Diagnostic Pathology

Front 1

what is the role of alanine aminotransferase

Back 1

cytoplasmic enzyme that catalyses the transamination of alpha-ketoglutarate and L-alanine to produce glutamate and pyruvate
high activity in striated and cardiac muscle

Front 2

ALT is a good indicator of hepatocellular injury in ruminants, pigs, horses and birds.
true or false?

Back 2

false

Front 3

AST is high in
a) acute liver injury
b) chronic liver injury
C) both acute and chronic liver inury
d) none of the above

Back 3

c) both acute and chronic

Front 4

what is the major interfering factor for AST (aspartate aminotransferase) levels? and what can be done to overcome this?

Back 4

skeletal muscle- there is no test to differentiate liver from muscle AST so measure CK

Front 5

what kind of drugs can induce some liver leakage enzymes?

Back 5

anti-convulsants, glucocorticoids, thiacetarsemide
some drugs cause liver damage hence leakage enzyme activity increases i.e. carprofen in dogs, tetracycline in cats

Front 6

what can lead to false positives and negatives for ALT levels?

Back 6

false positives: haemolysis and lipaemia
false negatives: enzyme degradation i.e. improper handling

Front 7

what limits SDH usefulness as diagnostic test?

Back 7

labile in vitro, very short half life (<12h), best analysed <4-6h post collection

Front 8

is GLDH good for identifying acute or chronic liver damage?

Back 8

acute

Front 9

what leakage liver enzyme do we use for pigs?

Back 9

OCT (ornithine carbamoyltransferase)

Front 10

name the induced hepatic enzymes commonly measured

Back 10

- ALP (alkaline phosphatase)
- GGT (gamma glutamyltransferase)

Front 11

what are common causes of increases in ALP and GGT

Back 11

- Cholestasis
- drugs
- hormonal effects

Front 12

what do marked ALP( alkaline phosphatase) levels in dogs often indicate?

Back 12

cholestasis

Front 13

what are some common causes of cholestasis?

Back 13

- cholangitis
- biliary cirrhosis
- extrahepatic bile duct obstruction i.e. pancreatitis

Front 14

when might you see increases in intestinal and placental ALP?

Back 14

- horses with colic
- late term pregnancy

Front 15

what limits the usefulness of liver ALP as a diagnostic tool in cats?

Back 15

- present in low levels
- short half life (6h)

Front 16

what enzyme is the preferred indicator of cholestasis in birds?

Back 16

GGT (gamma glutamyltransferase)

Front 17

what is the most commonly used test of liver function?

Back 17

bile acid testing

Front 18

what concentrations of bile acids post prandial indicate high probability of hepatobiliary disease in dogs and cats?

Back 18

dogs: >30umol/L
cats: >25umol/L

Front 19

what are some causes of increased bile acids?

Back 19

- porto-systemic shunts
- liver failure
- cholestasis
- inappropriate contraction of gall bladder
small intestinal bacterial overgrowth

Front 20

what is a good alternative to test for in malteses and maltese X instead of bile acids?

Back 20

ammonia

Front 21

hypoalbuminaemia would be a good indicator of acute liver disease?
true or false?

Back 21

false, hypoalbuminaemia is non-specific for liver diease
may occur with liver failure, need to have lost at least 75% functional mass before albumin levels decrease

Front 22

often have hyperglobulinaemia in chronic liver disease
true or false?

Back 22

true

Front 23

in severe liver failure what is the cause of hypoglycaemia?

Back 23

decreased gluconeogenesis and decreased clearance of insulin

Front 24

what is one major thing that must always be done before taking a liver biopsy?

Back 24

check clotting factors

Front 25

what are the vitamin K dependent clotting factors?

Back 25

II, VII, IX, X

Front 26

can cytology tell us about functional mass of the liver?

Back 26

no

Front 27

what can cytology tell us about the liver and function?

Back 27

- cellular infiltration i.e. inflammation vs neoplasia
- lipid or glycogen in hepatocytes i.e. diabetes, hyperadrenocorticism
- cholestasis
nodular hyperplasia

Front 28

what tests can be used for the diagnosis of Cushing's syndrome?

