General Pathology Flashcards
(108 cards)
1
Q
Nosology
A
Classification of diseases
2
Q
Pathophysiology
A
Physiological processes/mechanisms causing disease development and progress
3
Q
Anomaly
A
Condition existing before (or at) birth regardless the cause
4
Q
Disorder
A
Abnormality in function
Can be of unknown cause/aetiology
5
Q
Aetiology
A
Study of the causes of disease and it’s effects
6
Q
Endogenous cause
A
Cause coming from inside the patient
7
Q
Exogenous cause
A
Cause coming from outside the patient ex virus
8
Q
Predisposing cause
A
Mechanism making patient more susceptible to the cause
9
Q
Primary cause
A
Main factor causing the disease
10
Q
Secondary cause
A
Any factor assisting primary cause
11
Q
Semiotics
A
Study and meaning of signs
12
Q
Clinical picture
A
Set of specific signs typical for specific disease/disorder
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
14
Q
Pathognomonic sign
A
Sign who’s presence means that the disease is present beyond doubt
15
Q
Diagnostic sign
A
Signs leading to the recognition and identification of a disease
16
Q
Prognostic sign
A
Sign relating to outcome of the disease
17
Q
Main/major signs
A
Typical for specific disease or disorder
18
Q
Common signs
A
Unspecific, common in many clinical pictures
19
Q
Acute disease
A
Rapid onset (days) Resolved quickly (healing, chronification, death) Peracute or subacute
20
Q
Chronic disease
A
Slow onset (days to weeks) Little or no change
21
Q
Subclinical phase
A
Stage before symptoms/signs are noted
22
Q
Prodromal phase
A
Stage where early, unspecific signs are noted
23
Q
Clinical phase
A
Stage where normal, typical signs are present
24
Q
Decline phase
A
Disease progressing either to death or healing
Can become chronic
25
Stages of decline phase
Convalescence- period of recovery
Relapse- reappearance after vanished completely
Recurrence- activation before complete healing
26
Clinical judgement
Diagnosis
Prognosis
Treatment
27
Presumptive diagnosis
Based on presumption or probability with reasonable ground
28
Provisional diagnosis
Prognosis done before all tests are done
29
Definitive diagnosis
Diagnosis done after all available tests are done
30
Clinical diagnosis
Made on basis of medical signs rather than diagnostic tests
31
Differential diagnosis
The distinguishing between two or more diseases with similar signs
32
Diagnosis of exclusion
Diagnosis set after elimination of all other reasonable possibilities
33
Etiological diagnosis
Including a causative organism
34
Etiological treatment
Treating the cause, not the symptoms or consequences
35
Symptomatic treatment
Suppress undesirable signs
36
Palliative treatment
Relieve signs, improving quality of life
37
Preventive treatment
Preventing disease to occur
38
Specific treatment
Treatment particularly adapted to specific disease
39
Erythrocyte
Transportation of oxygen and CO2, maintain pH, blood viscosity
Biconcave, anucleated
Half-life ~100 days
40
Erythropoiesis
Production/formation of RBCs
Loss of nucleus
20% in baseline production
41
Anaemia
“Lack of blood”
Decrease in oxygen carrying capacity and delivery to tissues
Reduction of total RBCs, PCV or Hb concentration
42
Causes of anaemia
Loss of blood
Destruction of RBCs
Lack of production of RBCs
43
Regenerative anaemia
Due to loss or destruction
| Response from BM
44
Non-regenerative anaemia
Lack of production
| No response from Bm
45
Aetiology of regenerative anaemia
Haemorrhagic
| Haemolytic
46
Aetiology of non-regenerative anaemia
Primary BM anaemia
| Secondary BM anaemia (nutritional or hypoproliferative)
47
RBC indices of regenerative anaemia
Macrocyclic, hypochromic
Big RBC, low Hb concentration
High MCV, low MCHC/MHC
48
RBC indices of non-regenerative anaemia
Normocytic, normochromic
Normal erythrocyte
Low or normal MCV, high or normal MCHC
49
Polychromasia
Sign of regeneration
| Immature RBC without nucleus, tends to be larger than mature
50
Acanthocytes
Picked cell membrane/abnormal thorny projections
Can be due to
