pig, rabbit, dog
  2. diarrhoea, bleeding
  3. Brown adipose tissue
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96
Q

What are the Defence mechanisms Against falling body temperature

A
  • Contraction of muscles
    • Shivering
  • Vasoconstriction in the skin
  • Increased metabolism
    • Labile glycogen reserves are used up
  • Shallow and quick respiration
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97
Q

Name a HYPOTHERMIC wellknown disease

A

Baby pig disease

• Acute hypoglycemia of the newborn pigs

– Fatal if untreated
– Cold, starvation

• In newborn or young animals

– Heat regulation is not perfect

– Body surface is relatively large

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98
Q

What is autointoxication?

A

= Autotoxemia

Poisoning the body with endogenous toxins,

Self- poisoning, a pathological condition that occurs as a result of poisoning by substances produced in the body.

(➢Exogenous toxins subject of Toxicology)

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99
Q

Types of autointoxication

NEED TO KNOW

A
  1. Stuck of intermediary metabolism
  2. Retention autointoxication
  3. Hepatic autointoxication
  4. Putrid autointoxication
  5. Abnormal direction of metabolism
  6. Enterogenic autointoxication
  7. Resorption autointoxicationn
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100
Q

1. Stuck of intermediary metabolism

DIABETIC AUTOINTOXICATION

A

DIABETIC TOXINS = KETONE BODIES

Ketone bodies are 3 water-soluble molecules

  1. Acetoacetate,
  2. Beta-hydroxybutyrate and their spontaneous breakdown product,
  3. Acetone

Produced in LIVER from FATTY ACIDS

  1. Low food intake (fasting), carbohydrate restrictive diets, starvation,
  2. Prolonged intense exercise
  3. Untreated (or inadequately treated) TYPE 1 DM
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101
Q
  1. Stuck of intermediary metabolism

DIABETIC AUTOINTOXICATION

What is KETOSIS and KETOACIDOSIS

A
  1. Ketosis is a metabolic state in which most of the body’s energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis in which blood glucose provides most of the energy.
  2. KETOACIDOSIS (DKA) is a potentially life-threatening complication in people and animals with DM

➢ It happens predominantly in those with type 1 diabetes.

➢DKA results from a shortage of insulin; in response the body switches to burning fatty acids and producing acidic ketone bodies, causes most of the symptoms and complications.

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102
Q
  1. Stuck of intermediary metabolism

DIABETIC AUTOINTOXICATION

Symptoms of Diabetic ketoacidosis

A
  1. Nausea and vomiting,
  2. Pronounced thirst,
  3. Excessive urine production and
  4. Abdominal pain that may be severe.

➢Dehydration, such as a dry mouth and decreased skin turgor.

➢ Tachycardia (a fast heart rate) and low blood pressure.

➢ Cerebral edema, May cause

  • headache,
  • Coma,
  • loss of the pupillary light reflex, and
  • progress to DEATH.
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103
Q

Lesion

A

Diabetic autointoxication

(pancreas fibrosis, dog)

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104
Q

Lesion

A

Diabetic autointoxication (pancreas fibrosis, dog)

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105
Q

Lesion

A

Diabetic autointoxication

(Lipidosis in the liver, dog)

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106
Q

Lesion

A

Diabetic autointoxication

(Lipidosis in the LIVER, dog)

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107
Q

Lesion

A

Diabetic autointoxication

(Brain edema, dog)

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108
Q

LESION

A

Diabetic autointoxication

(Brain Edema, dog)

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109
Q

What is Retention autointoxication(2)

3 types

A

Develops in excretory organs, accompanied by a delay in the removal of metabolic products from the body.

➢Kidney failure = uremia

➢Uricosis (gout)

➢Icterus (hepatopathy)

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110
Q

Retention autointoxication(2)

Uremic autointoxication

Solutes/Uremic toxins

Classification of uremic toxins

A

Characterized by the retention of various solutes that would normally be excreted by the kidneys.

  1. Creatine,
  2. Creatinine,
  3. Urea
  4. Uric acid.

➢Low-molecular-weight, water-soluble uremic toxins

➢Protein-bound solutes
➢Middle-molecular-weight molecules

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111
Q

Retention autointoxication(2)

Uremic autointoxication

What are the consequences of UREMIA?

A
  • Seizure, coma, cardiac arrest, and death.
  • Spontaneous bleeding (vascular damage)
  • Electrolyte
  • Kidney failure
  • ➢MULTIORGAN FAILURE
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112
Q

Lesion

A

Uremia (kidney-fibrosis, dog)

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113
Q

Lesion

A

Uremia (kidney-fibrosis, dog)

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114
Q

Lesion

A

Uremia (kidney-fibrosis, dog)

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115
Q

Lesion

A

Uremia (necrotic glottisis, cat)

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116
Q

Lesion

A

Uremia (uremic gastritis, dog)

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117
Q

Lesion

A

Uremia

(uremic encephalopathy, dog)

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118
Q

Lesion

A

Uricosis (Bird)

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119
Q

Lesion

A

Uricosis

Granuloma (TOPHUS)

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120
Q

3. Hepatic autointoxication

A

Retention of bilirubin, decreased detoxification of the gastrointestinal toxins

(enterogenic autointoxication).

➢Damage of the liver parenchyma can occur:

▪ Hepatitis (inflammation)

▪ Hepatosis (degeneration)

▪ Tumor (primary, secondary)

▪ Fibrosis (necrosis, scar-formation)

▪ Cirrhosis

3 PHASES

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121
Q
  1. Hepatic autointoxication

PHASE I - Detoxification pathway

A

Consists of

  • Oxidation,
  • Reduction
  • Hydrolysis

Catalysed by enzymes referred to as the (=PROTECTION)

  • Cytochrome P450 enzyme group or
  • Mixed Function Oxidase enzymes (MFO).
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122
Q
  1. Hepatic autointoxication

What is Impaired hepatic detoxification?

A

Refers to decreased phase I and/or phase II enzyme activity

= The levels of hepatic detoxification enzymes decreased.

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123
Q
  1. Hepatic autointoxication

Phase II - detoxification pathway

A

This is called the conjugation pathway, whereby the liver cells add another substance (eg. cysteine, glycine or a sulphur molecule) to a toxic chemical or drug, to render it less harmful.

This makes the toxin or drug water-soluble, so it can then be excreted from the body via watery fluids such as bile or urine.

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124
Q
  1. Hepatic autointoxication

What is the toxic effect of BILIRUBIN

A

➢Bilirubin is toxic in most biological systems tested.

➢Several mechanisms have been suggested for this toxic effect,

  • Including inhibition of enzyme systems and
  • Inhibition of cell regulatory reactions (protein/peptide phosphorylation).
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125
Q
  1. Hepatic autointoxication

What is the toxic effect of BILIRUBIN in the BRAIN

A

When the serum level of unconjugated bilirubin exceeds the albumin binding capacity, bilirubin diffuses into the central nervous system and may result in permanent neurological damage or death

(bilirubin encephalopathy with kernicterus).

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126
Q
  1. Hepatic autointoxication

What is the toxic effect of BILIRUBIN in the BRAIN

What does BIND refer to?

A

Bilirubin-induced neurologic dysfunction (BIND) refers to the clinical signs associated with bilirubin toxicity (ie, hypotonia followed by hypertonia and/or opisthotonus or retrocollis) and is typically divided into acute and chronic phases.

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127
Q

Lesion

A
  1. Hepatic autointoxication

Toxic effect of Bilitubin to the brain

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128
Q

Lesion

Which toxic component?

A

Billirubin

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129
Q
  1. Hepatic autointoxication

➢Impaired hepatic detoxification can result from which intrahepatic causes:

A
  • exposure to
    • Food additives,
    • Solvents,
    • Toxins,
    • Viral infections,
    • Gilbert’s syndrome,
    • Hyperthyroidism,
    • Restricted bile flow (Cholestasis)
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130
Q
  1. Hepatic autointoxication COMPLICATIONS
A

➢The presence of chronic fatigue is a frequent symptom.

