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
2
Q
Forensic pathology
A
the purpose of an autopsy is to determine the nature of death from a legal perspective
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
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
5
Q
Comparative pathology
A
compares specific human pathologies with those seen in natural animal models
(tuberculosis, anthrax, erysipelas etc.)
6
Q
Disease - What do we examine in PATHOLOGY
A
2., Morphological changes
(→ Pathology)
→ Morphological examinations
7
Q
Most important Method to recognize/investigate the disease:
A
1., Autopsy
In the vast majority of the cases complementary investigations are necessary!
8
Q
What is Post-mortem and ante-mortem investigations
A
(excision, fine needle aspirate, biopsy samples from living animals)
9
Q
What is Pathogenesis
A
(how does the disease proceed)
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
11
Q
What is Special pathology/systemic pathology:
A
12
Q
Characteristic changes caused by well defined diseases, grouped according to organ systems
A
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
14
Q
A
Rupture large intestines - Horse
15
Q
Staining
A
Ziehl-Neelsen Staining
16
Q
Staining
A
Perls Staining
17
Q
A
Immunohistochemistry (IF, IPO), in situ hybridisation
18
Q
Special staining
A
MAC-387
19
Q
Type of lesion
A
Trichoblastoma, basalioma
20
Q
A
Foot and mouth disease in Cattle, Pig and Human
21
Q
Sanatio
A
Recovery/Healing
22
Q
• Recreatio
A
Mild degree of functional changes, reversible morphological alterations → revivification (recreatio)
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)
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)
25
• Reparatio
26
• Demarcatio
27
• Organizatio
28
**Demarcation (abscesses in the lung, horse)**
29
What is this an example of
**Callus formation**
## Footnote
Permanent morphological or structural changes (**restitutio cum defectu)** → **locus minoris resistentiae**
30
What is clinical death
Clinical death
## Footnote
(**no breathing, no heartbeat, but tissues and organs survive for a while** → resuscitation, grafts, transplantation, culturing) → **pathological agony („intermediate life”)** → **pathological or absolute death**
31
When is the recognition of death
Recognition of death:
no **heartbeat**, no responses to **sensory** or **sensitive** stimuli, no **reflexes** **(pupils → „brain death”)**
→ when **post mortem changes star**t: **obvious**
32
What are the postmortem changes?
* 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**
33
Name of lesion?
Due to?
Found where?
Desiccation - **exsiccatio postmortalis**
**Evaporation**
**Skin**
**Mucous membranes**
**Cornea**
**+ also in alive animals**
34
Characteristics of this postmortem change
**- complete dehydration of the tissues**
**- dry heat and/or air current**
- desert, chimney
- Function of the **putrefactive bacteria** is also hampered
35
Characteristics of this postmortem change
**Soaking, maceratio**
* **Skin, organs filled with fluid**
* **Foetuses**
* Aseptic autolysis
* **Carcasses staying in the water**
* **Also in living animals**
* flows on the skin!
36
**Rigor mortis**
**In which type of muscles?**
Nystens Rule
All 3 types of muslcles
Nystens rule - Direction of rigor mortis
37
* Skeletal muscles → rigor mortis timeline
* **2-4 hours** the **beginning** (head is stiff)
* **5-8 hours** becomes **general (body)**
* **24-48 hours** **starts to disappear**
* **48-60 passes off**
38
Rigor mortis in Heart Muscle
Systole or diastole?
Development?
Duration?
* Standstill in **diastole** – looks like systole
* Develops **fast (30 minutes)**
* **Lasts for 1 day**
39
Rigor Mortis Smooth muscles
Onset?
Duration?
* **Quick process (10-15 minutes)**
* **Lasts for 1 – 4 hours**
* Rigid intestines, arteries, spleen
40
**Onset and duration of RM**
**Rapid and short**
* **High** environmental and/or inner **temperature**
* **Prolonged** **muscular activity**
* **Young** and **elder animals**
* **Septicaemia**, wasting diseases
41
Onset and duration of RM
## Footnote
**Delayed**
* **Asphyxial death** (notably by carbon monoxide poisoning) = SUFFOCATION
* Severe **hemorrhage**, **cold surroundings**
* **Fails to develop In case of degenerative muscle changes**
42
What is this
Characteristics
* 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
43
Blood clot in the heart
44
* 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**
45
Sulfhemoglobin imbibition
46
Bile imbibition - From Gall bladder
47
Hemoglobin imbibition
48
**Self softening - Autolysis**
Autolytic ferments of the cell in the cytoplasm
* Autodigestio (self digestion)
* **Gastromalatia** due to gastric juice
* **Oesophagomalatia**
49
What is happening
**Postmortem destruction - putrefaction**
## Footnote
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**
50
Pase of Putrefaction
Rapid VS Slow
* 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**)
51
**Putrefaction**
52
**EMPHYSEMA POSTMORTALIS HEPATIS**
Due to **putrefaction**
53
Postmortal Tympany (gass accumulation)
54
**Sulph-hemoglobin imbibition**
## Footnote
Reaction of **Hb** (hemoglobin) plus **H2S** (hydrogen-sulphid) **greyish-green, paling off on air**
55
**Sulph-hemoglobin**
## Footnote
Reaction of Hb (hemoglobin) plus H2S (hydrogen-sulphid) greyish-green, paling off on air
56
Sulph-hemoglobin
Reaction of Hb (hemoglobin) plus H2S (hydrogen-sulphid) greyish-green, paling off on air
57
Sulph-hemoglobin
Reaction of Hb (hemoglobin) plus H2S (hydrogen-sulphid) greyish-green, paling off on air
58
**Pseudomelanosis**
* H2S + Fe (from Hb)
* Iron-sulphide
59
* **PM Wax - Adipocere**
* Saponification
* In wet, clayey soil
* Fatty acids and Ca++
* Form soaps, impregnate soft organs
* Sweetish odour
60
What are the causes of cellular damage?