Back 28

1. low dose dexmethasone test
2. ACTH stimulation test
3. endogenous ACTH assay
4. urine cortisol: creatinine ratio

Front 29

porto-systemic shunts have similar clinical signs to patients with

Back 29

hepatoencephalopathy

Front 30

pytalism is a common clinical sign seen in cats with what hepatic involving abnormality?

Back 30

porto-systemic shunt

Front 31

if animals with PSS are not diagnosed at young age when will they commonly be incidently diagnosed?

Back 31

when they are anaethetised for spay or castrate--> will have long anaesthetic recovery periods

Front 32

with congenital PSS you will see
a) microhepatica
b) hepatomegaly
c) liver will be normal size

Back 32

a) microhepatic bc the liver is never able to develop fully
it is often difficult to palpate

Front 33

what comprises a portal triad?

Back 33

1. hepatic artery
2. portal vein
3. bile duct

Front 34

what are the 3 major functions of bile synthesis

Back 34

1. excretion of waste products- cholesterol, bilirubin, metabolised xenobiotics
2. facilitate lipid digestion
3. buffering- neutralise pH of ingesta

Front 35

in zonal necrosis why is periacinar/centrilobular necrosis most common

Back 35

because this zone (3) is the furthest away from the arterial blood supply (portal triad) also this is the area of most drug metabolising ability (MFOs)

Front 36

define cirrhosis

Back 36

diffuse fibrosis with hyperplastic regenerative nodule formation

Front 37

name a bacterial agent that affects the liver of neonatal and foetal lambs and causes abortions

Back 37

Campylobacter fetus

Front 38

what are the predilection site(s) for canine adenovirus 1?

Back 38

hepatocytes, endothelium and renal epithelium

Front 39

is chronic liver disease most common in herbivores or carnivores?

Back 39

herbivores

Front 40

what are causes of chronic liver disease?

Back 40

- low dose chronic exposure to pyrrolyzidine alkaloidds, aflatoxins, lupinosis, primidone

Front 41

name 3 main ways ascites can be promoted

Back 41

1. hypoalbuminaemia = reduced plasma oncotic pressure (fluid mores out into extravascular space)
2. by portal hypertension
3. by retention of sodium and water y the kidneys (liver catabolises aldosterone..?)

Front 42

megalocytes are commonly seen with acute liver disease or chronic liver disease?

Back 42

chronic liver disease i.e. PAs +/- phomopsins, aflatoxins

Front 43

what is the name of the toxin that causes lupinosis

Back 43

Phomopsis leptostromiformis

Front 44

what is the major clinical manifestation presented due to PSS

Back 44

hepatoencephalopathy b/c directs toxins into systemic circulation
PSS acquired with chronic liver failure

Front 45

what is the cause of death for sheep with chronic copper poisoning?

Back 45

haemolytic anaemia (crisis)

Front 46

significant bilirubinuria is seen in intravascular haemolysis.
True or false?

Back 46

False. Only conjugated bilirubin is excreted in urine therefore bilirubinuria is significant in diffuse liver failure and pronounced in bile duct obstruction

Front 47

what is a cause of intrahepatic cholestasis in sheep?

Back 47

sporidesmin

Front 48

what toxin causes the so called "boxing glove liver"

Back 48

sporidesmin (atrophy of left lobe)

Front 49

what agents can cause photosensitisation secondary to bile obstruction in ruminants

Back 49

sporidesmin, PAs

Front 50

will thrombosis of the portal vein cause ascites?

Back 50

no

Front 51

briefly describe the pathogenesis initiating acute pancreatitis

Back 51

activation and release of pancreatic enzymes causing autodigestion and fulminant acute inflammation of surrounding tissues

Front 52

what conditions can cause serum amylase to be high?

Back 52

- acute pancreatitis
- pancreatic neoplasia
- decreased renal clearance
can be mildly elevated in some non-pancreatic diseases i.e. spey etc can cause increased AML

Front 53

what sample tube do you used for amylase

Back 53

heparin

Front 54

what can increase lipase in serum?

Back 54

- pancreatitis
- steroids
- hepatic and pancreatic neoplasia
- azotaemia
- GIT and hepatic disease
- following abdominal surgery

Front 55

what causes hypochromic RBCs?

Back 55

decreased haemoglobin content i.e. iron deficiency anaemia

Front 56

what are Howell-Jolly bodies?

