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General: Topic 21-30 Flashcards

1
Q

What is thrombocytopaenia?

A

(Having) a low number of platelets

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2
Q

What is the name / word for having a low number of platelets?

A

Thrombocytopaenia

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4
Q

What are the characteristics of platelet disorders?

A
  1. Coagulation time is increased or normal
  2. BT is increased
  3. PT /APTT is normal
  4. Platelet count if normal of low
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5
Q

What are the two types of thrombocytopathies?

A
  1. Congenital (rare)

2. Acquired (common)

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6
Q

What are the congenital types of thrombocytopathies?

A
  1. Membrane disorders (Glycoproteins deficiencies)
  2. Intracellular defects (Serotonin deficiency)
  3. Deficiency of Thromboxan synthesis (activate platelet aggregation)
  4. Von Willebrand’s disease
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7
Q

What are the acquired types of thrombocytopathies?

A
  1. Drug effects —> NSAIDs

2. Metabolic disorders (Uraemia, Diabetes mellitus)

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8
Q

What are the consequences of the acquired types of thrombocytopathies?

A
  1. Abnormal platelet adhesion
  2. Abnormal platelet aggregation
  3. Abnormal platelet contraction
  4. Abnormal platelet secretion
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9
Q

What is the name of the congenital form of thrombocytopaenia?

A

Werlhof disease

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10
Q

What type of disease is Werlhof’s disease?

A

It is an autoimmune disease that targets several platelet surface antigens. The result is thrombocytopaenia

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11
Q

What are the main types of acquired thrombocytopaenias?

A
  1. Impaired production of platelets (bone marrow failure)

2. Increased utilisation of platelets (in blood vessels)

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12
Q

What are some reasons for the decreased production of platelets (thrombocytopaenia)?

A
  1. Mycotoxins
  2. Chemical compounds (phenols)
  3. Leucosis
  4. Radiation
  5. Bracken fern poisoning
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13
Q

What are some reasons for an increased utilisation of platelets (thrombocytopaenia)?

A
  1. Idiopathic thrombocytopaenia purpura
  2. DIC
  3. Virus infection
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14
Q

What happens during Bracken fern poisoning?

A

There is a decreased number of thrombocytes (platelets)

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15
Q

What is the name of the congenital form of vasopathy?

A

Teleangiectasia

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16
Q

What are the acquired forms of vasopathy?

A
  1. Mechanical (e.g. forced coughing)
  2. Vitamin C deficiency (Scurvy)
  3. Allergic purpuras
  4. Symptomatic bleeding (bacterial toxins, effect of several viruses)
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17
Q

What are the characteristics of acquired vasopathies?

A
  1. Bleeding time is increased or normal
  2. Coagulation time is normal
  3. PT is normal
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18
Q

What is a thrombus?

A

A clot of blood formed intravasally

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19
Q

What is another word for blood clot?

A

Thrombus

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20
Q

What is an embolus?

A

A bit of a blood clot that is carried away from the main clot by the bloodstream

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21
Q

What is the name of a blood clot that is not attached?

A

Embolus

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22
Q

What is an embolism?

A

The occlusion of a blood vessel by an embolus

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23
Q

What is an infarct?

A

When there is local ischemic tissue necrosis due to inadequate blood flow

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24
Q

What does ischemia mean?

A

Restriction of blood supply to tissues, causing a shortage of oxygen needed for cellular metabolism. Generally caused by problems with blood vessels, sometimes caused by congestion (e.g. vasoconstriction, thrombosis, or embolism)

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25
Q

What is a macrothrombus?

A

A relatively large thrombus

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26
Q

What is the cause of macrothrombus?

A
  1. Stasis of bloodflow
  2. Strongylus (Horse; larvae settling in the endothel of mesenteric arteries)
  3. Iatrogenic (phlebitis; inflammation of vessels due to infusion of osmotically active substances)
  4. Endocarditis / Endocardosis (mitral valve disease of dogs) (bacteria, viruses)
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27
Q

What is the consequence of a macrothrombus?

A

Severe organ damage(s) and clinical symptoms

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28
Q

What is a microthrombus?

A

A small thrombus located in a capillary or other small blood vessel

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29
Q

What is the cause of microthrombus?