* 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
61
Luxation
62
**bite** (vulnus. morsum)
63
gun-shot **(vulnus. sclopetarium)**
64
Bleeding in the brain tissue
65
Rupture
66
Tituration
67
Sequelae of traumatic effects
• Local effects
– Lesions
– Tissue damage
– Port of entry!
68
Sequelae of traumatic effects
• General effects
**– General effect of a local infection**
• tetanus, gas-phlegmone
**– Loss of blood**
• Bleeding out
**– Functional disturbances**
• fractures, luxations
**– Embolism**
• fat, bone marrow
**– Traumatic shock**
69
Bleeding, Haemothorax
70
Loss of function
## Footnote
**disruption of the Achilles tendon**
71
Lesions in the tissues
Microscopical or Macroscopical
Macroscopic
## Footnote
**– Ruptures (ruptura)**
**– Fractures (fractura)**
**– Luxation (luxatio)
– Fissure**
**– Concussion (commotio)**
72
Lesions in the tissue leading to **Locus minoris resistenciae**
**– Ruptures (ruptura)**
**– Fractures (fractura)**
**– Luxation (luxatio)**
Locus minoris resistenciae
- sick animals
- bad condition
- dietetical problems
73
Lesions in the tissue
Where can you find Concussions
– Concussion (commotio)
– brain, spinal cord, bone marrow
– bony capsule!!!
– not always seen with naked eyes
74
Fractures
What do we have?
**Special form of fraction**
* **open** (fr. aperta) or **covered** (fr. optecta)
* special appaerance
– **Infraction** - **bone fracture marked by a small line that shows up in X-ray examination**
75
What can be seen
Dislocation of the broken ends
76
Which reaction can be seen?
What does it mean?
**Vital reaction**
**Happened in real life**
Edges of the wound
– Hemorrhages at the surrounding tissues – After soaking it disappears!
77
High temp as a cause of disease - Categories
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**
78
Appearance of the Burns
**C. erythematosa (1st degree)**
**Hyperaemic** area, **vasodilatation**, **edema**
79
Appearance of the Burns
**C. bullosa (2nd degree)**
* **Vesication,**
* **Denaturation of proteins,**
* **Pain**
80
Appearance of the burns
**C. escharotica (3rd degree)**
* **Coagulation necrosis of the tissues**
* **Hemostasis**
* **Thrombosis**
* **Pale**
* **Insensible**
81
Appearance of the Burn
**Carbonization (4th degree)**
* **Tissues are charred**
82
Inhalational Burns
**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
83
**Carbonization (4th degree)**
84
General effects of burns
| (exept hyperthermia)
* **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**
85
General effects of burn
HYPERTHERMIA
**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**
86
HYPERTHERMIA
HEAT STROKE
* **Heat stroke (\> 43°C)**
* Lesions
* **Heat spasms**
* electrolyte loss (sweating)
* **Heat distress**
* most often seen, collapse
* failure of cardiovascular compensatory mechanisms after hypovolemia
87
**Sunstroke - Insolation**
* **Infrared (ultraviolet?) radiation** of sunshine
* **Longlasting** or **strong impact of sunshine**
88
Low temperature as a cause of disease
LOCAL EFFECTS
* **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)
89
LESION
**C. erythematosa (1st)**
– bluish-red, swollen
90
LESION
**C. bullosa (2nd)**
– vesication, edema
91
LESION
**C. escharotica** (3rd)
– necrosis
92
LESION
**C. gangrenosa (4th)**
gangrene
93
Low temperature as a cause of disease
GENERAL effects
(Not hypothermia)
• General effects
– Gangrenous lesions, necrosis
**• Toxaemia**
94
Hypothermia at which temp?
Failure of the heat regulation – **around 35oC**
## Footnote
27-30 oC: **vital functions come to standstill**
20-25 oC: **death**
95
**Hypothermia**
1. Endangered species
2. Predisposing factors
3. Factor of great metabolic Activity
1. **pig, rabbit, dog**
2. **diarrhoea, bleeding**
3. **Brown adipose tissue**
96
What are the Defence mechanisms Against falling body temperature
* **Contraction** of muscles
* **Shivering**
* **Vasoconstriction** in the **skin**
* Increased **metabolism**
* Labile glycogen reserves are used up
* Shallow and quick **respiration**
97
Name a HYPOTHERMIC wellknown disease
**Baby pig disease**
## Footnote
• 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
98
What is autointoxication?
**= Autotoxemia**
## Footnote
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)
99
**Types of autointoxication**
NEED TO KNOW
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
100
**1. Stuck of intermediary metabolism**
**DIABETIC AUTOINTOXICATION**
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**
101
1. Stuck of intermediary metabolism
DIABETIC AUTOINTOXICATION
What is KETOSIS and KETOACIDOSIS
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.
102
1. Stuck of intermediary metabolism
DIABETIC AUTOINTOXICATION
Symptoms of Diabetic ketoacidosis
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**.
103
Lesion
**Diabetic autointoxication**
**(pancreas fibrosis, dog)**
104
Lesion
Diabetic autointoxication (pancreas fibrosis, dog)
105
Lesion
**Diabetic autointoxication**
**(Lipidosis in the liver, dog)**
106
Lesion
**Diabetic autointoxication**
| (Lipidosis in the LIVER, dog)
107
Lesion
**Diabetic autointoxication**
**(Brain edema, dog)**
108
LESION
**Diabetic autointoxication**
**(Brain Edema, dog)**
109
What is **Retention autointoxication**(2)
3 types
Develops in **excretory organs**, accompanied by a **delay** in the **removal of metabolic products** from the **body**.
## Footnote
➢**Kidney failure = uremia**
➢**Uricosis (gout)**
➢**Icterus (hepatopathy)**
110
Retention autointoxication(2)
**Uremic autointoxication**
Solutes/Uremic toxins
Classification of uremic toxins
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**
111
Retention autointoxication(2)
**Uremic autointoxication**
**What are the consequences of UREMIA?**
* Seizure, coma, cardiac arrest, and death.
