General Pathology Flashcards
Nosology
Classification of diseases
Pathophysiology
Physiological processes/mechanisms causing disease development and progress
Anomaly
Condition existing before (or at) birth regardless the cause
Disorder
Abnormality in function
Can be of unknown cause/aetiology
Aetiology
Study of the causes of disease and it’s effects
Endogenous cause
Cause coming from inside the patient
Exogenous cause
Cause coming from outside the patient ex virus
Predisposing cause
Mechanism making patient more susceptible to the cause
Primary cause
Main factor causing the disease
Secondary cause
Any factor assisting primary cause
Semiotics
Study and meaning of signs
Clinical picture
Set of specific signs typical for specific disease/disorder
Syndrome
Set of clinical signs associated with each other, and a specific disease
Collectively indicating or charcheterizing a disease, disorder or abnormal condition
Pathognomonic sign
Sign who’s presence means that the disease is present beyond doubt
Diagnostic sign
Signs leading to the recognition and identification of a disease
Prognostic sign
Sign relating to outcome of the disease
Main/major signs
Typical for specific disease or disorder
Common signs
Unspecific, common in many clinical pictures
Acute disease
Rapid onset (days) Resolved quickly (healing, chronification, death) Peracute or subacute
Chronic disease
Slow onset (days to weeks) Little or no change
Subclinical phase
Stage before symptoms/signs are noted
Prodromal phase
Stage where early, unspecific signs are noted
Clinical phase
Stage where normal, typical signs are present
Decline phase
Disease progressing either to death or healing
Can become chronic
Stages of decline phase
Convalescence- period of recovery
Relapse- reappearance after vanished completely
Recurrence- activation before complete healing
Clinical judgement
Diagnosis
Prognosis
Treatment
Presumptive diagnosis
Based on presumption or probability with reasonable ground
Provisional diagnosis
Prognosis done before all tests are done
Definitive diagnosis
Diagnosis done after all available tests are done
Clinical diagnosis
Made on basis of medical signs rather than diagnostic tests
Differential diagnosis
The distinguishing between two or more diseases with similar signs
Diagnosis of exclusion
Diagnosis set after elimination of all other reasonable possibilities
Etiological diagnosis
Including a causative organism
Etiological treatment
Treating the cause, not the symptoms or consequences
Symptomatic treatment
Suppress undesirable signs
Palliative treatment
Relieve signs, improving quality of life
Preventive treatment
Preventing disease to occur
Specific treatment
Treatment particularly adapted to specific disease
Erythrocyte
Transportation of oxygen and CO2, maintain pH, blood viscosity
Biconcave, anucleated
Half-life ~100 days
Erythropoiesis
Production/formation of RBCs
Loss of nucleus
20% in baseline production
Anaemia
“Lack of blood”
Decrease in oxygen carrying capacity and delivery to tissues
Reduction of total RBCs, PCV or Hb concentration
Causes of anaemia
Loss of blood
Destruction of RBCs
Lack of production of RBCs
Regenerative anaemia
Due to loss or destruction
Response from BM
Non-regenerative anaemia
Lack of production
No response from Bm
Aetiology of regenerative anaemia
Haemorrhagic
Haemolytic
Aetiology of non-regenerative anaemia
Primary BM anaemia
Secondary BM anaemia (nutritional or hypoproliferative)
RBC indices of regenerative anaemia
Macrocyclic, hypochromic
Big RBC, low Hb concentration
High MCV, low MCHC/MHC
RBC indices of non-regenerative anaemia
Normocytic, normochromic
Normal erythrocyte
Low or normal MCV, high or normal MCHC
Polychromasia
Sign of regeneration
Immature RBC without nucleus, tends to be larger than mature
Acanthocytes
Picked cell membrane/abnormal thorny projections
Can be due to
Excess of cholesterol in cell membrane
Severe hepatic disease
Target cell
“Bulls eye” Due to Iron deficiency anaemia Liver disease Post-splenectomy
Abnormal agglutination of RBCs
Agglutination or rouleaux formation Due to Inflammation Tumors Infection
Nucleated RBCs
Sign of regeneration
Metarubricytes or late rubricytes
Howell-Jowell bodies
Sign of regeneration
Basophilic nuclear remnants
Basophilic stippling
Sign of regeneration
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
Clinical signs of anaemia
Weakness/fatigue Excercise intolerance Pale mucous membrane May have: Jaundice, tachycardia, cardiac murmur, cardiomegaly, lymphnode enlargement, hepatomegaly, splenomegaly
Haemorrhagic anaemia
Acute- trauma, digestive bleeding, infections, clotting defects
Chronic- can lead to iron deficiency=non- regenerative
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
Blood smear in haemorrhagic anaemia
Reticulocytes increase after 3 days, max after 7, normal in 14
Immature RBCs/anycytosis remain longer
Extravascular haemolytic anaemia
RBCs loss due to mononuclear phagocytic system/MPS
Clinical signs as other anaemias, plus bilirubinaemia, haemoglobinuria
Intravascular haemolytic anaemia
Rupture of RBC inside blood vessels
Signs as other anaemias, plus bilirubinaemia, haemoglobinuria
Haemolysis
Reduced RBC lifespan due to destruction of RBC
Blood haematology & biochemistry in haemolytic anaemia
Low PCV