A
  1. Increased thromboplastin release (due to tissue damage)
  2. Bacteria
    a. Gram +: Thrombin-like effect
    b. Gram -: Endotoxins —> Platelet destruction
  3. Endothelial injury; Factor XII (11; Hagemann) increase (virus, hypoxia)
  4. Immunological disorders: Factor XII increase
  5. Chemical agents: Activating the first (contact) phase; e.g. IV applied dextran
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30
Q

What is the consequence of microthrombi?

A
  1. DIC (Disseminated intravascular coagulopathy)
  2. “Slight” tissue damage
  3. Vague clinical symptoms
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31
Q

Name some causes for the development of DIC

A
  1. Tissue breakdown products (necrosis, burns, cancer)
  2. Inflamed blood vessels
  3. Exposed collagen (denuding capillary endothelium)
  4. Bacteria, viruses
  5. Toxicosis
  6. Shock, vascular stasis, etc.
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32
Q

What is DIC?

A

A complex and acquired haemorrhagic disorder of coagulation- and platelet origin that arises due to abnormal activation of coagulation mechanisms by various factors

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33
Q

What does DIC lead to?

A

Diffuse formation of blood clots in the capillaries.

The initiation of fibrinolysis, depletion of platelets and other coagulation factors (Fibrinogen (I), Hagemann (XII)), and the production of fibrin degradation products (FDP) = anticoagulants.

All of the above potentiate BLEEDING

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34
Q

What are the 5 elements of inflammation?

A
  1. Heat (Calor)
  2. Redness (Rubor)
  3. Swelling (Tumor)
  4. Pain (dolor)
  5. Lack of function (Function laesa)
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35
Q

What are some defence mechanisms developed during phylogenesis?

A
  1. Regeneration
  2. Reparation
  3. Inflammation
  4. Haemostasis
  5. Antioxidant system
  6. Specific immune system
  7. General adaption syndrome (stress reaction)
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36
Q

What are the major parts of the inflammatory response?

A
  1. Haemodynamic changes
  2. Permeability changes
  3. Cells involved
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37
Q

What are the haemodynamic changes during inflammation?

A
  1. Transient vasoconstriction (few seconds - neural)
  2. Vasodilation
  3. Increased volume of blood flow
  4. Increased vascular permeability
  5. Speed of flow decreases
  6. Margination of leucocytes along the vessel walls
  7. Exudation
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38
Q

What type of reaction is the transient vasoconstriction during haemodynamic changes (in response to inflammation)?

A

It is a neural reaction

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39
Q

How does vasodilation occur during inflammation (haemodynamic changes)?

A

Starts after a few minutes, and lasts a few hours or longer

Release of histamine from mast cells
Generation of Nitric oxide (NO) and prostaglandins (PGD, PGE)

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40
Q

How does increased vascular permeability occur during inflammation (haemodynamic changes)?

A
  1. Histamine, Leukotriens (C4, D4, E4), bradykinin, and platelet activating factor (PAF) cause contraction of endothelial cells, resulting in gaps in the small vessels
  2. Complement factors (C5a and C3a) indirectly participate by inducing the release of histamine from mast cells
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41
Q

What is a direct vascular leakage?

A

An effect of any kind of structural injury to the microvasculature, affecting all types of vessels

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42
Q

What is an indirect vascular leakage?

A

Biochemical substances appearing in and around the site, and primarily affect the venules

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43
Q

What is the passive process of permeability?

A

The passage of fluid between endothelial cells

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44
Q

What is the active process of permeability?

A

Endothelial cells create enocytotic vesicles, and discharge the contents on the other side by active transport within the cell itself

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45
Q

Name some biochemical mediators that can affect permeability

A
  1. Plasma kinins (e.g. bradykinin)
  2. Complement factors (C5a, C3a)
  3. Leukotrienes (LTC4, LTD4, LTE4, LTB4)
  4. Prostaglandins (PGE2, PGI2)
  5. Cytokines (IL1, TNFalpha)
  6. Platelet activating factor (PAF)
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46
Q

What does PAF stand for?

A

Platelet activating factor

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47
Q

Which biochemical mediators cause contraction of the endothelial cells (and thereby increases permeability)?

A
  1. Histamine
  2. Leukotrienes (C4, D4, E4)
  3. Bradykinin
  4. Serotonin (rat mast cells)
  5. C5a, C3a
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48
Q

Which cells produce histamine?

A

Mast cells

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49
Q

What is a biochemical mediator?