* Spontaneous bleeding (**vascular damage)**
* Electrolyte
* Kidney failure
* **➢MULTIORGAN FAILURE**
112
Lesion
**Uremia (kidney-fibrosis, dog)**
113
Lesion
**Uremia (kidney-fibrosis, dog)**
114
Lesion
Uremia (kidney-fibrosis, dog)
115
Lesion
**Uremia (necrotic glottisis, cat)**
116
Lesion
**Uremia (uremic gastritis, dog)**
117
Lesion
**Uremia**
| (uremic encephalopathy, dog)
118
Lesion
Uricosis (Bird)
119
Lesion
Uricosis
Granuloma (TOPHUS)
120
**3. Hepatic autointoxication**
**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**
121
3. Hepatic autointoxication
## Footnote
**PHASE I - Detoxification pathway**
Consists of
* **Oxidation,**
* **Reduction**
* **Hydrolysis**
Catalysed by **enzymes** referred to as the (=PROTECTION)
* **Cytochrome P450** enzyme group or
* **Mixed Function Oxidase enzymes (MFO).**
122
3. Hepatic autointoxication
What is **Impaired hepatic detoxification**?
Refers to decreased **phase I** and/or **phase II enzyme activity**
**= The levels of hepatic detoxification enzymes decreased.**
123
3. Hepatic autointoxication
## Footnote
**Phase II - detoxification pathway**
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.**
124
3. Hepatic autointoxication
What is the toxic effect of BILIRUBIN
➢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).
125
3. Hepatic autointoxication
What is the toxic effect of BILIRUBIN in the BRAIN
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).**
126
3. Hepatic autointoxication
What is the toxic effect of BILIRUBIN in the BRAIN
What does BIND refer to?
**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.
127
Lesion
3. Hepatic autointoxication
Toxic effect of Bilitubin to the brain
128
Lesion
Which toxic component?
Billirubin
129
3. Hepatic autointoxication
➢**Impaired hepatic detoxification** can result from which **intrahepatic causes:**
* exposure to
* Food additives,
* Solvents,
* **Toxins**,
* **Viral infections,**
* **Gilbert's syndrome,**
* **Hyperthyroidism,**
* **Restricted bile flow (Cholestasis)**
130
3. Hepatic autointoxication **COMPLICATIONS**
➢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
131
Lesion
**Liver cirrhosis (dog)**
132
Lesion
ICHTERUS
Ichterus coagulopathy
133
4. Histolysis/heterolysis by gangrene = putrid autointoxication
What is gangrene?
Gangrene (or **gangrenous necrosis)** is a **type of necrosis** **(ichorous inflammation**).
134
4. Histolysis/heterolysis by gangrene = putrid autointoxication
Types of gangrene
The types of gangrene **differ in symptoms**, and include:
1. **dry gangrene,**
2. **wet gangrene,**
3. **gas gangrene,**
4. **internal gangrene.**
135
Lesion
Gangrene
136
4. Histolysis/heterolysis by gangrene = putrid autointoxication
## Footnote
**Dry Gangrene**
**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.**
137
Lesion
Dry gangrene
138
4. Histolysis/heterolysis by gangrene = putrid autointoxication
Wet Gangrene
**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.
139
Lesion
Wet Gangrene
140
Which bacterias can cause wet gangrene?
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.**
141
What happen due to wet gangrene?
➢ 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.
142
Lesion
**Pneumonia ichorosa (bo)**
143
Lesion
**Pneumonia ichorosa (bo)**
Wet gangrene
144
5) Abnormal direction of metabolism
Name a special type that accumulate with high metabolism = **abnormal metabolism**
The **porphyrias** are a group of **rare diseases**, in which chemical substances called **porphyrins** accumulate with high metabolism. (picture: swine) **abnormal metabolism**
145
Lesion
**Porphyrias** - porphyrins accumulate with high metabolism. (picture: swine) abnormal metabolism
146
**6. Enterogenic autointoxication, enterotoxaemia**
**How?**
**Why?**
**By what?**
– **Absorbed decomposition products from gastro- intestinal system**
**Grass fever**: methylindol, grass- sickness: **Cl. botulinum**,
**Enterotoxaemia**: **Cl. perfringens**
147
Lesion
**Enterogenic autointoxication, enterotoxaemia**
148
Lesion
**Enterogenic autointoxication, enterotoxaemia**
149
**6. Intestinal autointoxication/toxic colon**
Nothing highlighted
➢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.
150
Lesion
**Intestinal autointoxication/Toxic colon**
151
Lesion
**Intestinal autointoxication/Toxic colon**
152
7) Resorption autointoxication
**7. Absorbed metabolites from special cases:**
= Ruptured, perforated, **arrodated stomach**, intestine or urinary bladder.
153
Lesion
Ruptured, perforated, **arrodated stomach**, intestine or urinary bladder.
154
Lesion
Ruptured, perforated, **arrodated stomach**, intestine or urinary bladder.
155
Lesion
Ruptured, perforated, **arrodated stomach,** intestine or urinary bladder.
156
Lesion
Ruptured, perforated, **arrodated stomach,** intestine or urinary bladder.
157
Lesion
Ruptured, perforated, **arrodated stomach**, intestine or urinary bladder.
158
Morphological complications of the autointoxication
Degeneration and enlarged of parenchymal organs (liver, kidney, heart, CNS)
## Footnote
Hydropic or vacuolar degeneration: histopathologically large cytoplasm: swelling, enlarged mitochondria.
