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Path EOY - CLIN > Haematology and Biochem > Flashcards

Haematology and Biochem Flashcards

1
Q

albumins and globulins

A

albumin = most abundant, driver of oncotic pressure
- produced at constant rate by liver
- carries ion molecules

globulins = larger molecules, inflammatory cytokines and immunoglobulins
- produced by liver - acute phase proteins (inflammation) and coagulation proteins
- lymphocytes - immunoglobulins

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2
Q

hyperproteinemia

A

high albumin - dehydration
high globulin - dehydration, inflammation, neoplasia

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3
Q

hypoproteinemia

A

hypoalbuminemia -
reduce production - liver disease or inflammation
increased losses - renal disease (protein losing nephropathy, movement from blood into body cavity effusion

hypoglobulinemia -
rare
dehydration masking concurrent hypoalbuminemia
if actual hypoglobulinemia - immunodeficiency

panhypoproteinemia -
protein losing enteropathy - lymphoma, IBD, lymphangiectasia
protein losing dermatopathy - severe burns

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4
Q

liver markers - enzymes

A

Hepatocellular -
SDH - liver only - large animal
ALT - liver and muscle but mostly liver - not in large animal
GLDH - liver - more stable than SDH

Hepatobilliary -
ALP - biliary, bone, intestine, steroid - steroid only present in dogs
GGT - biliary only - small increases significant

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5
Q

liver markers - other

A

bile acids - specific to liver disease
bilirubin
cholesterol
albumin
glucose
coagulation factors

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6
Q

bile acid stimulation

A

produced by hepatocytes then degraded in gut and reuptaken to liver for processing

tests ability of liver to reuptake - good test of liver function

increase –> reduced liver function, portosystemic shunt, cholestasis

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7
Q

bilirubin

A

increased -
pre hepatic causes - excessive haem breakdown - haemolysis, fasting - unconjugate increased

hepatic causes - reduced ability to conjugate - toxic insult, lepto - conjugated and unconjugated both increased

post hepatic - gallstones, mucocoele, pancreatitis in cats - unconjugated increases first then both

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8
Q

cholesterol

A

produced by liver but also uptake from food and release from fat

increased -
cholestasis - increased bilirubin, GGT, ALT
starvation/anorexia - also increased triglycerides
recent meal - also increased triglycerides
neprhotic syndrome

decreased -
reduced intestinal absorption - GI disease, hypoadrenocorticism

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9
Q

hypoglycemia

A

diabetic ketoacidosis
starvation
insulinoma
artefact - wrong blood tube - should use fluoride oxalate

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10
Q

coagulation factors

A

synthesised by liver - liver failure –> increased coagulation times

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11
Q

muscular enzymes

A

creatinine kinase - muscle only - short half life
AST - muscle and liver - long half life
ALT - muscle and liver - more specific to liver

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12
Q

pancreatic markers

A

pancreatic lipase -
increased in pancreatitis and when GFR is reduced

amylase -
pancreatitis or reduced GFR

tli -
decreased in exocrine pancreatic insufficiency or up with pancreatitis or incomplete starvation

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13
Q

renal physiology

A

glomerulus - electrolytes out of blood, proteins stay in blood, RAAS

proximal tubule - resorption of electrolytes, vitamin D activation

loop of henle -
ascending - water absorption
descending - NaCl absorption
created medullary gradient to concentrate urine

distal tubule and collecting duct -
small amounts of electrolytes absorbed
reabsorbs water to concentrate urine

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14
Q

glomerular filtration rate

A

speed at which fluid is filtered out of blood into bowmans capsule

controlled by -
hydrostatic pressure - rate at which blood moves in and out of the glomerular capillaries and rate filtered fluid moves through renal tubules
oncotic pressure - amount of albumin in peripheral blood

hydrostatic changes -
increased inflow - high CO, high blood pressure
decreased inflow - low CO, water loss
increased flow through tubules - excretion of osmoactive substances (glucose, mannotol), diurectics, loss of medullt tonicity (psyhod=genic polydipsia, diabetes insipidus, liver failure)
decreased flow through tubules - injury to glomerulus, injury to tubules, urolithiasis

oncotic changes -
hypoalbuminemia - loss or decreased production
hyperalbuminemia - dehydration