➢Depression, general malaise
➢Headaches, digestive disturbances, allergies and chemical sensitivities, constipation

➢Mental confusion, mental illness, tingling in extremities, abnormal nerve reflexes, and other signs of impaired nervous system function

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131
Q

Lesion

A

Liver cirrhosis (dog)

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132
Q

Lesion

A

ICHTERUS

Ichterus coagulopathy

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133
Q
  1. Histolysis/heterolysis by gangrene = putrid autointoxication

What is gangrene?

A

Gangrene (or gangrenous necrosis) is a type of necrosis (ichorous inflammation).

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134
Q
  1. Histolysis/heterolysis by gangrene = putrid autointoxication

Types of gangrene

A

The types of gangrene differ in symptoms, and include:

  1. dry gangrene,
  2. wet gangrene,
  3. gas gangrene,
  4. internal gangrene.
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135
Q

Lesion

A

Gangrene

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136
Q
  1. Histolysis/heterolysis by gangrene = putrid autointoxication

Dry Gangrene

A

Dry gangrene is a form of coagulative necrosis that develops in ischemic tissue, where the blood supply is inadequate to keep tissue viable.

➢ The limited oxygen in the ischemic tissue limits putrefaction and bacteria fail to survive.

➢ The affected part is dry, shrunken and dark reddish-black.

➢ The line of separation usually leads to complete separation, with eventual falling off of the gangrenous tissue if it is not removed surgically, a process called autoamputation.

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137
Q

Lesion

A

Dry gangrene

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138
Q
  1. Histolysis/heterolysis by gangrene = putrid autointoxication

Wet Gangrene

A

Wet, or infected, gangrene is characterized by thriving bacteria and has a poor prognosis (compared to dry gangrene) due to sepsis resulting from the free communication between infected fluid and circulatory fluid.

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139
Q

Lesion

A

Wet Gangrene

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140
Q

Which bacterias can cause wet gangrene?

A

In wet gangrene, the tissue is infected by saprogenic microorganisms

(Clostridium perfringens or Bacillus fusiformis, for example),

which cause tissue to swell and emit a fetid smell.

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141
Q

What happen due to wet gangrene?

A

➢ The toxic products formed by bacteria are absorbed, causing the systemic manifestation of sepsis and finally death.

➢ Necrotoxins!!!

➢ The affected part is edematous, soft, putrid, rotten and dark.

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142
Q

Lesion

A

Pneumonia ichorosa (bo)

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143
Q

Lesion

A

Pneumonia ichorosa (bo)

Wet gangrene

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144
Q

5) Abnormal direction of metabolism

Name a special type that accumulate with high metabolism = abnormal metabolism

A

The porphyrias are a group of rare diseases, in which chemical substances called porphyrins accumulate with high metabolism. (picture: swine) abnormal metabolism

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145
Q

Lesion

A

Porphyrias - porphyrins accumulate with high metabolism. (picture: swine) abnormal metabolism

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146
Q

6. Enterogenic autointoxication, enterotoxaemia

How?

Why?

By what?

A

– Absorbed decomposition products from gastro- intestinal system

Grass fever: methylindol, grass- sickness: Cl. botulinum,

Enterotoxaemia: Cl. perfringens

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147
Q

Lesion

A

Enterogenic autointoxication, enterotoxaemia

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148
Q

Lesion

A

Enterogenic autointoxication, enterotoxaemia

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149
Q

6. Intestinal autointoxication/toxic colon

Nothing highlighted

A

➢The colon’s main responsibility is the elimination of toxins with the feces.

➢Toxins in the feces (intestinal toxins):

  • indol,
  • skatol,
  • phenol,
  • methylmercaptan,
  • urobilin,
  • histidine,
  • ammonia,
  • putrescine,
  • neurin,
  • cadaverin,
  • butyric acid,
  • cholin,
  • methylguandinine.

➢Constipation intestinal autointoxication/toxic colon.

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150
Q

Lesion

A

Intestinal autointoxication/Toxic colon

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151
Q

Lesion

A

Intestinal autointoxication/Toxic colon

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152
Q

7) Resorption autointoxication

7. Absorbed metabolites from special cases:​

A

= Ruptured, perforated, arrodated stomach, intestine or urinary bladder.

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153
Q

Lesion

A

Ruptured, perforated, arrodated stomach, intestine or urinary bladder.

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154
Q

Lesion

A

Ruptured, perforated, arrodated stomach, intestine or urinary bladder.

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155
Q

Lesion

A

Ruptured, perforated, arrodated stomach, intestine or urinary bladder.

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156
Q

Lesion

A

Ruptured, perforated, arrodated stomach, intestine or urinary bladder.

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157
Q

Lesion

A

Ruptured, perforated, arrodated stomach, intestine or urinary bladder.

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158
Q

Morphological complications of the autointoxication

A

Degeneration and enlarged of parenchymal organs (liver, kidney, heart, CNS)

Hydropic or vacuolar degeneration: histopathologically large cytoplasm: swelling, enlarged mitochondria.

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159
Q

Lesion

A

Toxic hepatopathy/vacuolar hepatopathy/non-specific hepatitis

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160
Q

LEsion

A

➢Toxic myodegeneration/myocardosis

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161
Q

LEsion

A

➢Toxic nephropathy/acut tubular degeneration-necrosis

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162
Q

Lesion

A

➢Toxic encephalopathy

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163
Q

Lesion

A

➢DIC (Disseminated intravascular coagulopathy/microthrombosis)

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164
Q
  1. Internal conditions of development of diseases
A

(predispositio) + resistance (resistentia)➔development of a disease.

Predisposition and resistance constitution) and acquired characteristics (condition).

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165
Q
  1. Internal conditions of development of diseases

What is Genetic predisposition

A

➢An individual may not be born with a disease but may be at high risk of acquiring it. This is called genetic predisposition or susceptibility.

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166
Q
  1. Internal conditions of development of diseases

What is Constitution

A

= Somatotype

Categorize the human physique according to the relative contribution of 3 fundamental elements, somatotypes

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167
Q
  1. Internal conditions of development of diseases

What are the different somatypes?

A

1) Normosom type (typus muscularis, typus athleticus) muscular-athletic physique [mesomorphic]
2) Leptosom type (typus respiratorius) prone to emaciation [ectomorphic]
3) Pycnic type (typus digestivus) prone to obesity [endomorphic]

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168
Q
  1. Internal conditions of development of diseases

What is diathesis?

A

„Defective” constitution➔predisposition for certain diseases (diathesis)

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169
Q
  1. Internal conditions of development of diseases

Diseases can be?

A

Congenital or Hereditiary

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170
Q
  1. Internal conditions of development of diseases

What is HEREDITIARY diseases?

A
  • The defective constitution and the connected functional changes are inherited
  • Can be dominant, recessive or intermedier
  • Can be recognized at parturition or can manifest later
  • If it is life-threatening: lethal factor
  • Predisposition for certain diseases: diathesis
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171
Q
  1. Internal conditions of development of diseases

What are CONGENITAL diseases?

A

Effects that harm the fetus

In avian species: ovogen infection (Salmonella gallinarum, goose parvovirus, etc.)

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172
Q

Important role in diatheses:

A
  • Species (susceptibility, eg. classical swine fever)
  • Breed, race (breeding those with natural resistence to a disease [eg. avian leukosis])
  • Gender
  • – ♀ cystitis
  • – ♂ urolithiasis
  • Age (young animal: omphalitis; old: digestive diseases)
  • Individual (not all individuals are affected by the same disease/agent)
  • Organ
  • – bone: fracture
  • – liver: rupture
  • – muscle: laceration
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173
Q

The congenital and acquired resistence is:?

A

IMMUNITY

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174
Q
  1. Infectious agents as causes of disease

What is infection?

A

Infection:

spreads from animal to animal, through direct or indirect route (fomites, vectors, iatrogen etc.)