159
Lesion
Toxic hepatopathy/vacuolar hepatopathy/non-specific hepatitis
160
LEsion
**➢Toxic myodegeneration/myocardosis**
161
LEsion
**➢Toxic nephropathy/acut tubular degeneration-necrosis**
162
Lesion
**➢Toxic encephalopathy**
163
Lesion
**➢DIC (Disseminated intravascular coagulopathy/microthrombosis)**
164
12. Internal conditions of development of diseases
(**predispositio**) + resistance (**resistentia**)➔**development of a disease.**
**Predisposition and resistance** constitution) and acquired characteristics (**condition**).
165
12. Internal conditions of development of diseases
What is Genetic predisposition
➢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.**
166
12. Internal conditions of development of diseases
What is Constitution
= **Somatotype**
Categorize the human physique according to the **relative contribution** of **3 fundamental elements, somatotypes**
167
12. Internal conditions of development of diseases
What are the different somatypes?
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]
168
12. Internal conditions of development of diseases
What is diathesis?
**„Defective” constitution**➔**predisposition for certain diseases** (**diathesis**)
169
12. Internal conditions of development of diseases
Diseases can be?
Congenital or Hereditiary
170
12. Internal conditions of development of diseases
What is HEREDITIARY diseases?
* 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**
171
12. Internal conditions of development of diseases
What are CONGENITAL diseases?
Effects that harm the fetus
In avian species: **ovogen infection** (Salmonella gallinarum, goose parvovirus, etc.)
172
Important role in diatheses:
* **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
173
The congenital and acquired resistence is:?
**IMMUNITY**
174
13. Infectious agents as causes of disease
What is infection?
**Infection**:
spreads from **animal** to **animal**, through **direct** or **indirect route** (fomites, vectors, iatrogen etc.)
175
13. Infectious agents as causes of disease
What is Invasiveness:
**Invasiveness:**
The pathogen is able to **spread inside the organism** (not all pathogens have this feature: e.g. Cl. tetani)
176
13. Infectious agents as causes of disease
## Footnote
**Infectious pathogens:**
**Parasites, fungi, bacteria, viruses, prions**
177
13. Infectious agents as causes of disease
## Footnote
**Parasites**
* **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
178
13. Infectious agents as causes of disease
**Fungi**
**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)
179
Lesion
**Fungi**
180
Lesion
**Fungal granuloma formation in the lung**
181
Lesion
**Fungal thalus formation in the air sac**
182
12. Infectious agents as causes of disease
## Footnote
**Bacteria**
* 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**
183
12. Infectious agents as causes of disease
## Footnote
**Viruses**
* 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**)
184
12. Infectious agents as causes of disease
**Prions**
* Modulator-proteins, modify the metabolic processes of the cell
* Damage: neuron degeneration, encephalosis
185
Lesion
Cause of lesion
Bovine spongiform encephalopathy (**BSE**), „**mad cow syndrom**
## Footnote
**PRIONS**
186
Immune response
Types
* **Innate**
* – Nonspecific for antigenes
* – Immediate reaction
* – No memory
**Adaptive**
– **Specific for antigenes**
– Slower reactions at first (days to weeks)
– Memory – fast reaction! (see vaccination)
187
Immune response
Innate immune response
**Anatomic barriers**
## Footnote
* **(skin, mucous membranes)** and
* **Physiologic properties** (stomach pH, body temperature) + **Phagocytosis**, **complement system**
188
Adaptive immunity
## Footnote
**Responses**
Adaptive immunity • 2responses:
## Footnote
– **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)**
189
Phagocytic cells include
* macrophages,
* dendritic cells,
* granulocytes (eosinophil, basophil,neutrophil),
* Mast cells
190
Types of cells
Macrophages
191
Types of cells
Dendritic cells
immature to the left, and mature to the right
192
Type of cells
NEUTROPHIL Granulocyte
193
Type of cell
EOSINOPHIL Granulocyte
194
Type of cell
BASOPHIL Granulocyte
195
Type of cell
MAST cell
196
Type of cell
NK-cells (phagocyting a tumor cell)
197
What is Mononuclear phagocytic system (MPS)
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
What is CYTOKINES
* 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
What is this
Mature Lymphocyte
200
What is this
Reactive lymphocytes
201
What are the 3 major groups of the immune system disorders?
1. **– Hypersensitivity reactions**
2. **– Autoimmune diseases**
3. **– Immunodeficiencies**
202
What is hypersensitvity? (immune system)
**1) Hypersensitivity**
**• Altered intensity** of immune response, leading to pathologic lesions
* **4 GROUPS**
203
What is **Type I hypersensitivity**
– Type I (**immediate**)
* **allergies,**
* **anaphylaxy**
204
What is **type II Hypersensitivity?**
**Type II**
* (**CYTOTOXIC**)
* **haemolytic anaemias**
205
What is **type III Hypersensitivity?**
**– Type III**
* **IMMUNE COMPLEX**
* **Arthus reaction,**
* Systemic lupus erythematosus (**SLE**),
* **Rheumatoid arthritis**
206
What is **type IV Hypersensitivity**
**– Type IV**
* **(DELAYED)**
* **tuberculin test,**
* **contact dermatitis**
207
Lesion
TYPE I Hypersensitivity
IMMEDIATE
ATOPIC DERMATITIS
208
LEsion
TYPE IV HYPERSENSITIVITY
## Footnote
**DELAYED**
**CONTACT DERMATITIS**
209
Lesion
TYPE III Hypersensitivity
IMMUNE COMPLEX
SLE = **Discoid lupus erythematosus (s= systemic)**
210
2) Autoimmune diseases
* 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
2) Autoimmune diseases
Example of a
1. • Autoreactive antibodies disease
2. • Lymphoplasmocytic inflammation and fibrosis
3. • Chronic inflammation
4. • Organ specific autoimmune diseases
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
Lesion
PEMPINGUS
Autoimmune disease
213
Lesion
**Uveodermatologic syndrome**
**Autoimmune disease**
214
LEsion
**Autoimmune disease**
Rheumatoid arthritis
215
**3) Immunodeficiency syndromes**
* 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
Lesion
**Normal and SCID Thymus (dog)**
217
Lesion
**Gingivostomatitis, cat**
FIV?