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15
Q

renal biomarkers

A

urea -
produced by liver in protein metabolism and excreted by kidneys
concentration dependant on production (liver failure, high protein diet, increased with GI bleeding) and rate of excretion (renal damage)

creatinine -
released by muscles at constant rate and excreted by kidneys
concentration dependant on production (mucle mass or wasting) and rate of excretion (Renal damage)

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16
Q

azotemia

A

increase in creatinine, urea and SDMA

pre-renal - problem with renal blood supply or increased urea production in liver

renal - problem with kidney itself

post-renal - obstruction of urine outflow

evaluation -
USG - low likely renal, high assess bladder size, CRT and dehydration
enlarged bladder and history of anuria - post renal
dehydration and normal CRT - pre renal

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17
Q

uremia

A

clinical signs associated with azotemia -
lethargy/depression
mucosal ulceration
vomiting/diarrhoea
respiratory signs - uremic pneumonitis, metastatic calcification
hypertension
hypokalemia myopathy - plantigrade stance (Cats)
hyperkalemia bradycardia - AKI and urinary obstruction
non-regenerative anemia

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18
Q

differences between AKI and CKD - electrolytes

A

Sodium - drops in both

chloride - follows sodium - if increasing independently then Fanconi’s syndrome

potassium -
increased in AKI
increased in CKD in dogs and horses, decreased in cats

calcium -
increased in AKI
increased then drops in CKD
drops in urinary obstruction

prosphate - increases in both

magnesium - increases in both

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19
Q

alabama rot

A

cutaneous and renal glomerular vasculopathy (CRGV)
skin lesions
acute renal failure

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20
Q

differences between AKI and CKD - signs

A

collapse - more acute
alabama rot - acute
non regenerative anemia - chronic
weight loss - chronic
severity of azotemia - more severe in acute

PUPD
anuria

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21
Q

sodium

A

most abundant electrolyte
maintains osmotic pressure

increase -
diabetes insipidus - free water loss
water deprivation
salt poisoning
ayperaldosteronism

decrease -
loss from GIT - diarrhoea vomiting
kidney failure - diabetes mellitus, medullary washout
addisons
cavity effusion
perspiration - horses

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22
Q

chloride

A

second most abundant
usually moves with sodium

greater chloride loss than sodium -
vomiting
pyloric outflow obstruction - GDV, LDA, foreign body

greater sodium loss -
proximal small intestinal diarrhoea - pancreatitis
renal tubular injury - fanconi’s
cushings

can use corrected chloride to work out if moving in same direction

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23
Q

potassium

A

regulates pH and cell electrochemical gradient - exchanged for H+ when blood pH altered

increases -
acidosis
reduced renal excretion - CKD, AKI, urinary obstruction, addisons
artefact - hemolysis, delayed serum separation

decreases -
alkalosis
decreased intake - anorexia in horses
perspiration - horses

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24
Q

metabolic and respiratory acidosis

A

metabolic - acids or bases building up in tissues
respiratory - affected by ability to exhale CO2

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25
Q

causes of metabolic acidosis

A

loss of sodium in excess of chloride - loss of sodium in bicarbm hydrochloric acid left behind - small intestinal diarrhoea, renal tubular injury (fanconis)

retained acids - ketones (diabetes), lactate (injured or hypoxic tissues), uremic acids (renal injury)

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26
Q

causes of metabolic alkalosis

A

loss of acid - loss of HCl through vomiting, GDV, LDA, gastric foreign body, gastrointestinal stasis

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27
Q

causes of respiratory acidosis

A

inadequate exhilation of CO2 - build up causes acidosis
respiratory tract obstruction
pulmonary fibrosis
pulmonary thromboembolism
pulmonary neoplasia
pneumonia