Excess of cholesterol in cell membrane
Severe hepatic disease
51
Target cell
```
“Bulls eye”
Due to
Iron deficiency anaemia
Liver disease
Post-splenectomy
```
52
Abnormal agglutination of RBCs
```
Agglutination or rouleaux formation
Due to
Inflammation
Tumors
Infection
```
53
Nucleated RBCs
Sign of regeneration
| Metarubricytes or late rubricytes
54
Howell-Jowell bodies
Sign of regeneration
| Basophilic nuclear remnants
55
Basophilic stippling
Sign of regeneration
56
Presence of reticulocytes in peripheral blood
Sign of regeneration
Increase of (or presence of in ruminants) Immature, anucleated erythrocytes
Horses have no reticulocytes in peripheral blood
57
Clinical signs of anaemia
```
Weakness/fatigue
Excercise intolerance
Pale mucous membrane
May have:
Jaundice, tachycardia, cardiac murmur, cardiomegaly, lymphnode enlargement, hepatomegaly, splenomegaly
```
58
Haemorrhagic anaemia
Acute- trauma, digestive bleeding, infections, clotting defects
Chronic- can lead to iron deficiency=non- regenerative
59
Blood haematology in haemorrhagic anaemia
Primary- loss of whole blood, PCV May be unchanged
| Secondary- after 24hrs blood replaced by IF, drop in PCV, serum protein drop
60
Blood smear in haemorrhagic anaemia
Reticulocytes increase after 3 days, max after 7, normal in 14
Immature RBCs/anycytosis remain longer
61
Extravascular haemolytic anaemia
RBCs loss due to mononuclear phagocytic system/MPS
| Clinical signs as other anaemias, plus bilirubinaemia, haemoglobinuria
62
Intravascular haemolytic anaemia
Rupture of RBC inside blood vessels
| Signs as other anaemias, plus bilirubinaemia, haemoglobinuria
63
Haemolysis
Reduced RBC lifespan due to destruction of RBC
64
Blood haematology & biochemistry in haemolytic anaemia
Low PCV
high billirubin
Normal or high protein
65
Blood smear in haemolytic anaemia
Increased number reticulocytes, more regenerative than haemorrhagic
Immature RBCs/anycytosis, remain longer
Cause of haemolysis may be identified
66
Signs of haemolytic anaemia
Intravascular- dark urine (haemoglobinuria), haemoglobinaemia, billirubinaemia
Extravascular- billirubinaemia
If both- also splenomegaly, hepatomegaly
67
Causes of extravascular haemolytic anaemia
```
Infectious
Immune-mediated
Fragmentation injury
Toxins
Inherited RBC defects
```
68
Causes of intravascular haemolytic anaemia
Cause related to RBC itself
Infectious
Immune-mediated
Inherited RBC defects
69
Infectious agent I haemolytic anaemia
Direct action of toxins
Invasion and destruction of RBC by organism
Immune- mediated mechanism
70
Immune-mediated haemolytic anaemia
IMHA
Primary- idiopathic
Secondary- RBC being infected by pathogen or coated by foreign antigen, neoplasia, drugs/vaccination, incompability transfusion reactions, oxidative stress
71
IMHA pathophysiology
Anti-RBC antibodies attach to RBC membrane
- Complement cascade
- removal of affected RBCs by MPS (extravascular)
72
Fragmentation injury/microangiopathic haemolytic anaemia
```
Damage to RBC caused by endothelial alteration in small vessels
Damaged/fragmented RBCs= scistocytes
By:
- disseminated intravascular coagulation
- inflammatory process
- hemangiosarcoma
- valve diseases
```
73
Oxidative stress haemolytic anaemia
```
Oxidative stress causing irreversible RBC damage
- methaemoglobin
- Heinz-bodies
- eccentrocytes
Visible in blood smear
```
74
Heinz-bodies
Hb precipitates over RBC inner surface
Fragile, undergo haemolysis in liver
Up to 10% is normal in cats
75
Eccentrocytes
Displaced Hb in one part of the cell, the rest with little
| Due to damaged membrane
76
Methaemoglobin
Hb containing Fe3 instead of Fe2
Cannot bind oxygen
Darker color than normal Hb
77
Causes of nutritional anaemias
Vitamin B12 and folic acid deficiency
Iron deficiency
Copper deficiency
78
Anaemia due to B12 and folic acid deficiency
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
Iron deficiency anaemia
Causes- chronic bleeding, low iron intake, malabsorption, high iron consumption
Blood smear- normo- or microcytic and normo- or hypochromic