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175
Q
  1. Infectious agents as causes of disease

What is Invasiveness:

A

Invasiveness:

The pathogen is able to spread inside the organism (not all pathogens have this feature: e.g. Cl. tetani)

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176
Q
  1. Infectious agents as causes of disease

Infectious pathogens:

A

Parasites, fungi, bacteria, viruses, prions

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177
Q
  1. Infectious agents as causes of disease

Parasites

A
  • Ectoparasites (dont enter organism)
    • stress, weakening factor (blood loss), „locus minoris resistentiae”
  • Endoparasites (infectious):
    • Multicellular
      • Malnutrition, blood loss, weakening, atrophy, mucosal membrane lesions, autointoxication
    • Unicellular
      • Intracellular Babesia causing cell damage
      • Extracellular toxoplasma causes formation of toxic products
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178
Q
  1. Infectious agents as causes of disease

Fungi

A

Mycotoxicosis(noinfection!)

Dermatomycosis (superficial invasion: skin, claw, hoof, mucosal membrane) → loss of hair, irritation, stress (itching), „locus minoris resistentiae” (changes in structure)

Visceral mycosis (local inflammatory processes, granuloma formation, thallus-formation, thrombotisation, thromboembolism, metastasis)

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179
Q

Lesion

A

Fungi

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180
Q

Lesion

A

Fungal granuloma formation in the lung

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181
Q

Lesion

A

Fungal thalus formation in the air sac

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182
Q
  1. Infectious agents as causes of disease

Bacteria

A
  • Obligatory and facultative pathogens, intracellular and extracellular
  • Bacterial Infections
    • Local
      • The pathogen enters the body, but does not certainly spread, often in wounds, abscesses
    • Systemic
      • Pathogen enters the body, and spreads → sepsis, bacteraemia
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183
Q
  1. Infectious agents as causes of disease

Viruses

A
  • Obligatory intracellular pathogens, modify the physiological metabolic processes of the infected cell
  • Local infection
  • Systemic infection (affects only a certain tissue type or organ system: e.g. rabies),
  • Generalised infection (viraemia)
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184
Q
  1. Infectious agents as causes of disease

Prions

A
  • Modulator-proteins, modify the metabolic processes of the cell
  • Damage: neuron degeneration, encephalosis
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185
Q

Lesion

Cause of lesion

A

Bovine spongiform encephalopathy (BSE), „mad cow syndrom

PRIONS

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186
Q

Immune response

Types

A
  • Innate
  • – Nonspecific for antigenes
  • – Immediate reaction
  • – No memory

Adaptive

– Specific for antigenes
– Slower reactions at first (days to weeks)
– Memory – fast reaction! (see vaccination)

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187
Q

Immune response

Innate immune response

A

Anatomic barriers

  • (skin, mucous membranes) and
  • Physiologic properties (stomach pH, body temperature) + Phagocytosis, complement system
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188
Q

Adaptive immunity

Responses

A

Adaptive immunity • 2responses:

– Cellular immunity (T lymphocytes against intracellular pathogens)

– Humoral immunity (B lymphocytes against extracellular pathogens and toxins)

T-Cell = Specific antigen binding molecule is T cell receptor (TCR) (only recognizes antigen if bound to MHC molecule!)

B-Cell = Membrane bound immunoglobulin (can recognize single antigen as well)

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189
Q

Phagocytic cells include

A
  • macrophages,
  • dendritic cells,
  • granulocytes (eosinophil, basophil,neutrophil),
  • Mast cells
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190
Q

Types of cells

A

Macrophages

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191
Q

Types of cells

A

Dendritic cells

immature to the left, and mature to the right

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192
Q

Type of cells

A

NEUTROPHIL Granulocyte

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193
Q

Type of cell

A

EOSINOPHIL Granulocyte

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194
Q

Type of cell

A

BASOPHIL Granulocyte

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195
Q

Type of cell

A

MAST cell

196
Q

Type of cell

A

NK-cells (phagocyting a tumor cell)

197
Q

What is Mononuclear phagocytic system (MPS)

A

Role in immunity, inflammatory processes,

• Monocyte is the name in circulation

In Tissues =

  • Histiocytes

– Resident macrophages

  • Kupffer-cells in liver,
  • Alveolar macrophages in lungs

Major role in phagocyting endogenous and exogenous pathogens

198
Q

What is CYTOKINES

A
  • Messenger molecules of the immune system
  • Low-molecular-weight
  • Soluble glycoprotein proteins
  • Largely, they are produced locally, and act LOCALLY
  • (but also SYSTEMIC effects: fever, lethargy, inappetence)
  • They direct the immune response
  • Oversecretion can be fatal: cytokine storm
199
Q

What is this

A

Mature Lymphocyte

200
Q

What is this

A

Reactive lymphocytes

201
Q

What are the 3 major groups of the immune system disorders?

A
  1. – Hypersensitivity reactions
  2. – Autoimmune diseases
  3. – Immunodeficiencies
202
Q

What is hypersensitvity? (immune system)

A

1) Hypersensitivity

• Altered intensity of immune response, leading to pathologic lesions

  • 4 GROUPS
203
Q

What is Type I hypersensitivity

A

– Type I (immediate)

  • allergies,
  • anaphylaxy
204
Q

What is type II Hypersensitivity?

A

Type II

  • (CYTOTOXIC)
  • haemolytic anaemias
205
Q

What is type III Hypersensitivity?

A

– Type III

  • IMMUNE COMPLEX
  • Arthus reaction,
  • Systemic lupus erythematosus (SLE),
  • Rheumatoid arthritis
206
Q

What is type IV Hypersensitivity

A

– Type IV

  • (DELAYED)
  • tuberculin test,
  • contact dermatitis
207
Q

Lesion

A

TYPE I Hypersensitivity

IMMEDIATE

ATOPIC DERMATITIS

208
Q

LEsion

A

TYPE IV HYPERSENSITIVITY

DELAYED

CONTACT DERMATITIS

209
Q

Lesion

A

TYPE III Hypersensitivity

IMMUNE COMPLEX

SLE = Discoid lupus erythematosus (s= systemic)

210
Q

2) Autoimmune diseases

A
  • Specific immune response to self-antigens
  • Multifactorial etiology
  • Autoantibodies
  • 2 main mechanisms:
    • normal immune response to abnormal antigen
    • abnormal immune response to normal antigen
  • Result: tissue damage and inflammation
211
Q

2) Autoimmune diseases

Example of a

  1. • Autoreactive antibodies disease
  2. • Lymphoplasmocytic inflammation and fibrosis
  3. • Chronic inflammation
  4. • Organ specific autoimmune diseases
A
  1. • Autoreactive antibodies disease = SLE (ANA-test)
  2. • Lymphoplasmocytic inflammation and fibrosis = keratoconjunctivitis sicca, KCS
  3. • Chronic inflammation = Rheumatoid arthritis
  4. • Organ specific autoimmune diseases = pemphigus, uveodermatologic syndrome, autoimmune haemolytic anaemia (AIHA)
212
Q

Lesion

A

PEMPINGUS

Autoimmune disease

213
Q

Lesion

A

Uveodermatologic syndrome

Autoimmune disease

214
Q

LEsion

A

Autoimmune disease

Rheumatoid arthritis

215
Q

3) Immunodeficiency syndromes

A
  • Failure Of The Immune System Response To pathogens
  • Can be primary (congenital or hereditary) or secondary (acquired)
  • Not always causing health issues (e.g. Pelger- Huët anomaly)
  • SCID (severe combined immunodeficiency)
    • failure to produce specific immunity
    • Can affect only T cells, T- and B cells
    • Mostly by fungi and viruses
  • Feline immunodeficiency virus (FIV), malnutrition, stress, tumors, aging, chronic diseases cause secondary immunodeficienies
216
Q

Lesion

A

Normal and SCID Thymus (dog)

217
Q

Lesion

A

Gingivostomatitis, cat

FIV?

218
Q

Lesion

A

Lymphoid depletion in Peyer’s patch, enteritis, cat small intestine

219
Q

Electricity as cause of disease

A

Electric shock – death: electrocution

The higher the voltage the less the resistance!!!

Alternity current is more dangerous than direct current!