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28
Q

causes of respiratory alkalosis

A

when CO2 exhaled excessively
tachypnoea

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29
Q

mixed acid base disorders

A

more than one acid base disorder occurring at the same time

renal failure with vomiting -
renal failure –> metabolic acidosis
vomiting –> metabolic alkalsosis

diabetic ketoacidosis with pancreatitis

septic abdomen (lactic acidosis) and hyperventilation

vomiting causing aspiration pneumonia

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30
Q

aberrations in calcium

A

balanced with phosphorus by PTH and vitamin D
excreted by kidneys and absorbed by kidneys

total calcium - bound to uremic acids and albumin so fluctuate with variations in these
free calcium - unbound, tightly controlled by PTH, vitamin D and calcitonin

hypercalcemia -
hyperparathyroidism - decreased excretion and increased bone resorption
addisons - decreased excretion
renal disease - decreased excretion
D-hypervitaminosis - psoriasis cream or rodenticide poisoning
idiopathic - cats
osteolytic - osteosarcoma
neoplastic - PTH related peptide secreated by tumours (anal sac carcinoma)
error, artefact

hypocalcemia -
nutrition - insufficient calcium or magnesium, or too much phosphorus
renal - insufficient vitamin D production, reduced reabsorption, urinary tract obstruction
pregnancy/lactation
pancreatic exocrine insufficiency or acute pancreatitis
tissue injury - necrosis, rhabdo
rumen overload

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31
Q

aberrations in phosphorus

A

increases -
decreased excretion - renal injury
release from injured cells - necrosis (tumours), rhabdo, excessive vitamin D

decreases -
increased excretion - hyperparathyroidism, fanconis, renal failure in horses
reduced intake
hypovitaminosis D

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32
Q

aberrations in magnesium

A

rarely measured

increases -
renal disease - reduced excretion

decreases -
dietary - staggers

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33
Q

precision and accuracy

A

accuracy = ability to get close to the right answers
precision = ability to give a repeatable result

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34
Q

grey zones

A

middle area where difficult to diagnose
seasonal or diurnal variation - ACTH peaks naturally in autumn so use different ranges for PPID in Autumn
breed and age variation
generic intervals used for exotics so less accurate

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35
Q

sensitivity and specificity

A

sensitivity = ability to accurately detect a sick patient
specificity = ability to accurately detect healthy patents

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36
Q

further tests

A

azotemia on biochem - urinalysis
severe liver enzyme elevations - bile acid stim
hyperkalemia and hyonatremia - basal cortisol

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37
Q

considerations in discordant results

A

calibration
grey zones
decision threshold reliability
hemolysed/lipemic/icteric samples
sample taking and handling
sensitivity or specificity of test
artefacts
individual variation
concurrent disease
history omissions

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38
Q

venepuncture sites - exotic mammals

A

cranial vena cava - GA, blind technique
jugular
cephalic
lateral saphenous - esp rabbits
lateral and dorsal tail veins - rats and mice
marginal ear vein - rabbits, small volumes

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39
Q

venepuncture sites - birds

A

wing/ulnar vein - fragile, prone to haemorrhage
medial tarsal vein - most species, harder in raptors, corvids, small passerines
right jugular - not in pigeons, waterfowl, gulls

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40
Q

venepuncture sites - chelonians

A

jugular - best
subcarapacial sinus - blind, large samples
dorsal tail - smaller samples
brachial plexus - large tortoises

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41
Q

venepuncture sites - squamates

A

ventral tail - care if autotomises, avoid hemipenes

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42
Q

venepuncture sites - reptiles

A

cardiocentesis - direct from ventricle, find heart with doppler

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43
Q

biochemistry - exotics

total protein

A

total protein -
increased - inflammation, vitellogenesis, lipemia
decreased - malnutrition, parasites, liver, kidnets, enteropathy, skin losses, lymph dilution

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44
Q

biochemistry - exotics

A

total protein -
increased - inflammation, vitellogenesis, lipemia
decreased - malnutrition, parasites, liver, kidnets, enteropathy, skin losses, lymph dilution

