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Second Year > General Pathology > Flashcards

General Pathology Flashcards

1
Q

Nosology

A

Classification of diseases

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2
Q

Pathophysiology

A

Physiological processes/mechanisms causing disease development and progress

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3
Q

Anomaly

A

Condition existing before (or at) birth regardless the cause

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4
Q

Disorder

A

Abnormality in function

Can be of unknown cause/aetiology

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5
Q

Aetiology

A

Study of the causes of disease and it’s effects

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6
Q

Endogenous cause

A

Cause coming from inside the patient

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7
Q

Exogenous cause

A

Cause coming from outside the patient ex virus

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8
Q

Predisposing cause

A

Mechanism making patient more susceptible to the cause

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9
Q

Primary cause

A

Main factor causing the disease

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10
Q

Secondary cause

A

Any factor assisting primary cause

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11
Q

Semiotics

A

Study and meaning of signs

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12
Q

Clinical picture

A

Set of specific signs typical for specific disease/disorder

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13
Q

Syndrome

A

Set of clinical signs associated with each other, and a specific disease
Collectively indicating or charcheterizing a disease, disorder or abnormal condition

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14
Q

Pathognomonic sign

A

Sign who’s presence means that the disease is present beyond doubt

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15
Q

Diagnostic sign

A

Signs leading to the recognition and identification of a disease

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16
Q

Prognostic sign

A

Sign relating to outcome of the disease

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17
Q

Main/major signs

A

Typical for specific disease or disorder

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18
Q

Common signs

A

Unspecific, common in many clinical pictures

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19
Q

Acute disease

A 
Rapid onset (days)
Resolved quickly (healing, chronification, death)
Peracute or subacute
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20
Q

Chronic disease

A 
Slow onset (days to weeks)
Little or no change
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21
Q

Subclinical phase

A

Stage before symptoms/signs are noted

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22
Q

Prodromal phase

A

Stage where early, unspecific signs are noted

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23
Q

Clinical phase

A

Stage where normal, typical signs are present

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24
Q

Decline phase

A

Disease progressing either to death or healing

Can become chronic

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25
Q

Stages of decline phase

A

Convalescence- period of recovery
Relapse- reappearance after vanished completely
Recurrence- activation before complete healing

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26
Q

Clinical judgement

A

Diagnosis
Prognosis
Treatment

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27
Q

Presumptive diagnosis

A

Based on presumption or probability with reasonable ground

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28
Q

Provisional diagnosis

A

Prognosis done before all tests are done

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29
Q

Definitive diagnosis

A

Diagnosis done after all available tests are done

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30
Q

Clinical diagnosis

A

Made on basis of medical signs rather than diagnostic tests

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31
Q

Differential diagnosis

A

The distinguishing between two or more diseases with similar signs

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32
Q

Diagnosis of exclusion

A

Diagnosis set after elimination of all other reasonable possibilities

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33
Q

Etiological diagnosis

A

Including a causative organism

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34
Q

Etiological treatment

A

Treating the cause, not the symptoms or consequences

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35
Q

Symptomatic treatment

A

Suppress undesirable signs

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36
Q

Palliative treatment

A

Relieve signs, improving quality of life

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37
Q

Preventive treatment

A

Preventing disease to occur

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38
Q

Specific treatment

A

Treatment particularly adapted to specific disease

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39
Q

Erythrocyte

A

Transportation of oxygen and CO2, maintain pH, blood viscosity
Biconcave, anucleated
Half-life ~100 days

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40
Q

Erythropoiesis

A

Production/formation of RBCs
Loss of nucleus
20% in baseline production

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41
Q

Anaemia

A

“Lack of blood”
Decrease in oxygen carrying capacity and delivery to tissues
Reduction of total RBCs, PCV or Hb concentration

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42
Q

Causes of anaemia

A

Loss of blood
Destruction of RBCs
Lack of production of RBCs

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43
Q

Regenerative anaemia

A

Due to loss or destruction

Response from BM

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44
Q

Non-regenerative anaemia

A

Lack of production

No response from Bm

45
Q

Aetiology of regenerative anaemia

A

Haemorrhagic

Haemolytic

46
Q

Aetiology of non-regenerative anaemia

A

Primary BM anaemia

Secondary BM anaemia (nutritional or hypoproliferative)

47
Q

RBC indices of regenerative anaemia

A

Macrocyclic, hypochromic
Big RBC, low Hb concentration
High MCV, low MCHC/MHC

48
Q

RBC indices of non-regenerative anaemia

A

Normocytic, normochromic
Normal erythrocyte
Low or normal MCV, high or normal MCHC

49
Q

Polychromasia

A

Sign of regeneration

Immature RBC without nucleus, tends to be larger than mature

50
Q

Acanthocytes

A

Picked cell membrane/abnormal thorny projections
Can be due to
Excess of cholesterol in cell membrane
Severe hepatic disease

51
Q

Target cell

A 
“Bulls eye”
Due to
Iron deficiency anaemia
Liver disease 
Post-splenectomy
52
Q