218
Lesion
Lymphoid depletion in Peyer’s patch, enteritis, cat small intestine
219
Electricity as cause of disease
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
Lesion
Common Kestrel (Falco tinnunculus)
221
Lesion
Lightning
222
Lesion
Lightning
223
**Radiant energy**
• Electromagnetic rays
## Footnote
– Ultra-short waves (microwaves - warming)
– Infrared waves (warm surface radiations)
– Visible rays (physiological effect)
– Ultraviolet rays (biological - path. effect!)
224
What is Radiant energy
**• 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
Irradiation sickness
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
Lesions
Radiations
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
What are the External causes of diseases
1. Physical effects
2. Chemical effects
1. • **toxicosis**
3. Biological effects
1. **Infectious agents**
2. **Virus, bacteria, fungi, prions, protozoa**
4. **Inad**equate supply Oxygen, water, nutrient
228
What are the Disturbances in oxygen supply
* 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
**Pathology of the suffocation**
* **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
Lesions due to
**Pathology of suffocation**
• Petechial hemorrhages
serosal membranes, larynx, trachea, heart
Acute dilation of the heart
Acute emphysema
Differentiate from septicaemia!
231
Lesions due to
**Pathology of suffocation**
## Footnote
Dark, unclotted blood
• Petechial hemorrhages
serosal membranes,
Acute lung hyperemia and edema
Acute emphysema
Differentiate from septicaemia!
232
Disturbances in water supply
* **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
Lesion
Dehydration
## Footnote
Lack of water intake
Increased fluid loss
- Diarrhea
234
Lesion
Dehydration
235
**Disturbances in nutrient supply**
**Total starvation**
Total starvation **(Inanitio completa)**
– No food intake (energy, protein)
– **40-50 % of the body: death (Cachexia)**
236
Disturbances in nutrient supply
## Footnote
**Partial starvation,**
**Malnutrition** **(Inanitio incompleta)**
## Footnote
**– Food supply is not adequate
– Deficiency diseases**
237
Disturbances in nutrient supply
## Footnote
**Obesity,**
**Overfeeding (Obesitas)**
## Footnote
– Surplus of feed or feed components
– Continuous or occasional (dilation and rupture of the stomach)
– Other causes (lack of movement, hormonal disorder)
238
Incomplete starvation, malnutrition
• Causes
**– 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
What is the Consequence of autointoxication (Nutrient)
– increased fat and protein catabolism → **ketonaemia**
240
Lesion
**Cachexia**
241
Lesion
Obesitas
242
Lesion
Cachexia
243
LEsion
Cachexia
244
Lesion
Cachexia
245
Lesion
**Oedema cachecticum**
246
Lesion
Cachexia
247
Infectious agent
Spreading?
Agents?
1. **Spreading among animals**
2. **Within the animal:** infectious agents, tumors as wel
1. Prion (TSE, BSE)
2. Viruses (DNS, RNS, enveloped, non enveloped)
3. Bacteria (Gr+, Gr-)
4. Chlamydia, Mycoplasma
5. Fungi
6. Protozoa
7. Helminths
8. Ectoparasites
248
**Skin infections**
**– Transcutan infection**
## Footnote
* **Intakt skin:** **dermatophytosis**, **Malassezia**
* Through **lesions**: papilloma, rabies (!), tetanus
* Arbo = **arthropode** born: **babesiosis**, **Lyme-disease,** infec. anaemia, **WNV, African swine fever**
249
Spread of pathological procecces in GI tract
Gastrointestinal tract
* Gastric **acidity, pH 1-2
* Viscous****mucus**
* Digestive **enzymes**, detergents in the bile
* Defensins
* Normal intestinal flora
* Secreted IgA antibodies **(MALT)**
250
Lesion
RESPIRATORY
**Type II pneumocyte**s (surfactant, regeneration,
phagocytosis, immunregulation)
251
What is an AEROSOL
Aerogen (airborne) infection
252
Oronasal, conjunctival infection affects
bird flu, fowl cholera
253
urogenital infection:
– venereal infection, semen, or erosions on the mucus membranes (**Brucellosis**, AIDS, dourine)
– urinary or genital infections: FLUTD, cystitis; **pyometra**
254
Infections via the umbilical cord,
**omphalogen**:
E. coli,
Salmonella
255
Vertical infections
**transplacental** or **intrauterine** infection (BVD, PRRSV)
**ovogen infection**: Salmonella
256
Incetions caused by the veterinarian
**Iatrogenic infection: PCV2, EBL**
257
What are the Factors affecting spread of pathogens and the disease:
**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
Spread of pathological processes in the organism
1. Pathogen in the organism
2. At the site of entry **(portal of entry)**
3. **Primary process**
4. **Metastasis**
259
What is **METASTASIS**
= SPREADING of PAHOGEN
## Footnote
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
Types of metastasis
1. **Local**
2. **Regional**
3. **Distant**
261
Local metastasis
to the surrounding areas
## Footnote
**direct spread**
262
Regional Metastasis
to regional **lymph nodes**
via the **lymphatic circulation**
263
Distant Metastasis
= To Distant organs
1. **lymphogen** = retrograde lymphogen metastasis
2. **haematogen =** phagocytotic embolic
3. **Intracanalicular =** ascending descending
264
Spread of pathological processes in the organism
Mostly spread through the
Veins
## Footnote
V. portae V. hepatica
V. pulmonalis V. umbilicalis
265
What is the outcome of Spreading of pathological processes in the organism?