ALT - not useful, not released in liver damage

ALP - bone damage only

AST - liver and muscle damage, assessed with ck

CK -
bird - tissue/muscle damage
reptile - muscle damage
mammal - any muscle disease process
NB increases associated with traumatic venepucture

GLDH -
bird - hepatocellular damage
reptile - hepatocellular damage

GGT - cholestasis

bile acids -
mammal - hepatic coccidiosis
bird - liver insufficiency (decreased in microhepatica)
reptile - varying usefullness

bile pigments -
birds - somtimes bilirubin - liver disease
reptiles - biliverdin - liver disease

glucose -
mammals - stress, pain, food, GI obstruction, GI stasis. decreased with insulinomas, septicemia, severe liver disease, starvation
reptile - vary by species

lactate -
increased - shock, low CO, liver failure, sepsis, seizures
birds - capture myopathy
reptile - anaerobic metabolism

uric acid -
renal insufficieny
bird - main renal indicator, postpranddial, egg production, gout. decreased in liver disease and starvation
reptile - renal indicator

urea -
mammal - main renal marker

creatinine - consistently low in birds and reptiles

calcium - huge increase in egg laying females
mammal - neoplasia, renal failure, impaired excretion, dietary

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45
Q

exotics biochem species differences

A

birds -
uric acid for renal
low protein normal
stable glucose
calcium affected by egg laying

reptile -
lymph dilution common - reduces everything
effects of sex and season
AST - muscle, with CK
GGT for renal
GDH for heptocellular necrosis
biliverdin
uric acid for renal - fasted samples in carnivores
calcium - egg laying species

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46
Q

metabolic bone disease

A

hypocalcemia - calcium leached from bones
collapse
seizures
tremors

47
Q

egg laying biochem

A

increased total protein, globulin, uric acid, ALP, total calcium - constituents of egg and shell

check ionised calcium

48
Q

haematopoiesis

A

formation of all cellular components of blood
in bone marrow
some in liver and spleen - extramedullary

49
Q

erythropoiesis

A

kidney cells detect tissue hypoxia –> erythropoeitin –> signalling cascade –> progenitors differentiate to erythrocytes

50
Q

myelopoiesis

A

white blood cells

stimulated by IL3, GM-CSF, G-CSF
unregulated production in response to inflammation

51
Q

thrombopoiesis

A

plasma

thrombopoietin produced by liver (stimulates production)

52
Q

neutrophils

A

first response
phagocytosis
degranulation
extracellular traps

53
Q

eosinophils

A

parasites
allergic responses

54
Q

basophils

A

parasites
allergic response
histamine release

55
Q

lymphocytes

A

t cells - immune medaited immunity
b cells - humoral - antibody production
NK cells - innate - phagocytosis

56
Q

monocytes

A

macrophages in tissue
immune response regulation
phagocytosis
microbicidal

57
Q

spherocytes

A

dogs
small, round erythrocytes
dense staining

58
Q

agglutination

A

grapes

59
Q

rouleux

A

stack of coins

60
Q

hypochromia

A

iron deficiency

erythrocytes
increased central palor

61
Q

band neutrophils

A

released from bone marrow early
increased demand

62
Q

toxic change neutrophils

A

released too early from bone marrow

63
Q

howell jolly body

A

remnants of RBC nuclei - usually removed by spleen
splenic dysfunction

64
Q

heinz bodies and eccentrocytes

A

oxidative damage - hemoglobin oxidised and pushed to cell margin

paracetamol in cats
some other toxins
diabetic ketoacidosis

65
Q

regenerative vs non-regenerative anemia

A

regenerative - bone marrow responding - reticulocytes (polychromatiphils, uneven sized RBCs (ansiocytosis), nucleated RBCs, howell jolly bodies
^ short ddx list

non-regenerative - long ddx list

66
Q

schistocytes

A

red cell fragments - cells squeezed through abnormal vessels (haemoangiosarcoma) or fragile (iron deficiency)