Abnormal agglutination of RBCs

A 
Agglutination or rouleaux formation
Due to
Inflammation
Tumors
Infection
53
Q

Nucleated RBCs

A

Sign of regeneration

Metarubricytes or late rubricytes

54
Q

Howell-Jowell bodies

A

Sign of regeneration

Basophilic nuclear remnants

55
Q

Basophilic stippling

A

Sign of regeneration

56
Q

Presence of reticulocytes in peripheral blood

A

Sign of regeneration
Increase of (or presence of in ruminants) Immature, anucleated erythrocytes
Horses have no reticulocytes in peripheral blood

57
Q

Clinical signs of anaemia

A 
Weakness/fatigue
Excercise intolerance
Pale mucous membrane 
May have:
Jaundice, tachycardia, cardiac murmur, cardiomegaly, lymphnode enlargement, hepatomegaly, splenomegaly
58
Q

Haemorrhagic anaemia

A

Acute- trauma, digestive bleeding, infections, clotting defects
Chronic- can lead to iron deficiency=non- regenerative

59
Q

Blood haematology in haemorrhagic anaemia

A

Primary- loss of whole blood, PCV May be unchanged

Secondary- after 24hrs blood replaced by IF, drop in PCV, serum protein drop

60
Q

Blood smear in haemorrhagic anaemia

A

Reticulocytes increase after 3 days, max after 7, normal in 14
Immature RBCs/anycytosis remain longer

61
Q

Extravascular haemolytic anaemia

A

RBCs loss due to mononuclear phagocytic system/MPS

Clinical signs as other anaemias, plus bilirubinaemia, haemoglobinuria

62
Q

Intravascular haemolytic anaemia

A

Rupture of RBC inside blood vessels

Signs as other anaemias, plus bilirubinaemia, haemoglobinuria

63
Q

Haemolysis

A

Reduced RBC lifespan due to destruction of RBC

64
Q

Blood haematology & biochemistry in haemolytic anaemia

A

Low PCV
high billirubin
Normal or high protein

65
Q

Blood smear in haemolytic anaemia

A

Increased number reticulocytes, more regenerative than haemorrhagic
Immature RBCs/anycytosis, remain longer
Cause of haemolysis may be identified

66
Q

Signs of haemolytic anaemia

A

Intravascular- dark urine (haemoglobinuria), haemoglobinaemia, billirubinaemia
Extravascular- billirubinaemia
If both- also splenomegaly, hepatomegaly

67
Q

Causes of extravascular haemolytic anaemia

A 
Infectious
Immune-mediated
Fragmentation injury
Toxins
Inherited RBC defects
68
Q

Causes of intravascular haemolytic anaemia

A

Cause related to RBC itself
Infectious
Immune-mediated
Inherited RBC defects

69
Q

Infectious agent I haemolytic anaemia

A

Direct action of toxins
Invasion and destruction of RBC by organism
Immune- mediated mechanism

70
Q

Immune-mediated haemolytic anaemia

A

IMHA
Primary- idiopathic
Secondary- RBC being infected by pathogen or coated by foreign antigen, neoplasia, drugs/vaccination, incompability transfusion reactions, oxidative stress

71
Q

IMHA pathophysiology

A

Anti-RBC antibodies attach to RBC membrane

  • Complement cascade
  • removal of affected RBCs by MPS (extravascular)
72
Q

Fragmentation injury/microangiopathic haemolytic anaemia

A 
Damage to RBC caused by endothelial alteration in small vessels
Damaged/fragmented RBCs= scistocytes
By:
- disseminated intravascular coagulation
- inflammatory process
- hemangiosarcoma
- valve diseases
73
Q

Oxidative stress haemolytic anaemia

A 
Oxidative stress causing irreversible RBC damage 
- methaemoglobin
- Heinz-bodies 
- eccentrocytes 
Visible in blood smear
74
Q

Heinz-bodies

A

Hb precipitates over RBC inner surface
Fragile, undergo haemolysis in liver
Up to 10% is normal in cats

75
Q

Eccentrocytes

A

Displaced Hb in one part of the cell, the rest with little

Due to damaged membrane

76
Q

Methaemoglobin

A

Hb containing Fe3 instead of Fe2
Cannot bind oxygen
Darker color than normal Hb

77
Q

Causes of nutritional anaemias

A

Vitamin B12 and folic acid deficiency
Iron deficiency
Copper deficiency

78
Q

Anaemia due to B12 and folic acid deficiency

A

Cause- diet deficiencies, malabsorption syndrome, increased requirement, chemotherapy
Pathophysiology- inhibition in synthesis of DNA, inefficient erythropoiesis
Gives- macrocyclic and normochromic anaemia
Diagnosis- by blood smear, big RBCs, RBC precursors present, hypersegmented neutrophils

79
Q

Iron deficiency anaemia

A

Causes- chronic bleeding, low iron intake, malabsorption, high iron consumption
Blood smear- normo- or microcytic and normo- or hypochromic

80
Q

Copper deficiency anaemia

A

Copper needed for iron absorption and release of iron stores in body
Signs- neorological and haematological, low growth rate, GI signs