**GENERALIZATION**
266
DIFFERENT FORMS of spreading of pathological process in the organism
**• Bacteriaemia**
## Footnote
– 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
What could lead to **Septicaemia**
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
What does SIRS stand for
Systemic inflammatory response syndrome
269
Result of SIRS
* High **TNFα** and **LPS** (Gr- bact) levels: **DIC**
* **Liver damage: decreasing glyconeogenesis**
* **High NO levels:** **vasodilatation** – **decrease blood pressure**
* **SEPTIC SHOCK**
270
Pathology of SEPTICEMIA
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
Lesion
Septicemia
Enlarged Spleen
272
Lesion
Septicemia
Generalized lymphadenomegaly
273
Lesion
Septicaemia
**Cloudy swelling** in the **parenchymatous** organs (liver, kidneys, **heart** and skeletal muscle)
274
Mechanisms of cell injury
**GENERAL CONSIDERATIONS**
* 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
Mechanisms of cell injury
**ATP synthesis**
Oxidative phosphorylation, anaerobic glycolysis (liver cell vs. neuron)
1. 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
What is REPERFUSION INJURY
• In certain cases cells may undergo **more severe damage after** the blood flow is **restored after ischemia**
277
What is the different nuclear changes?
Nuclear changes
1. Nuclear membrane hyperchromatosis
2. Karyopycnosis
3. Karyorhexis
4. Karyolysis
278
Lesion
Karyorhexis
279
Lesion
Damage of the cell surface organelles
280
Regressive changes in the organs
ATROPHY
281
Factors of the circulatory system
Circulatory system
## Footnote
**• 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
Normal circulation depends on
* 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
Regulation of blood circulation depends on
1. • **Hydrodynamic factors**
2. **• Neurohormonal regulation**
3. **• Vasomotion control**
1. maintaining harmonized calibre change in the vessels
4. **• Terminal circulatory bed**
284
What is importaint about the Terminal circulatory bed
* Section between the arterioles and venules
* Major place of circulatory disturbances
285
What is the Role of the **endothelium**
• Function:
## Footnote
* 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
What are the circulatory disturbances?
**=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
What is Prehemostasis
**• Plasma leakage**
• **Extravasation**
– RBCs
– WBCs
**• In case of inflammation**
**• Strong stimuli**
– mechanical, thermal, chemical or toxic
288
Pathology of circulatory disturbances
**• 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
Lesion
Circulatory disturbances
HYPERAEMIA?
290
What is this a picture of
Hyperaemia due to decreased blood flow
291
what is this a picture of
Local Congestion
292
Circularoty disturbance
Local Congestion, what does it mean
Local congestion
## Footnote
**• 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
Lesion
Circulatory disturbance
## Footnote
**Local congestion**
294
Pathology of congestion
• 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
LEsion
Congestion
296
Lesion
Congestion due to torsion of one uterine horn
297
Lesion
Congestion
298
What is Infarceratio
= 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
Lesion
Slow occlusion
300
What is slow occlusion
Slow occlusion
## Footnote
* Collaterals enlarge
* Remodel
* Drainage is maintained
• Liver cirrhosis
301
Lesion
Systemic Venous Congestion
302
What is Systemic venous congestion
• **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
Pathology of Systemic Venous Congestion
**• 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
Lesion
Systemic venous congestion
305
Lesion
Chronic case of systemic venous congestion of the liver
NUTMEG
306
Lesion
**Congestive induration - Liver**
307
What is Congestive INDURATION
Congestive induration
**• Chronic congestion**
**• Parenchyma is destroyed**
* **Replaced** by **collagen fibrous connective tissue**
* Pathology:
**– Firm, moist content is less on the cut surface**
308
What is ISCHAEMIA
Ischaemia
• **Local inadequate blood supply**
– **General**: anemia, hypovolemia
**• Physiological**
**– Digestion,** uneven distribution of blood
• **Pathological**
1. **– Compression**
2. **– Obturation**
3. **– Vasoneurotic disturbance**
• **Consequences**
309
What are the different types of ISCHAEMIA
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
Name the cases
A= Thrombosis
B= Compression
C= Embolism
D= Vasculitis
311
Name the cases
E= Spasm
F= Steal
G= Atheroma
H= Hyperviscosity
312
What are the Consequences of the ischaemia
• Depends on
– **degree** and **type of narrowing**, **time**, **type** of tissue, **collaterals** (lung, liver)
• Collapsus / **shock**
• **Necrosis** - Infarct:
**– Infarctus haemorrhagicus**
**– Infarctus ischaemicus**
313
What is an infarct
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
What is an Ischemic infarct
* • 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
* Infarct pathology
* 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
Older/chronic infact with demarcation
317
Ischemic infarcts, kidney, swine, cross section
318
Infarct
319
Infarct
320
Colonic mucosal necrosis, horse
321
Ischemic infarct, heart
322
What is Hemorrhagic infarct
• Double circulation
– In the necrotic area the vessels are filled with RBCs
• Red (darker), dry
– Location
• Lungs, kidney, spleen, liver
323
Haemorrhagic infarct, testicle, dog
324
Haemorrhagic infarcts, spleen, dog
325
Haemorrhagic infarcts, kidney
326
Haemorrhagic infarcts,
327
Consequences of an infarct
**• 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
Consequenses of an infarct
329
Infarct =
arterial occlusion
330
Infarceration =
venal occlusion
331
What is Haemostasis
**arrest of bleeding**
• finely regulated physiologic response
332
Steps of Haemostasis
* Steps of hemostasis
* 1. **Primary**
* Transient **vasoconstriction**, **platelet aggregation** to form a platelet plug
* 2. **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
What are the Disturbances of microcirculation
* **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
Stasis
335
Definision of SHOCK
**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
* Types of Shock
* **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
What is the cause of septic shock
Caused by
## Footnote
**Gr- lipopolisacharid (LPS)**;
**(Gr+, fungi as well without LPS)** and
**Cytokins, vasoactive mediators**
338
What are the phases of Shock
**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
Pathology of Shock
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
Shock
Haemorrhages
341
Liver edema
Cause of shock
342
Ischaemia in the kidney
Shock
343
Shock gut piglett
344
What is an Hemorrhage
– extravasation in a live animal
345
What is • Thrombosis
(Embolism)
## Footnote
– inappropriate formation of intravascular thrombus
346
• Hemorrhage + thrombosis =
**(DIC)**
347
**Expressions**
## Footnote
Epistaxis?