high billirubin
Normal or high protein
Blood smear in haemolytic anaemia
Increased number reticulocytes, more regenerative than haemorrhagic
Immature RBCs/anycytosis, remain longer
Cause of haemolysis may be identified
Signs of haemolytic anaemia
Intravascular- dark urine (haemoglobinuria), haemoglobinaemia, billirubinaemia
Extravascular- billirubinaemia
If both- also splenomegaly, hepatomegaly
Causes of extravascular haemolytic anaemia
Infectious Immune-mediated Fragmentation injury Toxins Inherited RBC defects
Causes of intravascular haemolytic anaemia
Cause related to RBC itself
Infectious
Immune-mediated
Inherited RBC defects
Infectious agent I haemolytic anaemia
Direct action of toxins
Invasion and destruction of RBC by organism
Immune- mediated mechanism
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
IMHA pathophysiology
Anti-RBC antibodies attach to RBC membrane
- Complement cascade
- removal of affected RBCs by MPS (extravascular)
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
Oxidative stress haemolytic anaemia
Oxidative stress causing irreversible RBC damage - methaemoglobin - Heinz-bodies - eccentrocytes Visible in blood smear
Heinz-bodies
Hb precipitates over RBC inner surface
Fragile, undergo haemolysis in liver
Up to 10% is normal in cats
Eccentrocytes
Displaced Hb in one part of the cell, the rest with little
Due to damaged membrane
Methaemoglobin
Hb containing Fe3 instead of Fe2
Cannot bind oxygen
Darker color than normal Hb
Causes of nutritional anaemias
Vitamin B12 and folic acid deficiency
Iron deficiency
Copper deficiency
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
Iron deficiency anaemia
Causes- chronic bleeding, low iron intake, malabsorption, high iron consumption
Blood smear- normo- or microcytic and normo- or hypochromic
Copper deficiency anaemia
Copper needed for iron absorption and release of iron stores in body
Signs- neorological and haematological, low growth rate, GI signs
Hypoproliferative anaemia
Due to: -Inflammation, metabolic disease - chronic renal or hepatic failure -Neoplasia -Endocrine disease Anaemias usually mild Normocytic and normochronic
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%)
Neoplasia causing anaemia
Reasons may be: -Chronic disease - blood loss - immune-mediated haemolysis - chronic antineoplastic treatment Blood smear= inflammatory anaemia, normocytic, normochromic
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
Liver disease in anaemia
Anaemia of chronic disease
Interfere with EPO synthesis
Altered iron metabolism
Endocrine diseases in anaemia
Diabetes mellitus- diabetic ketoacidosis
Hypothyroidism- general decrease in metabolism, low EPO, low proliferation of RBC precursors in BM
Aplastic anaemia
Destruction of BM hematopoietic cells
- pancytopenia
- pure red cell aplasia
Mieloptisis
Primary BM anaemia
BM infiltration
- myeloproliferative or lymphoproliferative diseases (WBC precursors neoplasia)
Pancytopenia
BM produces NO blood cells (WBC+RBC) - replacement of normal BM cells by fat Caused by: - infection - drugs - immune- mediated
Red cell aplasia
Involving only RBC precursors - normocytic, normochromic - reticulocytopenia - absence of red cell precursors Causes: - immune mediated - infectious
Polycuthaemia/erythrocytosis
Absolute increase in RBC mass
Increased hematocrit
Increased haemoglobinuria concentration
Relative or absolute
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)
Absolute polycythaemia/polycythaemia Vera
Myeloproliferative disorder w abnormal increase of RBC production
Serum EPO activity typically decreased
Secondary polycythaemia
High EPO
Physiological- compensation of tissue hypoxia
Pathological- due to renal tumor, extrarenal, excessive EPO administration
Consequences of erythrocytosis
Hyperviscosity syndrome (spontaneous bleeding from mucous membranes, visual disturbances/retinopathy, neurological signs
Heart failure
Hypoxia
Granulocytes
Specific cytoplasmic granules, segmented nuclei
- neutrophils
- eosinophils
- basophils
Agranulocytes/mononuclear cells
No granules, non-segmented nuclei
- lymphocytes
- monocytes
Neutrophils
Granulocytes, pink granules
Main target:
- bacteria
- fungi
Eosinophils
Granulocytes, red granules
Main target:
-Larger parasites
- inflammatory responses
Basophils
Granulocytes, purple granules
Unknown main function
Mononuclear cells
Lymphocytes- round, large nuclei
Monocytes- pleomorphic nuclei, can be lobulated with “fat” lobules
Lymphocytes
B-cells= antibody production, activation of T-cells T-cells= CD4+, CD8+, regulatory T-cells, NK-cells
Monocytes
Becomes macrophages in tissue
Leukogram
- total WBC count
- differential cell count
- WBC morphological features
Pathophysiology of neutrophils
Most abundant WBC
First line of defence
Increased segmentation when mature, 3-5 segments normal
Regulated by G-CSF (inflammation)
1st Neutrophilic medullary compartments
Proliferation pool- dividing cells (48-60hrs)
Maturation pool- metamielocytes, band neutrophils (46-70hrs)
Storage/reserve pool- mature neutrophils
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
Neutrophilic
Increased number of mature neutrophils Causes: - shift from MNP to CNP, stress - increased BM production (corticosteroids, inflammation) - granulocytic leukemia