Medium amperage cause disturbances
– Brain – loss of consciousness,

– Heart failure – cardiac arrest

220
Q

Lesion

A

Common Kestrel (Falco tinnunculus)

221
Q

Lesion

A

Lightning

222
Q

Lesion

A

Lightning

223
Q

Radiant energy

A

• Electromagnetic rays

– Ultra-short waves (microwaves - warming)

– Infrared waves (warm surface radiations)

– Visible rays (physiological effect)

– Ultraviolet rays (biological - path. effect!)

224
Q

What is Radiant energy

A

• Ionizing rays

  • positive or negative charges

– Effect: dose, ionization, penetrability

– Cosmic rays

– Particular radiations (alpha, beta, proton, neutron, deuteron rays)

– Electromagnetic rays (X- and gamma rays)

225
Q

Irradiation sickness

A
  1. Phase I (initial phase – after 1-2 hours)
    1. dizziness, vomiting, exhaution, anorexia, nervousness – alopecia
  2. Phase II (latent phase) – 1-2 days without signs
  3. Phase III (sickness – after a week)
    1. Bone marrow lesions: hemopoietic insufficiency
    2. No phagocytosis, no antibody production
  4. Phase IV (break down - 4-5 months after)
    1. diarrhea,
    2. anemia,
    3. kidney & liver failures etc.
      1. malignant tumors
226
Q

Lesions

Radiations

A

Lymphocytes
– lymphopenia, smaller lymphonodes

Bone marrow – hypoplasia

Testicles, ovaries – atrophia, fibrosis

Lens
– opacity

Skin
– ulcers,tumors

Cartilage
– retarded growth, malformation of the legs

Fetus
– developmental anomalies

227
Q

What are the External causes of diseases

A
  1. Physical effects
  2. Chemical effects
    1. • toxicosis
  3. Biological effects
    1. Infectious agents
    2. Virus, bacteria, fungi, prions, protozoa
  4. Inadequate supply Oxygen, water, nutrient
228
Q

What are the Disturbances in oxygen supply

A
  • Suffocation = (asphyxia) – lack of air
  • Hypoxaemia = insufficient saturation of the blood
  • Hypoxia = insufficient saturation of the tissues
  • Hypercapnia = increased CO2 level in the tissues
229
Q

Pathology of the suffocation

A
  • Dark, unclotted blood
  • • Petechial hemorrhages
    • serosal membranes, larynx, trachea, heart
  • Acute lung hyperemia and edema
  • Acute dilation of the heart
  • Acute emphysema
  • Differentiate from septicaemia!
230
Q

Lesions due to

A

Pathology of suffocation

• Petechial hemorrhages

serosal membranes, larynx, trachea, heart

Acute dilation of the heart

Acute emphysema

Differentiate from septicaemia!

231
Q

Lesions due to

A

Pathology of suffocation

Dark, unclotted blood

• Petechial hemorrhages

serosal membranes,

Acute lung hyperemia and edema

Acute emphysema

Differentiate from septicaemia!

232
Q

Disturbances in water supply

A
  • Exsiccosis, dehydration
    • Lack of water intake
      • Fluid loss never stops – eg. evaporation
      • Relatively high mineral content, pH shift
    • Increased fluid loss
      • Vomiting, diarrhea, perspiration
  • Hyperhydratio (water toxicosis)
    • Loss of minerals and electrolites
  • Pathological changes seen in skin (skin fold test), sunken eyes
233
Q

Lesion

A

Dehydration

Lack of water intake

Increased fluid loss

  • Diarrhea
234
Q

Lesion

A

Dehydration

235
Q

Disturbances in nutrient supply

Total starvation

A

Total starvation (Inanitio completa)

– No food intake (energy, protein)
– 40-50 % of the body: death (Cachexia)

236
Q

Disturbances in nutrient supply

Partial starvation,

A

Malnutrition (Inanitio incompleta)

– Food supply is not adequate
– Deficiency diseases

237
Q

Disturbances in nutrient supply

Obesity,

A

Overfeeding (Obesitas)

– Surplus of feed or feed components
– Continuous or occasional (dilation and rupture of the stomach)

– Other causes (lack of movement, hormonal disorder)

238
Q

Incomplete starvation, malnutrition

• Causes

A

– Feed
• Quantity or quality (ingredients)

– Normal feed, but
• Inadequate food uptake
• Pathological lesions of the digestive tract

• Digestion - Maldigestion
• Absorption - Malabsorption
• Deficiencies

– Increased need
• Consequence: deficiency diseases

239
Q

What is the Consequence of autointoxication (Nutrient)

A

– increased fat and protein catabolism → ketonaemia

240
Q

Lesion

A

Cachexia

241
Q

Lesion

A

Obesitas

242
Q

Lesion

A

Cachexia

243
Q

LEsion

A

Cachexia

244
Q

Lesion

A

Cachexia

245
Q

Lesion

A

Oedema cachecticum

246
Q

Lesion

A

Cachexia

247
Q

Infectious agent

Spreading?

Agents?

A
  1. Spreading among animals
  2. Within the animal: infectious agents, tumors as wel
  3. Prion (TSE, BSE)
  4. Viruses (DNS, RNS, enveloped, non enveloped)
  5. Bacteria (Gr+, Gr-)
  6. Chlamydia, Mycoplasma
  7. Fungi
  8. Protozoa
  9. Helminths
  10. Ectoparasites
248
Q

Skin infections

A

– Transcutan infection

  • Intakt skin: dermatophytosis, Malassezia
  • Through lesions: papilloma, rabies (!), tetanus
  • Arbo = arthropode born: babesiosis, Lyme-disease, infec. anaemia, WNV, African swine fever
249
Q

Spread of pathological procecces in GI tract

A

Gastrointestinal tract

  • Gastric **acidity, pH 1-2
  • Viscous**mucus
  • Digestive enzymes, detergents in the bile
  • Defensins
  • Normal intestinal flora
  • Secreted IgA antibodies (MALT)
250
Q

Lesion

A

RESPIRATORY

Type II pneumocytes (surfactant, regeneration,

phagocytosis, immunregulation)

251
Q

What is an AEROSOL

A

Aerogen (airborne) infection

252
Q

Oronasal, conjunctival infection affects

A

bird flu, fowl cholera

253
Q

urogenital infection:

A

– venereal infection, semen, or erosions on the mucus membranes (Brucellosis, AIDS, dourine)

– urinary or genital infections: FLUTD, cystitis; pyometra

254
Q

Infections via the umbilical cord,

A

omphalogen:

E. coli,

Salmonella

255
Q

Vertical infections

A

transplacental or intrauterine infection (BVD, PRRSV)

ovogen infection: Salmonella

256
Q

Incetions caused by the veterinarian

A

Iatrogenic infection: PCV2, EBL

257
Q

What are the Factors affecting spread of pathogens and the disease:

A

Infectivity (ability of pathogen to establish infection)

Pathogenicity (capacity to cause disease)

Virulence (ability to decrease the fitness of the host)

Host specificity (PRRSV, Aujeszky disease)

Invasivity (tetanus, anthrax, FIPV!!)

Immunological function of the host

Contagiousness (ability to spread) rabies, FMD

– Temperature (CHV, rhinoviruses)
– Humidity, other environmental factors

258
Q

Spread of pathological processes in the organism

A
  1. Pathogen in the organism
  2. At the site of entry (portal of entry)
  3. Primary process
  4. Metastasis
259
Q

What is METASTASIS

A

= SPREADING of PAHOGEN

metastasis is the name of – the process
– the secondary lesion

• metastasis: a lesion identical to the original (primary) one

Can be an active process: migrating parasites!!!

260
Q

Types of metastasis

A
  1. Local
  2. Regional
  3. Distant
261
Q

Local metastasis

A

to the surrounding areas

direct spread

262
Q

Regional Metastasis

A

to regional lymph nodes

via the lymphatic circulation

263
Q

Distant Metastasis

A

= To Distant organs

  1. lymphogen = retrograde lymphogen metastasis
  2. haematogen = phagocytotic embolic
  3. Intracanalicular = ascending descending
264
Q

Spread of pathological processes in the organism

Mostly spread through the

A

Veins

V. portae V. hepatica
V. pulmonalis V. umbilicalis

265
Q

What is the outcome of Spreading of pathological processes in the organism?