nosebleed
348
Expressions
## Footnote
Hematemesis
– bloody vomit
349
**Expressions**
## Footnote
Hemoptoe
expectoration
350
Expressions
## Footnote
Haemarthros
blood in the joints
351
Expressions
## Footnote
Hematuria
blood in the urine
352
Expressions
## Footnote
Metrorrhagia
hemorrhage in the uterus
353
Expressions
## Footnote
Enterorrhagia
intestinal hemorrhage
354
Expressions
## Footnote
Hematochezia
- bloody feces (associated with lower GI tract bleeding)
355
Expressions
## Footnote
Melaena
bloody feces because of enterorhagia
356
Expressions
## Footnote
Hemopericardium, -thorax, -peritoneum
Heart, thorax, abdomen
357
Expressions
## Footnote
(haemaspiratio
- inhalation of blood)
358
Haemorrhages in the pelvis of the kidney, swine
359
Hemorrhage in the Bowman’s capsule
360
Heamorrhage in the spleen
361
Forms of hemorrhage
• By origin
**– hemorrhage by rhexis**
– rhexis = breaking forth
* Vessel wall continuity defect
* Physically disrupted vessel
362
Pars esophagica ulceration, stomach, pig. **Rhectic hemorrhage.**
363
Ascending pyelonephritis, **rhectic hemorrhage, dog**
364
Forms of haemorrhages
## Footnote
By origin
– hemorrhage by **diapedesis**
**• 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
Forms of Haemorrhage
**By appearance**
From small to large
**– Petechial (vibex)** \< **Ecchymotic**Suffusion \< **Hematoma** \< **Apoplexy**
366
**Petechiae, gut, horse**
367
**Ecchymosis, dog**
368
Purpura
369
Petechiae and ecchymoses, epicardium
370
Petechiae, meninges, swine
371
**Elongated hemorrhages (vibex), muscle**
372
**Intramuscular haemorrhages, poultry**
373
Suffusions, mesentery
374
Haematoma, liver
375
Sublingual haematoma, dog
376
Perirenal haematoma, swine
377
**Perirenal haematoma, cat**
378
**Apoplexy, cat**
379
Petechial bleeding, Thymus cattle BNP
380
Old haematoma liver
381
After bleeding
382
What are the Signs of hemorrhages
* Hemorrhagic infiltration of lymph nodes
* Brownish red color from haemoglobin
* Degradation of haemoglobin
383
Haemorrhagic infiltration
of lymph nodes, large intestine, swine
384
Pseudomelanosis, salmonellosis, swine
385
Factors predisposing to thrombosis (Virchow’s triad)
1. **Alterations in the vascular endothelium**
2. **Alterations in blood flow**
3. **Alterations in blood constituents = HYPERCOAGULOBILITY**
386
Thrombosis of the arteria iliaca externa, horse
387
Umbilical vein foal
388
Red thrombus characteristics
**• 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
What is the Mechanism of Stasis
– Plasma leakage
– Higher viscosity
– Higher resistance in the lumen
– Slowing down of the blood flow
390
Stasis
391
Recanalisation of a thrombus, submucosa, horse
392
Thrombosis in species
• Horse
– a. mesenterialis cran., abdominal aorta
393
Thrombosis in species
• Cattle
– in the wall of the uterus (septic metritis)
394
Thrombosis in species • Human!
• Cat
– abdominal aorta
395
Thrombosis in species
• Other species (swine, cattle, dog)
endocarditis
396
Vegetative valvular endocarditis
heart
**white thrombus**
(Endocarditis thrombo-ulcerosa)
397
What is EMBOLISM
**Embolus**
## Footnote
– 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
Types of EMBOLI
**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
**Air embolism, dog**
400
**Cause of embolism**
* Trauma
* Sudden movements
* Forced abdominal pressure
* Coughing
* Inflammation, malignant tumor
* Iatrogen cause
401
**Outcome of embolism**
## Footnote
**Local: infarct**
– **Venous** – pulmonary circulation
– **Arterious** – smaller artery downstream
**Metastasis of pathogens,** spreading of pathogenic processes
**Sudden death (lung, brain)**
402
**Anaemic infarcts, kidney, swine**
403
What are Regressive changes
**Edema**, disturbances in **water balance** of cells and the organism, disturbances in **fat metabolism**
404
Location of water intracellular is called?
* Intercellular (in tissue spaces) = **edema**
* Transcellular (in the **lumen** of the organs)
* intestines, body cavities
405
What regulates the water balance?