81
Q

Hypoproliferative anaemia

A 
Due to:
-Inflammation, metabolic disease
- chronic renal or hepatic failure
-Neoplasia
-Endocrine disease
Anaemias usually mild
Normocytic and normochronic
82
Q

Inflammation/chronic disease causing anaemia

A

due to:
-Inflammatory cytokines reducing iron availability
-Inhibition of EPO production or release
-Decreased biological activity of EPO
-Decreased RBC lifespan
Blood smear= normocytic, normochromic, mild anaemia (Hct>20%)

83
Q

Neoplasia causing anaemia

A 
Reasons may be:
-Chronic disease
- blood loss
- immune-mediated haemolysis
- chronic antineoplastic treatment
Blood smear= inflammatory anaemia, normocytic, normochromic
84
Q

Renal disease in anaemia

A

Causes:

  • EPO deficiency
  • effects of uremic toxins: GI ulcers, suppression of BM, shortened RBC lifespan by mild haemolysis (urea)
  • chronic inflammatory disease
85
Q

Liver disease in anaemia

A

Anaemia of chronic disease
Interfere with EPO synthesis
Altered iron metabolism

86
Q

Endocrine diseases in anaemia

A

Diabetes mellitus- diabetic ketoacidosis

Hypothyroidism- general decrease in metabolism, low EPO, low proliferation of RBC precursors in BM

87
Q

Aplastic anaemia

A

Destruction of BM hematopoietic cells

  • pancytopenia
  • pure red cell aplasia
88
Q

Mieloptisis

A

Primary BM anaemia
BM infiltration
- myeloproliferative or lymphoproliferative diseases (WBC precursors neoplasia)

89
Q

Pancytopenia

A 
BM produces NO blood cells (WBC+RBC)
- replacement of normal BM cells by fat
Caused by:
- infection
- drugs
- immune- mediated
90
Q

Red cell aplasia

A 
Involving only RBC precursors
- normocytic, normochromic
- reticulocytopenia
- absence of red cell precursors
Causes:
- immune mediated
- infectious
91
Q

Polycuthaemia/erythrocytosis

A

Absolute increase in RBC mass
Increased hematocrit
Increased haemoglobinuria concentration
Relative or absolute

92
Q

Relative polycythaemia

A

Decreased plasma volume in relation to RBC
Haemogram= high PCV, high TP
Types:
-Haemoconcentration (loss of fluids)
-Splenic contraction (stress in horses & greyhounds)

93
Q

Absolute polycythaemia/polycythaemia Vera

A

Myeloproliferative disorder w abnormal increase of RBC production
Serum EPO activity typically decreased

94
Q

Secondary polycythaemia

A

High EPO
Physiological- compensation of tissue hypoxia
Pathological- due to renal tumor, extrarenal, excessive EPO administration

95
Q

Consequences of erythrocytosis

A

Hyperviscosity syndrome (spontaneous bleeding from mucous membranes, visual disturbances/retinopathy, neurological signs
Heart failure
Hypoxia

96
Q

Granulocytes

A

Specific cytoplasmic granules, segmented nuclei

  • neutrophils
  • eosinophils
  • basophils
97
Q

Agranulocytes/mononuclear cells

A

No granules, non-segmented nuclei

  • lymphocytes
  • monocytes
98
Q

Neutrophils

A

Granulocytes, pink granules
Main target:
- bacteria
- fungi

99
Q

Eosinophils

A

Granulocytes, red granules
Main target:
-Larger parasites
- inflammatory responses

100
Q

Basophils

A

Granulocytes, purple granules

Unknown main function

101
Q

Mononuclear cells

A

Lymphocytes- round, large nuclei

Monocytes- pleomorphic nuclei, can be lobulated with “fat” lobules

102
Q

Lymphocytes

A 
B-cells= antibody production, activation of T-cells
T-cells= CD4+, CD8+, regulatory T-cells, NK-cells
103
Q

Monocytes

A

Becomes macrophages in tissue

104
Q

Leukogram

A
  • total WBC count
  • differential cell count
  • WBC morphological features
105
Q

Pathophysiology of neutrophils

A

Most abundant WBC
First line of defence
Increased segmentation when mature, 3-5 segments normal
Regulated by G-CSF (inflammation)

106
Q

1st Neutrophilic medullary compartments

A

Proliferation pool- dividing cells (48-60hrs)
Maturation pool- metamielocytes, band neutrophils (46-70hrs)
Storage/reserve pool- mature neutrophils

107
Q

Neutrophils 2nd vascular compartment

A

Two pools after leaving BM
- circulatory neutrophilic pool (CNP), in larger vessels
- marginated neutrophilic pool (MNP), in small vessels
50-50
When stress neutrophils leave MNP to CNP=increased nr of neutrophils in peripheral blood
Half-life 6-7hrs
Tissue migration within 2 hrs, no return to circulation

108
Q

Neutrophilic

A 
Increased number of mature neutrophils
Causes:
- shift from MNP to CNP, stress
- increased BM production (corticosteroids, inflammation)
- granulocytic leukemia

Second Year (40 decks)

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