A

Any messenger / cell that act on blood vessels

Can be inflammatory cells, or other cells that contribute to an inflammatory response

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50
Q

What are the compounds of the immediate / early phase of exudation (acute inflammation)?

A
  1. Histamine

2. Serotonin

51
Q

What are the compounds of the delayed / late phase of exudation (acute inflammation)?

A
  1. Hagemann factor-dependent pathways
    a. Coagulation factors
    b. Fibrinolytic factors
    c. Kinins
    d. Complement factors
  2. Lipid mediators
52
Q

What is the precursor of histamine?

53
Q

Which enzyme trust histidine into histamine, and in which cells does this occur?

A

Histidine carboxylase

Mast cells and basophil granulocytes

54
Q

When is histamine released?

A

In response to:

  1. Immunological processes
  2. Physical injury / mechanical damage
  3. Irradiation
  4. Heat
  5. Chemical agents (e.g. toxins, snake or bee venom, etc)
55
Q

Which receptors does histamine affect?

A
  1. Pericyte H2 receptors: Relaxation

2. Endothel H1 receptors: Contraction

56
Q

What is the consequence of histamine binding to receptors?

A
  1. Vasodilation and increased capillary permeability
  2. Development of pain
  3. Immediate (anaphylactic, type 1) hypersensitivity reaction
57
Q

What can inhibit histamine?

A
  1. Antihistamines
  2. Adrenalin (epinephrine)
  3. PGE2
58
Q

What is the precursor of serotonin?

A

Tryptophan

59
Q

Where is serotonin released from?

A
  1. From platelets

2. From neurons

60
Q

When is serotonin released from platelets?

A

During the platelet-release reaction, which is triggered by stimuli such as;

Trypsin, collage, antigen-antibody complexes, Globin-coated surfaces, snake venoms, epinephrine, PAF and ADP

61
Q

Which parts of the brain are associated with serotonin?

A

Higher centres involved in memory, appetite, sleep, and learning

62
Q

What is the effect of serotonin?

A
  1. Vasoconstriction in the smooth muscles (inc. permeability)
  2. Bronchial muscle contraction (Associated with asthma)
  3. Increase in intestinal peristalsis (can lead to diarrhoea)
63
Q

What inhibits serotonin?

A
  1. LSD

2. Tissue enzymes

64
Q

What is chemotaxis?

A

The phenomenon of directional migration in response to a gradient of chemoattractants

65
Q

Name some endogenous chemoattractants

A 
From plasma:
1. Complemet system
2. Fibrinogen
From cells:
3. Arachidonic acid derivatives 
a. Leukotrienes (LT)
b. Interleukins (IL-1, IL-9)
c. PAF
66
Q

Name some exogenous chemoattractants

A
  1. Bacterial chemotaxins
  2. Viruses
  3. Parasites
  4. Dead cells (nectrotaxins)
  5. Superoxide anion radical
  6. Endotoxins
67
Q

What are the effects of chemotaxis?

A
  1. Increased WBC migration, which causes temporary neutropenia
  2. Increased cell adhesion
  3. Increase in lysosomes
  4. Increased O2 consumption and O2 radical formation
68
Q

What can inhibit chemotaxis?

A
  1. Neutrophil immobilising factor (NIF)
  2. Leukocyte immobilising factor (LIF)
  3. Lysosomal pro teases (elastase, proteases)
69
Q

Describe the process of phagocytosis

A
  1. Chemotaxis by agent
  2. Neutrophil and monocyte migration increases
  3. Connection develops between the phagocyte and the opsonised pathogen —> Phagocytosis (phagosoma develops)
  4. Digestion of pathogen (phagolysosoma develops)
  5. Oxygen dependent / independent killing
70
Q

In phagocytosis, what is oxygen-dependent killing?

A

Killing via an “oxidative-burst”, using reactive metabolites, halides, etc. (-Obr, -OCl, etc.)

71
Q

In phagocytosis, what is oxygen-independent killing?

A

Killing via lysosomal enzymes

72
Q

How can phagocytosis be decreased?

A

It can be decreased due to an increase in the adrenocortical function (Cushing’s syndrome, GCC therapy)

73
Q

What activates factor XII / Hagemann?

A
  1. Collagen contact (exposed collagen)
  2. Activated platelets
  3. Various negatively charged surfaces (including glass)
74
Q

What does the activation of Hagemann Factor-dependent pathways cause (inflammation)?