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
**What causes Increased Retention of water**
INCREASED
## Footnote
**• Hydrostatic pressure** – venous congestion
**• Colloid osmotic pressure** of the interstitium
**• Vascular permeability**
407
What causes Decreased Retention of water
DECREASED
## Footnote
**• Colloid osmotic pressure** of the plasma
* *• Tissue tension** - starvation
* *• Capacity of the lymph vessels**
- Electrolite imbalance – kidney failure
408
Nomenclature of the water balance disturbances
**• Hyperhydria**
• **Anasarca**
Fluid accumulation in the **subcutaneous tissue**
409
Nomenclature of the water balance disturbances
**• Hyperhydria**
**• Hydrops**
**•transudate – exudate**
•hydrops haemorrhagicus acutus
* hydrops adiposus
* hydrops chylosus
410
Nomenclature of the disturbances
• Hyperhydria
**•Ascites**
Fluid accumulation in the abdomen
Offen cause of **cirrhose**
411
Nomenclature of the disturbances
* Hyperhydria
* **Hydrothorax**
**•Hydropericardium**
Water accumulation in the thorax, heart pericardium
412
Nomenclature of the disturbances
• Hyperhydria
**• Edema**
– **intercellular** water accumulation
413
HYDROTHORAX
414
**Hydrops chylosus**
415
**Disse space**
416
Fluid in the transcellular space
417
**Classification of the edema**
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
**Cell swelling**
**Functional disturbances of the sodium pump result in water influx**
419
Vacuolar degeneration
420
Hydropic degeneration
421
Reticulated degeneration
422
Balloning degeneration
423
Balloning degeneration
424
**Vesicular degeneration**
425
Water disturbances Causes in cell
* Hypoxia
* autointoxication
* burns, frostbites
* extended tissue necrosis
* acidosis, alkalosis
* infectious diseases
* exogenous toxins
* Hypoproteinemia
426
Where do we find Simple fats DEPOT
## Footnote
•
* Subcutaneous fat,
* kidney,
* under serous membranes,
* bonemarrow
427
Pathology of Disturbances in water balance of cells
* Organs are swollen, enlarged, and pale
* Dried cut surface
* Epithelial layers such as skin and mucosal membranes can be dry or jelly like
428
Staining methods of FATS
**• Physical**
• Sudan III, scarlet red
* Sudan black, osmic acid
* Oil-red-O
**• Chemical**
• Nile blue
* PAS
* Schultz method (cholesterol)
429
**Physiological fatty infiltration**
430
Centrilobular fatty infiltration
431
Centrilobular fatty infiltration
432
Diffuse pathological fatty infiltration
433
Diffuse pathological fatty infiltration
434
Nutmeg pattern fatty infiltration
435
Pathological simple fatty infiltration
436
Pathological necrobiotic fatty infiltration
437
LOCAL Lipoidoses
* **Cholesteatoma in the choroid plexus**
* **On the pleura**
* **Atherosclerosis**
438
Systemic LIPIDOSES
**•Hereditary, congenital**
## Footnote
**•Sphyngomyelin, gangliosid, kerazine**
439
Lipidoses
440
Demonstration of glycogen
• Stainings
– PAS (diastase controll)
– Lugol’s solution (brown)
**– Best’s carmine (red)**
441
**Best’s carmine (red) staining of glycogen**
442
Regulation of glucose metabolism
1) glucose production of the liver (GNG, GGL)
2) glucose uptake of the peripheries (skeletal myocytes, adipocytes)
**3) insulin & antagonists (glucagon, STH etc.)**
443
Function of insulin
* Promotes **fuel storage after a meal**
* Promote **growth**
444
Metabolic Pathway affected by INSULIN
* 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
Function of **GLUCAGON**
**• Mobilizes fuels**
• **Maintains blood glucose levels during fasting**
446
* Activates **gluconeogenesis** and **glycogenolysis** (liver) **during fasting**
* **Activates FA release** from **adipose tissue**
447
**Increased glycogen production or/and accumulation**
**Overfeeding**
**Increased activity**
**Glycogen storage diseases**
448
**Glycogen storage disease**
**Species**
**Horses, cattle, sheep, dogs, and cats**
449
Name a Glycogen Storage Disease
**Gierke’s disease**
450
**Less glycogene**
**• Decreased production – toxical chemicals**
– bacterial toxin (??)
– mycotoxins
## Footnote
**• Increased mobilization – starvation**
451
What is DIABETES MELLITUS
Cluster of metabolic disorders associated with **hyperglycemia**.
Permanent hyperglycaemia results in **secondary lesions** in different organ systems.
452
Major types of DIABETES
Human
## Footnote
**Type I** – **decreased insulin production** due to **ß-cell damage**
**Type II** – **Insulin-resistance** of the **peripheries** (rel. ins. deff.)
453
Which type of Diabetes show KETOACIDOSIS
Type I - insulin dependent
454
Which type of DIABETES are most common in Cats?
TYPE II
455
Which type of DIABETES are most common in Dogs?
TYPE I
456
**Consequences of DM**
Attributed to persistent hyperglycemia and...
• glucose concentration of body fluids and excretes
Polyuria & polydipsia
Emphysematous cystitis (dogs, cats)
Glycogen accumulation in the kidney
457
**Mitotic activity of different cells**
* **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
Microglial cells
459
Oligodendroglia, oligocytes
460
**Mononuclear-phagocyta system (MPS)**
* **Part of the immune system**
* **Proliferate**
* **Clear**
* removal, absorption
* phagocytosis (pathogens, destruction of RBCs)
* **Produce antibody**
461
What are the different **phagocytes**
* microphages (granulocytes)
* macrophages
462
Direct forms of repair
* **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
**Indirect forms of repair**
**• 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 i**nternal architecture**
464
**What is Metaplasia**
* **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
What is **indirect** metaplasia
– 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
**Causes of metaplasia**
* **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
**Metaplasia of laryngeal respiratory epithelium**
## Footnote
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
**Metaplasia of esophageal squamous mucosa to gastric type columnar mucosa at the left – Barrett’s oesophagus (human)**
469
Mesenchymal metaplasia (abdominal hernia)
470
What is Pseudometaplasia
* 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
What is **Allomorphia, dismorphia**
• change in **shape**, but **not in type**
## Footnote
**• reversible**
472
What is Atrophy
Decrease of the size of an organ or cell by reduction in cell size and/or reduction in cell numbers
473
What is • Hypoplasia
• Failure of normal development of an organ: **developmental anomaly**
474
What is Involution
• „Physiological atrophy”
– response to the **decreased requirement** of the body for the function of a particular cell or organ
475
Unilateral kidney hypoplasia, cat
476
Muscular hypoplasia, pig
477
What are the forms of ATROPHY
• Physiological - pathological
* Simple – degenerative
* Reversible – irreversible
* Regional – complete
• Numeric atrophy
478
Examples of involutions
Involution (physiological atrophy)
## Footnote
**• 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
Pathological atrophy
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
Cysticercus cysts, brain, monkey
481
Cysticercus tenuicollis cyst, liver, pig
482
Atrophy of the cerebral cortex and cerebellar hypoplasia, calf
483
Urolithiasis in the kidney calyces, cattle
484
Cachexia, bone marrow, cattle
485
The atrophied tissue is replaced by another (e. q. connective or fatty) tissue is called?
• muscular pseudohypertrophy
486
Muscular pseudohypertrophy, horse; cattle
487