67
Q

PCR with anemia

A

hemotropic mycoplasmas in cats
babesia in dogs
ehrlichia and anaplasma in dogs
FIV/FeLV

68
Q

serology with anemia

A

lepto
panleukopenia
parvo
Equine infectious anemia
FeCOV

69
Q

slide agglutination

A

IMHA

70
Q

coombs test

A

IMHA

71
Q

fecal occult blood with anemia

A

can test even if not grossly visible
blood loss in GIT

72
Q

Anemia - biochem

A

reduced red cell mas
reduced hemoglobin
reduced PCV
reduced red blood cell count

73
Q

anemia - pathophysiology and compensatory mechanisms

A

reduced oxygenation of tissues

compensation -
increased oxygen delivery
increased CO
increased RBC production
vasoconstriction to shunt blood away from tissue with lower O2 demand

74
Q

anemia - signs

A

pale mm
lethargy
exercise intolerance
tachypnoea
tachycardia
collapse
icterus
melaena - black, tarry stool
pica

75
Q

anemia - classification

A

severity
based on MCV values - low in iron deficiency, high if presence of immature RBCs
non-regenerative vs regenerative

76
Q

regenerative anemia

A

haemorrhage, hemolysis

3-5 days for marrow to respond - pre-regenerative
prolonged regenerative –> iron deficiency –> non-regenerative

no iron defiency

seen in severe paracitism

hemolysis -
extravascular - more common
intravascular - acute and severe - hemoglobulinuria, haemoglobulinemia
primary - IMHA - immune mediated - common - breed disposition, more in males
secondary - secondary to infections (babesia, mycoplasma), neoplasia, drugs
tocins - oxidation of hemoglobin - heinz bodies

77
Q

IMHA signs

A

lethargy
anorexia
pale mm
bounding pulses
murmur
tachypnoea
jaundice
hepatosplenomegaly
pyrexia

diagnoses - hematology, agglutination, coombs test

78
Q

non-regenerative anemia

A

chronic inflammation most common

endocrine - hypothyroidism, addisons

renal - chronic failure - decreased erythropoietin, and decreased RBC lifespan due to uremic toxins

primary bone marrow disorders -
aplastic anemia
pure red cell aplasia
myelophthisis
myelobirosis

79
Q

erythrocytosis

A

increased red cell mass - increased hemoglobin, PCV, hemocrit, red blood cell count

dehydration - increased serum proteins, increased USG

Primary erythrocytosis -
bone marrow neoplasia
failure in RBC feedback mechanisms
low erythropoietin
signs - neurological, cardiopulmonary, retinal changes

secondary erythrocytosis -
hypoxia
solid tumours
renal carcinoma

80
Q

neutrophilia

A

to meet demand - infection, immune mediated disease, inflammation, neoplasia

independent of demand - leukemia

persistence in circulation - chronic stress, steroids

redistribution - shift from marginating to circulating pool - excitement, stress, increased blood pressure

81
Q

signs of toxicity in cells

A

dohle bodies - blue cytoplasmic inclusions
foamy cytoplasm
blueish cytoplasm
toxic granules

82
Q

lyphocytosis

A

increased to meet demand - persistent antigenic stimulation

without demand - lymphoid leukemia, lymphoma

redistribution - excitement/acute stress, addisons

83
Q

monocytosis

A

to meet demand - infections, immune mediated disease, inflammation, necrosis, sepsis, neoplasia

without demand - leukemia

redistribution - chronic stress, steroids

84
Q

eosinophilia

A

to meet demand - allergic reaction, parasites, inflammation of mast cell rich tissue

without demand - neoplasia (lymphoma, mast cell tumour, squamous cell carcinoma), hypereosinophilic syndrome, eosinophilic leukemia