A
  1. Blood clotting
  2. The fibrinolytic system
  3. Generation of kinins
  4. Activation of the compliment cascade
75
Q

What is the effect of the Hagemann Factor-dependent pathways?

A
  1. (Further increase of) Vasodilation
  2. (Further increase of) Permeability
  3. Chemotaxis
  4. Pain

(Effects are similar to histamine)

76
Q

Name the inhibitors of Hagemann Factor-dependent pathways

A
  1. Protease inhibitors
  2. Alpha-2 macroglobulin
  3. Antitrypsin, antithrombin III
  4. Kinases (Mainly from the endothelial cells, esp. in the lungs)
77
Q

What does COX mean?

A

Cyclo-oxygenase

78
Q

What does COX 1 do?

A

It is responsible for regulating blood flow by inducing moderate vasodilation, and for stimulating the cells of the gastric mucosa to secrete mucous

Needed for everyday “housekeeping” activities in the body

79
Q

What does COX 2 do?

A

It allows the generation of more prostaglandins and thromboxane than what would normally be produced by a particular tissue, and thereby contributes to the inflammatory process

80
Q

What are the effects of lipid mediators?

A
  1. Vasodilation
  2. Increased vascular permeability
  3. Chemotactic effects on neutrophils (LTB4)
  4. Pain (PGE2, PGI2)
  5. Smooth muscle contraction (LTC4, LTD4, LTE4)
  6. Histamine-like effect
81
Q

What is the cause of chronic inflammation?

A

The prolonged or repeated action of a mild irritant (e.g. silica), so that interleukins induce the synthesis of GCC

82
Q

What is the result of chronic inflammation?

A
  1. Secondary immune mechanism(s) (autoimmune) develop

2. Deficient acute phase response

83
Q

What are the characteristics of chronic inflammation?

A
  1. Continuous cell migration (mainly mononuclear cells)
  2. Fibroblast appearance —> Collagen production increase
  3. Recapillarization leading to regeneration and reparation
84
Q

Name some reasons for a decreased food intake

A
  1. Starvation (no access)
  2. Secondary ketosis
  3. Baby pig disease
  4. Iron deficiency
  5. Anaemia
85
Q

Name some reasons for an increased utilisation / demand of food

A
  1. Primary ketosis
  2. Milk fever
  3. Lipid metabolisation syndrome —> Production decreases
86
Q

When does absolute starvation occur?

A
  1. During the course of serious diseases

2. Due to local causes

87
Q

When does relative starvation occur?

A
  1. Decreased intake of food
  2. Bad quality food
  3. Malabsorption / maldigestion
  4. Increased loss (GI, kidney)
  5. Increased demand
88
Q

What are the general effects of starvation?

A
  1. Decreased production
  2. Decreased reproductive function
  3. Decreased defence mechanisms
  4. Altered blood composition
  5. Cahexia
  6. Oedema
89
Q

Which organ functions are most affected by starvation?

A
  1. Liver: affects the carbohydrate / lipid / protein metabolism
  2. Endocrine organs
  3. Muscles
  4. Blood
  5. Skeletal system
  6. Adipose tissue
90
Q

What happens in the Rumen during starvation?

A
  1. Motility decreases
  2. VFA production decreases
  3. Ph and ammonia concentration increases
91
Q

What happens in the Liver of ruminants during starvation?

A
  1. More urea is produced (Limit = availability of ATP)
  2. Blood urea is increased
  3. Urea appears in milk and urine
  4. GNG and ketogenesis both increase
92
Q

What happens in the Blood of ruminants during starvation?

A
  1. Immediate hypoglycaemia
  2. Far increase
  3. Secondary ketosis
  4. Compensated metabolic acidosis
93
Q

What are some reasons for an increased food intake?

A
  1. Overfeeding
  2. Ammonia toxicosis
  3. Lactate or salt poisoning
94
Q

What are some reasons for a decreased food utilisation?

A
  1. Diabetes mellitus

2. Storage diseases

95
Q

What are some endogenous reasons for obesity?

A
  1. Diabetes mellitus

2. Hypothyroidism

96
Q

What is an exogenous reasons for obesity?

A

Fat cow syndrome

97
Q

What are the general effects of obesity?

A
  1. The activity of the defence mechanisms decreases
  2. Morbidity (the ratio of the number of sick animals in a population) increases
  3. Lifespan decreases
98
Q

What are some disorders of the organ function during obesity?