A

GENERALIZATION

266
Q

DIFFERENT FORMS of spreading of pathological process in the organism

A

• Bacteriaemia

– bacteria in low number

– only temporarily

• Septicaemia - sepsis

– lots of bacteria
– for prolonged time

• Pyaemia

– pus gets in the circulation
– the content of an abscess gets in the bloodstream

• Viraemia

– free or cell-associated

267
Q

What could lead to Septicaemia

A
  1. Bacteria in the organs as well
  2. Settlement in the organs (bacterial-emboli, phagocytotic metastasis)
  3. Septicemia by Mycoplasmas – Mycoplasmaemia
  4. Pyogen bacteria (sepsis)
  5. Rottening bacteria (sapraemia)
268
Q

What does SIRS stand for

A

Systemic inflammatory response syndrome

269
Q

Result of SIRS

A
  • High TNFα and LPS (Gr- bact) levels: DIC
  • Liver damage: decreasing glyconeogenesis
  • High NO levels: vasodilatation – decrease blood pressure
  • SEPTIC SHOCK
270
Q

Pathology of SEPTICEMIA

A
  1. Incomplete rigor mortis
  2. Dark red blood, incomplete post mortem coagulation
    1. – fast putrefaction, and haemoglobin imbibition
  3. Spleen enlargement (septic splenitis)
  4. Generalized lymphadenomegaly
  5. Acute catarrhal inflammation in the GI tract
  6. Haemorrhages everywhere
    1. – Mucous membranes, under the serous membranes, in the cortex of the kidneys
  7. Cloudy swelling in the parenchymatous organs (liver, kidneys, heart and skeletal muscle)
271
Q

Lesion

A

Septicemia

Enlarged Spleen

272
Q

Lesion

A

Septicemia

Generalized lymphadenomegaly

273
Q

Lesion

A

Septicaemia

Cloudy swelling in the parenchymatous organs (liver, kidneys, heart and skeletal muscle)

274
Q

Mechanisms of cell injury

GENERAL CONSIDERATIONS

A
  • Cellular response depends on the – type, duration, severity of the harm
  • Consequences depend on the – type, condition, adaptability of the cell
  • Cellular injury results from functional, and biochemical abnormalities in one or more

essential cell component:

275
Q

Mechanisms of cell injury

A

ATP synthesis

Oxidative phosphorylation, anaerobic glycolysis (liver cell vs. neuron)

    1. If ATP decreases (hypoxia, or toxin)
  2. Rise in IC Ca++ : enzyme activation
  3. Mitochondrial damage (increased Ca++ levels, phospholipases, ROS)
    1. – Cytochrome c leakage - APOPTOSIS
  4. ​ROS levels rising (free radicals)
  5. Membrane permeability defects
276
Q

What is REPERFUSION INJURY

A

• In certain cases cells may undergo more severe damage after the blood flow is restored after ischemia

277
Q

What is the different nuclear changes?

A

Nuclear changes

  1. Nuclear membrane hyperchromatosis
  2. Karyopycnosis
  3. Karyorhexis
  4. Karyolysis
278
Q

Lesion

A

Karyorhexis

279
Q

Lesion

A

Damage of the cell surface organelles

280
Q

Regressive changes in the organs

A

ATROPHY

281
Q

Factors of the circulatory system

A

Circulatory system

• Blood

• Heart

• Network of vessels
– Blood distribution – arteries – Blood collection – veins

• Microcirculation
– between blood and extravascular tissue – exchange of nutrient and waste products

• Lymphatics

– draining fluid into the blood vascular system

282
Q

Normal circulation depends on

A
  • Heart (mechanical energy)
  • Valves (cardiac, aortic, venous)
  • Elastic walls of blood vessels
  • Pressure differentials
  • Volume of the blood
  • Distribution of the blood

• Hydrodynamic factors

283
Q

Regulation of blood circulation depends on

A
  1. • Hydrodynamic factors
  2. • Neurohormonal regulation
  3. • Vasomotion control
    1. maintaining harmonized calibre change in the vessels
  4. • Terminal circulatory bed
284
Q

What is importaint about the Terminal circulatory bed

A
  • Section between the arterioles and venules
  • Major place of circulatory disturbances
285
Q

What is the Role of the endothelium

A

• Function:

  • To maintain blood in a fluid state
  • Anti-thrombotic and pro-fibrinolytic
  • Upon injury opposite effect

• Critical participant:

  • Fluid distribution, inflammation, immunity
  • Angiogenesis, hemostasis
286
Q

What are the circulatory disturbances?

A

=Alterations in blood flow and perfusion

• Local:

  1. Hyperemia
    1. In the artery
      1. Active hyperemia
      2. A slowdown of the arterial flow
    2. • In the vein:
      1. Local venous congestion
      2. Systemic venous congestion
  2. Ischaemia

• General:

– collapse

– shock

287
Q

What is Prehemostasis

A

• Plasma leakage

• Extravasation

– RBCs

– WBCs

• In case of inflammation

• Strong stimuli

– mechanical, thermal, chemical or toxic

288
Q

Pathology of circulatory disturbances

A

• On the body surfaces of alive animals

• Increased blood flow
– Bright red, slightly swollen, warm area

• Decreased blood flow
– Bluish red, swollen, colder

• Distended blood vessels appear

– Vascular injection

289
Q

Lesion

A

Circulatory disturbances

HYPERAEMIA?

290
Q

What is this a picture of

A

Hyperaemia due to decreased blood flow

291
Q

what is this a picture of

A

Local Congestion

292
Q

Circularoty disturbance

Local Congestion, what does it mean

A

Local congestion

• Passive process

• Blood accumulates and slows down in the venous circulation

– prehemostasis, hemostasis

• Vein is obstructed or compressed

– Torsion of the intestine
– Strangulation of the spleen
– Thrombosis

293
Q

Lesion

A

Circulatory disturbance

Local congestion

294
Q

Pathology of congestion

A

• ORGANS

– Dark red, bluish red, cyanotic

– Swollen

– Large amount of blood on the cut surface

• Mucosal membranes (SKIN)

– Dark red, bluish-red, swollen

– Edemic submucosa
– Wrinkled

– Serous fluid in the lumen of the organ

295
Q

LEsion

A

Congestion

296
Q

Lesion

A

Congestion due to torsion of one uterine horn

297
Q

Lesion

A

Congestion

298
Q

What is Infarceratio

A

= Venous Infarct

  • • Infarceratio haemorrhagica
  • • Long lasting or final obstruction of a vein

– No nutrient or oxygen supply

– Plasma and RBCs in the tissues

– Necrosis of large area
(similar to hemorrhagic infarct)

299
Q

Lesion

A

Slow occlusion

300
Q

What is slow occlusion

A

Slow occlusion

  • Collaterals enlarge
  • Remodel
  • Drainage is maintained

• Liver cirrhosis

301
Q

Lesion

A

Systemic Venous Congestion

302
Q

What is Systemic venous congestion

A

• Not only the terminal circulatory bed is affected

• Causes
– Acute or chronic heart failure
– Paralysis of the vasomotor center

– Shock

• Appearance
– In all the organs

303
Q

Pathology of Systemic Venous Congestion

A

• Liver
– First centrilobular, than general

– Chronic case: nutmeg liver

  • *• Spleen**
  • *– Hyperemic septic splenitis !**
  • Kidneys (medulla only)
  • Lung (plus edema)

• Intestines
– Dark from the serous membranes

304
Q

Lesion

A

Systemic venous congestion

305
Q

Lesion

A

Chronic case of systemic venous congestion of the liver

NUTMEG

306
Q

Lesion

A

Congestive induration - Liver

307
Q

What is Congestive INDURATION

A

Congestive induration

• Chronic congestion

• Parenchyma is destroyed

  • Replaced by collagen fibrous connective tissue
  • Pathology:

– Firm, moist content is less on the cut surface

308
Q

What is ISCHAEMIA

A

Ischaemia

• Local inadequate blood supply

– General: anemia, hypovolemia

• Physiological

– Digestion, uneven distribution of blood

• Pathological

  1. – Compression
  2. – Obturation
  3. – Vasoneurotic disturbance

• Consequences

309
Q

What are the different types of ISCHAEMIA

A

Ischaemia

  1. Ischaemia compressiva– Tympany (horse, cow, rabbit, etc.) – Tumors
  2. Ischaemia obturativa – Thrombus, embolus
  3. Vasoneurotic ischaemia– Angiospasm (CNS, cold, chemical subs.)
  4. Collateral ischaemia
310
Q

Name the cases

A

A= Thrombosis

B= Compression

C= Embolism

D= Vasculitis

311
Q

Name the cases

A

E= Spasm

F= Steal

G= Atheroma

H= Hyperviscosity

312
Q

What are the Consequences of the ischaemia

A

• Depends on
– degree and type of narrowing, time, type of tissue, collaterals (lung, liver)

• Collapsus / shock

• Necrosis - Infarct:
– Infarctus haemorrhagicus

– Infarctus ischaemicus

313
Q

What is an infarct

A

Infarct

Definition

  • Necrosis of circumscribed area of a tissue due to acute ischemia
    • The vessels are obturated

The circulation of tissue

  • End arteries
    • No anastomotic channel
  • Anastomotic arteries
    • Kidneys
314
Q

What is an Ischemic infarct

A
  • • End arteries
    • Area becomes bloodless, necrotic
    • Appearence:
      • Pale grey, dry
      • The margin of the infarct is reddish
        • The collateral vessels are full with RBCs
  • Location
    • Kidneys,
    • heart,
    • spleen,
    • brain
315
Q
  • Infarct pathology
A
  • Formation of the infarct
    • Pale, swollen, no sharp edges
    • Histochemical methods are needed
  • Fresh infarct
    • Cone shaped, pale, enlarged, sharp
    • edged, cut surface is still moist (!)
  • Evolved infarct
    • Cut surface dry, homogenous, crumbled
    • Dark red, hyperaemic rim
  • Older or chronic infarct: Surrounded by demarcation zone, scar
316
Q
A

Older/chronic infact with demarcation

317
Q
A

Ischemic infarcts, kidney, swine, cross section

318
Q
A

Infarct

319
Q
A

Infarct

320
Q
A

Colonic mucosal necrosis, horse

321
Q
A

Ischemic infarct, heart

322
Q

What is Hemorrhagic infarct

A

• Double circulation

– In the necrotic area the vessels are filled with RBCs

• Red (darker), dry

– Location
• Lungs, kidney, spleen, liver

323
Q
A

Haemorrhagic infarct, testicle, dog

324
Q
A

Haemorrhagic infarcts, spleen, dog

325
Q
A

Haemorrhagic infarcts, kidney

326
Q
A

Haemorrhagic infarcts,

327
Q

Consequences of an infarct

A

• Nature of vascular supply

– Double (lungs, liver) or end-arterial (kidney, spleen)

• Rate of occlusion development
– If it is slow, collateral blood supply maydevelop

• Vulnerability to hypoxia
– Neurons (3–4 min)
– Myocardial cells (20–30 min) – Fibroblasts (hours)

• Oxigen content of the blood

• Death

– Insufficient – Heart

– Lung

• Survival
– Reactive inflammation
– Repair
– Organisatio – connective tissue

328
Q
A

Consequenses of an infarct

329
Q

Infarct =

A

arterial occlusion

330
Q

Infarceration =

A

venal occlusion

331
Q

What is Haemostasis

arrest of bleeding

• finely regulated physiologic response

A
332
Q

Steps of Haemostasis

A
  • Steps of hemostasis
      1. Primary
        * Transient vasoconstriction, platelet aggregation to form a platelet plug
      1. Secondary
        * Coagulation to form a meshwork of fibrin
        * intrinsic (XII activation) and extrinsic (TF – VII activation)
        * common pathway activation of X, FIBRIN formation
    • 3. Thrombus dissolution
      • thrombus retraction by plasmin, fibrinolysis
    • 4. Tissue repair at the damaged site
333
Q

What are the Disturbances of microcirculation

A
  • Prehemostasis –blood flow slows down
  • Hemostasis – stop of the blood flow
    • In the terminal bed
    • Leakage
    • Reversible
  • Posthemostasis – start of the blood flow
  • Peristasis – slow bloodflow
334
Q
A

Stasis

335
Q

Definision of SHOCK

A

Cardiovascular collapse

– A syndrome resulting from a disproportion between blood volume and volume of the circulatory system (1:6)

– Profound circulatory failure resulting in life-threatening hypoperfusion of vital organs

336
Q
  • Types of Shock
A
  • Cardiogenic: Acute or chronic heart failure
  • Hypovolemic
    • Blood loss and Reduced circulating blood volume
    • Fluid loss is secondary from vomiting, diarrhea, burn
  • Blood maldistribution
    • Neurogenic → vasodilatation (paralysis of the vasomotor center)
    • Anaphylactic - type I hypersensitivity reaction
    • Septic (endotoxin)
337
Q

What is the cause of septic shock

A

Caused by

Gr- lipopolisacharid (LPS);

(Gr+, fungi as well without LPS) and

Cytokins, vasoactive mediators

338
Q

What are the phases of Shock

A

1. non-progressive

– compensation

– baroreceptors

2. progressive

– inadequate compensation

3. irreversible

– severe metabolic acidosis

– Insufficient blood supply of the vital organs (brain, kidneys), DIC

339
Q

Pathology of Shock

A
  1. Hemorrhages
  2. Congestion in the abdominal organs (intestines)
  3. Transsudate in the abdominal cavity, liver and lung edema
  4. Acute dilatation of the heart
  5. Ischemia in the kidney (oliguria)
  6. Hyalin-thrombus in the small blood vessels
  7. Subacute case

– degeneration in liver, kidney, heart muscle

340
Q
A

Shock

Haemorrhages

341
Q
A

Liver edema

Cause of shock

342
Q
A

Ischaemia in the kidney

Shock

343
Q
A

Shock gut piglett

344
Q

What is an Hemorrhage

A

– extravasation in a live animal

345
Q

What is • Thrombosis

A

(Embolism)

– inappropriate formation of intravascular thrombus

346
Q

• Hemorrhage + thrombosis =

A

(DIC)

347
Q

Expressions

Epistaxis?

A

nosebleed

348
Q

Expressions

Hematemesis

A

– bloody vomit

349
Q

Expressions

Hemoptoe

A

expectoration

350
Q

Expressions

Haemarthros

A

blood in the joints

351
Q

Expressions

Hematuria

A

blood in the urine

352
Q

Expressions

Metrorrhagia

A

hemorrhage in the uterus

353
Q

Expressions

Enterorrhagia

A

intestinal hemorrhage

354
Q

Expressions

Hematochezia

A
  • bloody feces (associated with lower GI tract bleeding)
355
Q

Expressions

Melaena

A

bloody feces because of enterorhagia

356
Q

Expressions

Hemopericardium, -thorax, -peritoneum

A

Heart, thorax, abdomen

357
Q

Expressions

(haemaspiratio

A
  • inhalation of blood)
358
Q
A

Haemorrhages in the pelvis of the kidney, swine

359
Q
A

Hemorrhage in the Bowman’s capsule

360
Q
A

Heamorrhage in the spleen

361
Q

Forms of hemorrhage

• By origin

– hemorrhage by rhexis

A

– rhexis = breaking forth

  • Vessel wall continuity defect
  • Physically disrupted vessel
362
Q
A

Pars esophagica ulceration, stomach, pig. Rhectic hemorrhage.