80
Copper deficiency anaemia
Copper needed for iron absorption and release of iron stores in body
Signs- neorological and haematological, low growth rate, GI signs
81
Hypoproliferative anaemia
```
Due to:
-Inflammation, metabolic disease
- chronic renal or hepatic failure
-Neoplasia
-Endocrine disease
Anaemias usually mild
Normocytic and normochronic
```
82
Inflammation/chronic disease causing anaemia
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
Neoplasia causing anaemia
```
Reasons may be:
-Chronic disease
- blood loss
- immune-mediated haemolysis
- chronic antineoplastic treatment
Blood smear= inflammatory anaemia, normocytic, normochromic
```
84
Renal disease in anaemia
Causes:
- EPO deficiency
- effects of uremic toxins: GI ulcers, suppression of BM, shortened RBC lifespan by mild haemolysis (urea)
- chronic inflammatory disease
85
Liver disease in anaemia
Anaemia of chronic disease
Interfere with EPO synthesis
Altered iron metabolism
86
Endocrine diseases in anaemia
Diabetes mellitus- diabetic ketoacidosis
| Hypothyroidism- general decrease in metabolism, low EPO, low proliferation of RBC precursors in BM
87
Aplastic anaemia
Destruction of BM hematopoietic cells
- pancytopenia
- pure red cell aplasia
88
Mieloptisis
Primary BM anaemia
BM infiltration
- myeloproliferative or lymphoproliferative diseases (WBC precursors neoplasia)
89
Pancytopenia
```
BM produces NO blood cells (WBC+RBC)
- replacement of normal BM cells by fat
Caused by:
- infection
- drugs
- immune- mediated
```
90
Red cell aplasia
```
Involving only RBC precursors
- normocytic, normochromic
- reticulocytopenia
- absence of red cell precursors
Causes:
- immune mediated
- infectious
```
91
Polycuthaemia/erythrocytosis
Absolute increase in RBC mass
Increased hematocrit
Increased haemoglobinuria concentration
Relative or absolute
92
Relative polycythaemia
Decreased plasma volume in relation to RBC
Haemogram= high PCV, high TP
Types:
-Haemoconcentration (loss of fluids)
-Splenic contraction (stress in horses & greyhounds)
93
Absolute polycythaemia/polycythaemia Vera
Myeloproliferative disorder w abnormal increase of RBC production
Serum EPO activity typically decreased
94
Secondary polycythaemia
High EPO
Physiological- compensation of tissue hypoxia
Pathological- due to renal tumor, extrarenal, excessive EPO administration
95
Consequences of erythrocytosis
Hyperviscosity syndrome (spontaneous bleeding from mucous membranes, visual disturbances/retinopathy, neurological signs
Heart failure
Hypoxia
96
Granulocytes
Specific cytoplasmic granules, segmented nuclei
- neutrophils
- eosinophils
- basophils
97
Agranulocytes/mononuclear cells
No granules, non-segmented nuclei
- lymphocytes
- monocytes
98
Neutrophils
Granulocytes, pink granules
Main target:
- bacteria
- fungi
99
Eosinophils
Granulocytes, red granules
Main target:
-Larger parasites
- inflammatory responses
100
Basophils
Granulocytes, purple granules
| Unknown main function
101
Mononuclear cells
Lymphocytes- round, large nuclei
| Monocytes- pleomorphic nuclei, can be lobulated with “fat” lobules
102
Lymphocytes
```
B-cells= antibody production, activation of T-cells
T-cells= CD4+, CD8+, regulatory T-cells, NK-cells
```
103
Monocytes
Becomes macrophages in tissue
104
Leukogram
- total WBC count
- differential cell count
- WBC morphological features
105
Pathophysiology of neutrophils
Most abundant WBC
First line of defence
Increased segmentation when mature, 3-5 segments normal
Regulated by G-CSF (inflammation)
106
1st Neutrophilic medullary compartments
Proliferation pool- dividing cells (48-60hrs)
Maturation pool- metamielocytes, band neutrophils (46-70hrs)
Storage/reserve pool- mature neutrophils
107
Neutrophils 2nd vascular compartment
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
Neutrophilic
```
Increased number of mature neutrophils
Causes:
- shift from MNP to CNP, stress
- increased BM production (corticosteroids, inflammation)
- granulocytic leukemia
```