A

Dysfunction of:

  1. Blood circulation (heart)
  2. Thermoregulation
  3. Water balance
  4. Reproductive functions
  5. Locomotor functions
99
Q

Name the three primary amino acid disorders

A
  1. Decreased intake / increased loss
  2. Antagonism (similar chemically structured molecules)
  3. Overload and toxicity
100
Q

What are the results of a Tryptophan deficiency?

A
  1. Synthesis of niacin and niacin decreases
  2. Vitamin B utilisation decreases
  3. Diseases like Pellagra and blacktongue (dog) can manifest
  4. General deficiency symptoms like Appetite loss and poor growth
101
Q

What are some important physiological processes that require lysine?

A
  1. Pigment production

2. Collagen production

102
Q

What happens in the case of a methionine overdose?

A

Methionine has the highest toxicity out of all the amino acids

  1. Impairment of growth
  2. Dilates tubules
  3. Pancreas / liver damage
  4. Haemoglobin breakdown
103
Q

What happens in the case of a phenylalanine overdose?

A
  1. Impaired growth

2. Impaired albumin production

104
Q

What happens in the case of a tyrosine overdose?

A

Necrosis of hepatocytes

105
Q

What happens in the case of a tryptophan overdose?

A
  1. Decreased kidney growth

2. Convulsions (caused by a high level of serotonin in the brain)

106
Q

What are the most common reasons for secondary amino acid disorders?

A
  1. Alteration of protein metabolism
  2. Inadequate supplementation (farm animals)
  3. Liver malfunction, portosystemic shunt (pets)
107
Q

What are the 3 main causes for protein deficiency?

A
  1. Decreased intake (ow low quality food)
  2. Decreased synthesis (liver)
  3. Decreased utilisation or absorption (malabsorption, maldigestion)
  4. Increased loss (kidney failure, parasites, chronic bleeding, Protein Losing Enteropathy (PLE))
108
Q

What are the main consequences of protein deficiency?

A
  1. Reduced performance / production
  2. Impairment of defence mechanisms
  3. Alteration of blood constituents
  4. Decrease in organ function
109
Q

What are the consequences for performance and production in the case of protein deficiency?

A
  1. Retarded growth
  2. Weakness of muscles
  3. Drop in egg / milk production
  4. Loss of body weight
  5. Retarded embryonic development
110
Q

What are the consequences for the defence mechanisms in the case of protein deficiency?

A

Decrease in:

  1. Antibody and WBC production
  2. Phagocytise activity
  3. Collagen formation
  4. Wound healing
111
Q

What are the consequences for blood constituents in the case of protein deficiency?

A
  1. Decreased blood cell production
  2. Decreased plasma protein synthesis (Hypoalbuminaemia, hypoproteinaemia)
  3. Consequent decreased total Ca2+ level
  4. Relative increase in the ionised Ca20 level
112
Q

What are the consequences for liver function in the case of protein deficiency?

A
  1. Decreased synthesis of albumin and coagulation factors

2. Decreased detoxification and deamination of the blood

113
Q

What are the consequences for GI tract function in the case of protein deficiency?

A
  1. Decrease in digestive enzymes

2. Disturbed digestion (anorexia, dyspepsia)

114
Q

What are the consequences for endocrine function in the case of protein deficiency?

A
  1. Adrenocortical hyperfunction

2. Decrease in gonadotropin hormones and TSH

115
Q

What are the consequences for the cornified tissue in the case of protein deficiency?

A

Disorders of pigmentation, feather formation, and wool production

116
Q

What are the consequences for bones in the case of protein deficiency?

A

Osteoporosis

117
Q

What are the causes of protein overload / excess?

A
  1. Increased intake of protein of NPN
  2. Neoplasm (tissue necrosis)
  3. Inflammation (including immune mediated disorders)
118
Q

What are the consequences of protein excess?

A
  1. Athletic conditions

2. Alterations in plasma proteins

119
Q

What happens in the case of phenylalanine overload?

A
  1. Decreased growth and food intake (in poultry)

2. Impaired albumin formation

120
Q

What happens in the case of tyrosine overload?

A

Necrosis of hepatocytes

121
Q

What happens in the case of tryptophan overload?

A
  1. Cessation of growth (in poultry)

2. Kidney changes

Pathophysiology (5 decks)

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