363
Q
A

Ascending pyelonephritis, rhectic hemorrhage, dog

364
Q

Forms of haemorrhages

By origin
– hemorrhage by diapedesis

A

• Small defects in otherwise intact blood vessels

• Increased vessel wall permeability (RBCs in small number)

• Decreased coagulability (thrombocytopenias)

• Clotting factor deficiencies (von Willebrand’s disease)

• Acquired coagulation disorders
– Vitamine K deficiency, warfarin toxicosis, liver disease

• DIC

365
Q

Forms of Haemorrhage

By appearance

From small to large

A

– Petechial (vibex) < EcchymoticSuffusion < Hematoma < Apoplexy

366
Q
A

Petechiae, gut, horse

367
Q
A

Ecchymosis, dog

368
Q
A

Purpura

369
Q
A

Petechiae and ecchymoses, epicardium

370
Q
A

Petechiae, meninges, swine

371
Q
A

Elongated hemorrhages (vibex), muscle

372
Q
A

Intramuscular haemorrhages, poultry

373
Q
A

Suffusions, mesentery

374
Q
A

Haematoma, liver

375
Q
A

Sublingual haematoma, dog

376
Q
A

Perirenal haematoma, swine

377
Q
A

Perirenal haematoma, cat

378
Q
A

Apoplexy, cat

379
Q
A

Petechial bleeding, Thymus cattle BNP

380
Q
A

Old haematoma liver

381
Q
A

After bleeding

382
Q

What are the Signs of hemorrhages

A
  • Hemorrhagic infiltration of lymph nodes
  • Brownish red color from haemoglobin
  • Degradation of haemoglobin
383
Q
A

Haemorrhagic infiltration
of lymph nodes, large intestine, swine

384
Q
A

Pseudomelanosis, salmonellosis, swine

385
Q

Factors predisposing to thrombosis (Virchow’s triad)

A
  1. Alterations in the vascular endothelium
  2. Alterations in blood flow
  3. Alterations in blood constituents = HYPERCOAGULOBILITY
386
Q
A

Thrombosis of the arteria iliaca externa, horse

387
Q
A

Umbilical vein foal

388
Q

Red thrombus characteristics

A

• Like clotting

• Stasis!

• Cellular damage (RBCs)

• Usually together with white thrombus

• BUT stasis for any reason

– Heart failure – all over

– Right side failure
• Truncus pulmonalis, lung

– Hypoalbuminaemia
• cachexia, liver or kidney failure

389
Q

What is the Mechanism of Stasis

A

– Plasma leakage
– Higher viscosity
– Higher resistance in the lumen

– Slowing down of the blood flow

390
Q
A

Stasis

391
Q
A

Recanalisation of a thrombus, submucosa, horse

392
Q

Thrombosis in species

• Horse

A

– a. mesenterialis cran., abdominal aorta

393
Q

Thrombosis in species

• Cattle

A

– in the wall of the uterus (septic metritis)

394
Q

Thrombosis in species • Human!

• Cat

A

– abdominal aorta

395
Q

Thrombosis in species

• Other species (swine, cattle, dog)

A

endocarditis

396
Q
A

Vegetative valvular endocarditis
heart
white thrombus

(Endocarditis thrombo-ulcerosa)

397
Q

What is EMBOLISM

A

Embolus

– a solid mass or gas bubble of either internal or external origin carried by the bloodstream sticks in a narrower blood vessel

– free-floating foreign material within the blood

• Embolism: transport process

398
Q

Types of EMBOLI

A

Thrombus or a part of it ( - thombo-embolism)

– emboli derived from fragments of a thrombus

Cells or cell groups

Air or gas bubble

Fat droplets–from bone marrow after fracture

Parasites–Dirofilaria, flukes

Aggregates of bacteria,fungi
Tumor cells

Tissue fragments(skin)

Solid foreign material

399
Q
A

Air embolism, dog

400
Q

Cause of embolism

A
  • Trauma
  • Sudden movements
  • Forced abdominal pressure
  • Coughing
  • Inflammation, malignant tumor
  • Iatrogen cause
401
Q

Outcome of embolism

A

Local: infarct
– Venous – pulmonary circulation
– Arterious – smaller artery downstream

Metastasis of pathogens, spreading of pathogenic processes

Sudden death (lung, brain)

402
Q
A

Anaemic infarcts, kidney, swine

403
Q

What are Regressive changes

A

Edema, disturbances in water balance of cells and the organism, disturbances in fat metabolism

404
Q

Location of water intracellular is called?

A
  • Intercellular (in tissue spaces) = edema
  • Transcellular (in the lumen of the organs)
    • intestines, body cavities
405
Q

What regulates the water balance?

A
  1. •Nervous system
    1. • Hypothalamus
      1. • Kidney, sweating, respiration, gastric juice
  2. •Hormonal regulation
    1. • endocrine glands
      1. • Hypophysis (vasopressin, aldosterone), thyroid gland (tiroxin)
  3. •Physical-chemical factors
    1. • maintenance of constant osmotic pressure
406
Q

What causes Increased Retention of water

A

INCREASED

• Hydrostatic pressure – venous congestion

• Colloid osmotic pressure of the interstitium

• Vascular permeability

407
Q

What causes Decreased Retention of water

A

DECREASED

• Colloid osmotic pressure of the plasma

  • *• Tissue tension** - starvation
  • *• Capacity of the lymph vessels**
  • Electrolite imbalance – kidney failure
408
Q

Nomenclature of the water balance disturbances

• Hyperhydria

• Anasarca

A

Fluid accumulation in the subcutaneous tissue

409
Q

Nomenclature of the water balance disturbances

• Hyperhydria

• Hydrops

A

•transudate – exudate

•hydrops haemorrhagicus acutus

  • hydrops adiposus
  • hydrops chylosus
410
Q

Nomenclature of the disturbances

• Hyperhydria

•Ascites

A

Fluid accumulation in the abdomen

Offen cause of cirrhose

411
Q

Nomenclature of the disturbances

  • Hyperhydria
  • Hydrothorax

•Hydropericardium

A

Water accumulation in the thorax, heart pericardium

412
Q

Nomenclature of the disturbances

• Hyperhydria
• Edema

A

– intercellular water accumulation

413
Q
A

HYDROTHORAX

414
Q
A

Hydrops chylosus

415
Q
A

Disse space

416
Q
A

Fluid in the transcellular space

417
Q

Classification of the edema

A
  1. Time of the appearance
    1. Oe. congenitale or aquisita
  2. Pathogenesis
    1. Oe. stagnationis
      1. cardiale
    2. Oe. dysoricum
      1. • inflammatorium, toxicum, allergicum, angioneuroticum
    3. • Oe. ex hypoproteinaemia (hydraemia)
      1. • cachecticum, renale (oedema ex vacuo)
    4. • Oe. lymphangioticum
    5. • Oe. hormonale - myxoedema
418
Q

Cell swelling

A

Functional disturbances of the sodium pump result in water influx

419
Q
A

Vacuolar degeneration

420
Q
A

Hydropic degeneration

421
Q
A

Reticulated degeneration

422
Q
A

Balloning degeneration

423
Q
A

Balloning degeneration

424
Q
A

Vesicular degeneration

425
Q

Water disturbances Causes in cell

A
  • Hypoxia
  • autointoxication
  • burns, frostbites
  • extended tissue necrosis
  • acidosis, alkalosis
  • infectious diseases
  • exogenous toxins
  • Hypoproteinemia
426
Q

Where do we find Simple fats DEPOT

•

A
  • Subcutaneous fat,
  • kidney,
  • under serous membranes,
  • bonemarrow
427
Q

Pathology of Disturbances in water balance of cells

A
  • Organs are swollen, enlarged, and pale
  • Dried cut surface
  • Epithelial layers such as skin and mucosal membranes can be dry or jelly like
428
Q

Staining methods of FATS

A

• Physical
• Sudan III, scarlet red

  • Sudan black, osmic acid
  • Oil-red-O

• Chemical

• Nile blue

  • PAS
  • Schultz method (cholesterol)
429
Q
A

Physiological fatty infiltration

430
Q
A

Centrilobular fatty infiltration

431
Q
A

Centrilobular fatty infiltration

432
Q
A

Diffuse pathological fatty infiltration

433
Q
A

Diffuse pathological fatty infiltration

434
Q
A

Nutmeg pattern fatty infiltration

435
Q
A

Pathological simple fatty infiltration

436
Q
A

Pathological necrobiotic fatty infiltration

437
Q

LOCAL Lipoidoses

A
  • Cholesteatoma in the choroid plexus
  • On the pleura
  • Atherosclerosis
438
Q

Systemic LIPIDOSES

A

•Hereditary, congenital

•Sphyngomyelin, gangliosid, kerazine

439
Q
A

Lipidoses

440
Q

Demonstration of glycogen

• Stainings

A

– PAS (diastase controll)

– Lugol’s solution (brown)

– Best’s carmine (red)

441
Q
A

Best’s carmine (red) staining of glycogen

442
Q

Regulation of glucose metabolism

A

1) glucose production of the liver (GNG, GGL)
2) glucose uptake of the peripheries (skeletal myocytes, adipocytes)

3) insulin & antagonists (glucagon, STH etc.)