85
Q

basophilia

A

to meet demand - hypersensitivities, parasitism, inflammation

without demand - paraneoplastic syndromes (mast cell), basophilic leukemia

86
Q

neutropenia

A

increased demand - migration into tissue - bacterial sepsis, abscess, endotoxemia, tumour, necrosis

redistribution - acute endotoxemia

decreased production - bone marrow disease, drugs

increased destruction - immune mediated

87
Q

leukopenia

A

loss of lymphocytes - loss of chylous fluid (lymph), protein losing enteropathy, chylothorax

decreased production - viral infections, lympholytic drugs

redistribution - chronic stress, steroids

88
Q

stress leukogram

A

leukocyte pattern due to increased cortisol

neutrophilia, lymphopenia, eosinophilia

reverse in addisons

89
Q

red cell morphology by species

A

dog - most obvious central pallor
alpaca - oval, no nucleus
birds and reptiles - nucleated red blood cells

90
Q

variation in regenerative response by species

A

horses - no polychromatophils, can’t use this to assess regeneration

91
Q

variation in leukocyte response by species

A

cats - more extreme response to epinephrine
dog - complete stress glucocorticoid response most common
cattle - neutropenia common

92
Q

feline haemotrophic mycoplasma

A

haemoparasite

feline infectious anemia - acute hemolytic anemia
transmission in blood
male cats with outdoor access

species -
m. hemofelis - most pathogenic - mild to severe disease in healthy cats
candidatus m. haemomimutum - milder unless immunosuppressed
candidatus m. turicensis - unlikely to cause clinical anemia unless concurrent disease

one or combination

PCR

carrier

signs -
related to anemia
weakness
lethargy
pale mm
intermittent fever
tachycardia
tacypnea
haemic murmur
depression
collapse

regenerative or pre-regenerative
non-regenerative in immune compromised patients

diagnosis - coombs and agglutination

rods, cocci or rings on surfaces of RBCs

cant be cultures

93
Q

babesia canis

A

hemoparasite
tick bourne

sporozoites invade RBCs –> differentiate and divide –> rupture RBCs –> invade neighbouring RBCs
hemolytic anemia
regnerative
can be associated with development of autoantibodies

mild to moderate disease
carrier

signs -
fever
lethargy
anorexia
jaundice
vomiting
mild to severe

diagnosis - hemolysed serum, spherocytes, positive coombs test, thrombocytopenia, neutropenia
blood smear - large paired piriform organisms inside RBCs
PCR - protozal DNA
serology

94
Q

heaptozoonosis

A

hemoparasite
tick borne - eaten and sporozoites penetrate intestinal epithelium
–> spread to lymphatics –> monozoites infect neutrophils

signs -
related to severity of parasite burden
low burdens may be asymptomatic
risk of secondary infection - infected neutrophils
non-specific signs
hypoglobulinemia, hypoalbuminemia
non-regenerative anemia
neutrophilia

diagnosis - blood smear
PCR

95
Q

heartworm

A

hemoparasites
mosquito vector
dog definitive host

nematode - dirofilaria immitis

3 stages -
microfilaria - in blood
larvae - in mosquito and tissue
adult - pulmonary artery or right atrium in heavy burdens

signs -
mild - asymptomatic or cough
moderate - cough, exercise intolerance, abnormal lungs sounds
severe - above + dyspnoea, abnormal heart sounds, syncope, ascities, death
caval syndrome - sudden onset, severe lethargy and weakness, hemoglobinuria and haemoglobinemia

diagnosis - antigen detection, modified knotts

NB cats - can get it but not definitive host - less signs and testing not reliable, use radiography and echo

96
Q

bovine babesiosis

A

hemoparasite
babesia divergens
red water fever

merozoites invade RBCs –> burst –> intravascular hemolytic anemia

mild to severe disease

signs -
related to severity of hemolysis
fever
depression
icterus
anorexia
tachycardia/tachypnoea
pale mm
haemoglobinuria
abortion
milk drop

diagnosis - PCR, blood smear evaulation - pear shaped structures in cytoplasm

97
Q

bovine anaplasmosis

A

hemoparasite
tick borne
a. phagocytophilium
obligate intracellular bacteria - neutrophils

disease via immunosuppresion
persistent carrier status - up to 2 years

diagnosis -
blood smear - mulberry looking colonies of coccobacilliary bacteria
PCR
serology - not widely used

98
Q

equine piriplasmosis

A

hemoparasite
tick borne
babesia equi (theileria equi) or babesia caballi

replicates in RBCs –> burst –> merozoites released into bloodstream –> infect more RBCs

signs -
acute - hemolytic anemia, icterus, hemoglobinuria, thrombocytopenia, fever, inappetence
usually mild and non specific - indistinguishable from chronic inflammatory disorder

99
Q

candidatus mycoplasma hemolamae

A

camelid hemoparasite
regenerative anemia
associated with chronic disease

combined with hemonchus cause more anemia

blue dots on RBCs
PCR

100
Q

hemonchus contortus

A

camelid GIT parasite
most common camelid source of anemia
higher in gut –> more severe

combined with haemolamae cause more anemia

101
Q

benefits of cytology

A

no anaesthetic
low risk complications
quick
non-invasive
rapid results
tumour grading
surgical planning
tumour staging
fluid classification
identifying infections
used for anciliary tests - PARR, flow cytometry, PCR

102
Q

greasy slide ddx

A

lipoma

steatititis/panniculitis
pernodal fat
mast cell tumour
liposarcoma
other soft tissue sarcoma

103
Q

cytology stains

A

in house - diff-quik, MGG
lab - modified wrights

104
Q

hemodilution

A

too many erythrocytes or platelets on a slide, obscured rest of sample

105
Q

identifying inflammation on cytological specimen

A

white blood cells -
neutrophils - well preserved or degenerate (pale blue swollen nucleus) - microorganisms and necrosis
macrophages - activated (vacuolated and foamy) - phagocytosis and cell debris

acute/suppurative - neutrophils
chronic active/pyogrnulomatous - neutrophils and macrophages
chronic/granulomatous - macrophages
specific - eg eosinophils
concurrent tissue reaction - hyperplasia/dysplasia

106
Q

hyperplasia

A

increased in number of cells in a tissue

non-neoplasic

often hormonal influence

cytology (FNA) -
high cellularity
may have mild criteria of malignancy
mildly increased N:C
more prominent nucleoli
finer chromatin

107
Q

dysplasia

A

disordered growth

common in epithelial tissue secondary to inflammation

loss of uniformity
disordered architecture

FNA -
Nuclear to cytoplasmic asynchrony
cytoplasmic basophilia
anisokaryosis and ansiocytosis (uneven cell size and nuclear size)
difficult to distinguish from neoplasia

108
Q

neoplasia

A

abnormal and excessive tissue growth

growth uncoordinated with normal tissue
irreversible - autonomous

109
Q

epithelial neoplasias

A

squamous cell carcinoma
adenoma
adenocarcinoma

110
Q

mesenchymal neoplasia

A

osteosarcoma
haemoangiosarcoma
lipoma
lipsarcoma

111
Q

round cell neoplasias

A

mast cell tumour
lymphoma
leukemia
histiocytoma/histocytic sarcoma
plasma cell tumour
transmissible veneral tumour

112
Q

neuroendocrine neoplasia

A

thyroid tumours
pheochromacytomas

113
Q

criteria of malignancy

A

anisocytosis - uneven cell size
anisokaryosis - variation in nuclear size
increased N:C
mitotic figures
multinucleation
nuclear moulding
angular nuceli
coarse clumped chromatin
prominent nucleoli
necrosis
phagocytosis
emperipoeisis - intact cells inside cytoplasm of other cells
crowded cells

114
Q

lymphoma subtyping

A

small, intermediate or large lymphocytes
presence or absence of nucleoli
position of nucleus in cell
shape of nucleus
relative volume of cytoplasm
presence/absence of golgi zone
relative numbers of mitotic figures
dimorphic lymphocyte distribution
presence on ancilliary cells

PARR
Flow cytometry
IHC

Path EOY - CLIN (4 decks)

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