443
Q

Function of insulin

A
  • Promotes fuel storage after a meal
  • Promote growth
444
Q

Metabolic Pathway affected by INSULIN

A
  • Stimulates glucose storage as glycogen (muscle, liver)
  • Stimulates FA synthesis and storage after a high-carbohydrate meal
  • Stimulates amino acids uptake and protein synthesis
445
Q

Function of GLUCAGON

A

• Mobilizes fuels

• Maintains blood glucose levels during fasting

446
Q
  • Activates gluconeogenesis and glycogenolysis (liver) during fasting
  • Activates FA release from adipose tissue
A
447
Q

Increased glycogen production or/and accumulation

A

Overfeeding

Increased activity

Glycogen storage diseases

448
Q

Glycogen storage disease

Species

A

Horses, cattle, sheep, dogs, and cats

449
Q

Name a Glycogen Storage Disease

A

Gierke’s disease

450
Q

Less glycogene

A

• Decreased production – toxical chemicals
– bacterial toxin (??)
– mycotoxins

• Increased mobilization – starvation

451
Q

What is DIABETES MELLITUS

A

Cluster of metabolic disorders associated with hyperglycemia.

Permanent hyperglycaemia results in secondary lesions in different organ systems.

452
Q

Major types of DIABETES

A

Human

Type I – decreased insulin production due to ß-cell damage

Type II – Insulin-resistance of the peripheries (rel. ins. deff.)

453
Q

Which type of Diabetes show KETOACIDOSIS

A

Type I - insulin dependent

454
Q

Which type of DIABETES are most common in Cats?

A

TYPE II

455
Q

Which type of DIABETES are most common in Dogs?

A

TYPE I

456
Q

Consequences of DM

A

Attributed to persistent hyperglycemia and…

• glucose concentration of body fluids and excretes

Polyuria & polydipsia

Emphysematous cystitis (dogs, cats)

Glycogen accumulation in the kidney

457
Q

Mitotic activity of different cells

A
  • Stem cells (multipotent umbilical stem cells)
  • Labile cells (surface epithelial cells)
    • vegetative intermitotic
  • Stabile cells (hepatocytes, renal tubular epithelial cells)
    • reverzible postmitotic
  • Permanent cells (nerve cells, striatedmuscle cells)
    • fix postmitoticus
458
Q
A

Microglial cells

459
Q
A

Oligodendroglia, oligocytes

460
Q

Mononuclear-phagocyta system (MPS)

A
  • Part of the immune system
  • Proliferate
  • Clear
    • removal, absorption
    • phagocytosis (pathogens, destruction of RBCs)
  • Produce antibody
461
Q

What are the different phagocytes

A
  • microphages (granulocytes)
  • macrophages
462
Q

Direct forms of repair

A
  • Hypotypia
    • Original cells, but not the original structure
  • Heteromorphosis
    • Instead of original cells other (not connective tissue) type of cells
  • Hyperregeneration, hypermorphosis
    • Fill the area, but continue proliferation
  • Repair
    • Organisation, Demarcation
463
Q

Indirect forms of repair

A

• Accommodation (adaptation) after irrevocable, permanent dysfunction

  • Atrophy
  • Hypertrophy (increase in size)
  • Hyperplasia (increase in number)
  • Metaplasia (change in the tissue type)
  • Transformation
    • certain changes in internal architecture
464
Q

What is Metaplasia

A
  • Special case of defective healing
    • One type of differentiated tissue is replaced by another type of differentiated tissue
  • Limited possibility of changing
  • Only two types of tissue
    • – epithelial tissue to epithelial tissue
    • – connective tissue to connective tissue
  • NO OTHER POSSIBILITIES!
465
Q

What is indirect metaplasia

A

– multipotent cells replace the degenerated tissue

– differentiate in a different way
(columnar epithelium simple epithelium = basal cell metaplasia)

– prosoplasia (more differentiated)

– anaplasia (less differentiated)

466
Q

Causes of metaplasia

A
  • every kind of cell damage, but…
  • …presence of certain conditions

– vitamin A deficiency in poultry

– irritation of the mucosal membranes

by external factors or chronic inflammation

– F-2 toxins in the uterus

– bone tissue formation in a wound

(ovariectomy, chronic hernia, hematoma)

– ossification of the left atrium

467
Q
A

Metaplasia of laryngeal respiratory epithelium

The chronic irritation has led to an exchanging of one type of epithelium (the normal respiratory epithelium at the right) for more resilient squamous epithelium (left).

468
Q
A

Metaplasia of esophageal squamous mucosa to gastric type columnar mucosa at the left – Barrett’s oesophagus (human)

469
Q
A

Mesenchymal metaplasia (abdominal hernia)

470
Q

What is Pseudometaplasia

A
  • appearences mimicking metaplasia
  • different kinds of tissue in a certain place
  • originating from choristia

– tonsils–> cartilage

– gastric mucosal tissue—> oesophagus islets

– lung –> kidney tissue
– spinal cord —> some portions of intestines
– simple epithelium of vagina —> columnar ep

471
Q

What is Allomorphia, dismorphia

A

• change in shape, but not in type

• reversible

472
Q

What is Atrophy

A

Decrease of the size of an organ or cell by reduction in cell size and/or reduction in cell numbers

473
Q

What is • Hypoplasia

A

• Failure of normal development of an organ: developmental anomaly

474
Q

What is Involution

A

• „Physiological atrophy”

– response to the decreased requirement of the body for the function of a particular cell or organ

475
Q
A

Unilateral kidney hypoplasia, cat

476
Q
A

Muscular hypoplasia, pig

477
Q

What are the forms of ATROPHY

A

• Physiological - pathological

  • Simple – degenerative
  • Reversible – irreversible
  • Regional – complete

• Numeric atrophy

478
Q

Examples of involutions

A

Involution (physiological atrophy)

• Embryo or fetus
– Müllerian/Wolffian duct system

• Neonate
– Ductus arteriosus

• Earlyadult

– Thymus

• Adult female
– Cyclic changes in the endometrium

• Old age
– Endometrium, testicles, bone, cerebrum etc.

479
Q

Pathological atrophy

A
  1. Decreased function – „disuse”
    1. Muscle atrophy in fractured limbs
  2. Loss of innervation
    1. Injury, inflammation, tumors of nerves etc.
  3. Pressure atrophy
    1. Internal= Tumors - Parasites - CSF-accumulation
    2. External = „Bed sores”
  4. Lack of nutrient supply
    1. Cachexia
  5. Blood supply distrubances
    1. Thrombosis
  6. Disturbances of endocrine stimulation
    1. Skin atrophy in Cushing’s disease
  7. Atrophy due to drug application
    1. Topical steroids
480
Q
A

Cysticercus cysts, brain, monkey

481
Q
A

Cysticercus tenuicollis cyst, liver, pig

482
Q
A

Atrophy of the cerebral cortex and cerebellar hypoplasia, calf

483
Q
A

Urolithiasis in the kidney calyces, cattle

484
Q
A

Cachexia, bone marrow, cattle

485
Q

The atrophied tissue is replaced by another (e. q. connective or fatty) tissue is called?

A

• muscular pseudohypertrophy

486
Q
A

Muscular pseudohypertrophy, horse; cattle

487
Q
A

General Pathology (8 decks)

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