Back 56

remnant of previous mitosis consisting of DNA therefore stain purple on Wright's stain. Usually quite small and towards periphery of RBCs
may indicate regeneration

Front 57

what commonly causes Burr cells?

Back 57

uraemia (renal failure) and electrolyte depletion

Front 58

what types of anaemias are likely to show pancytopenia or bicytopenia?

Back 58

1. aplastic anaemia
2. myelopthisic anaemia
reflect defects in stem cells or marrow micro-environment

Front 59

what conditions are dacryocytes seen with?

Back 59

- iron deficiency anaemia
- myelopthisic anaemia

Front 60

what is the protein that plays a major role in iron regulation especially in inflammatory conditions?

Back 60

hepcidin

Front 61

what is the mechanism behind anaemias due to defects in nucleotide synthesis and name two examples.

Back 61

stem cells and cytokines are normal or increased but marrow microenvironment and nutrients are deficient. The marrow cells respond to increased epo but the cells produced are defective
1. vit B12 deficiency
2. folate deficiency

Front 62

why are vitamin B12 deficiencies uncommon in large herbivores?

Back 62

because they produce it from microbes in the rumen and large intestine

Front 63

what plant can cause deficient folate leading to anaemia in cattle?

Back 63

macrozamia palm

Front 64

what is the most common heart disease we see in dogs?

Back 64

mitral valve disease

Front 65

where is the mitral valve located?

Back 65

it is the left atrioventricular or bicuspid valve between the left atrium and left ventricle

Front 66

what are the clinical signs of heart disease?

Back 66

1. altered rate
2. altered rhythm
3. presence of adventitious sounds
4. altered area of auscutation
5. altered audibility (fluid)

Front 67

define murmur

Back 67

auditory vibration of long duration than normal heart sounds created when laminar flow is disrupted

Front 68

define arrhythmia

Back 68

a disturbance in the normal cardiac rhythm due to an abnormality in impulse initiation and impulse propagation

Front 69

the clinical signs of heart failure are attributable to?

Back 69

1. accumulation of fluid (congestion)
2. tissue/organ ischaemia (decreased CO)

Front 70

what are the clinical signs of decreased CO?

Back 70

- pale mm
- weak pulse
- cold extremities
- prolonged CRT
- tachycardia (compensatory)

Front 71

describe the body's compensatory mechanisms to decreased CO

Back 71

1. SNS
- decreased CO--> baroceptors become desensitised due to low blood volume and pressure and hence decreased stretch of blood vessels therefore they cannot induce PNS so SNS stimulation dominates = increased myocardial contractility and vasoconstriction = increased HR, BP and CO
2. RAAS --> low CO = decreased renal perfusion which stimulates release of renin--> ANGI-->ANGII = vasoconstriction (increased BP= increased afterload)--> aldosterone = sodium and water resorption = increased blood volume (increased preload)- oedema

Front 72

what are the clinical signs of LS CHF?

Back 72

- pulmonary oedema
- crackles
- cyanosis
- tachypnoea

Front 73

what are the clinical signs of RS CHF?

Back 73

- ascites
- pleural effusion
- peripheral oedema
- jugular pulses
- hepatojugular reflex

Front 74

what is the most common cardiomyopathy in cats?

Back 74

hypertrophic cardiomyopathy (HCM)

Front 75

what are the main mechanisms of cardiac failure in heart disease that will cause decreased CO?

Back 75

1. sustained pressure overload
2. sustained volume overload
3. altered normal contractility
4. altered normal compliance
5. altered normal rate and rhythm

Front 76

what are haemodynamic disorders characterised by?

Back 76

1. an abnorml pattern of blood flow through the heart (increased preload) i.e. valvular insufficiency
2. an impedence to chamber inflow or outflow (increased afterload)i.e. pulmonic stenosis

Front 77

what are the pathological changes associated with sustained pressure overload?

Back 77

1. concentric ventricular hypertrophy
2. post stenotic valvular dilation due to pressure build up
3. systolic murmur (turbulent blood flow)

Front 78

what are the causes of pulmonary hypertension?

Back 78

1. pulomnary artery hypertension
- idiopathic
- dirofilariasis
- congenital L-R shunts i.e. patent ductus arteriosus
2. LS heart disease
- cardiomyopathy
- valvular disease
back up of fluid on LS
3. lung diseases +/- hypoxaemia
- COPD
- intersitial lung disease
- alveolar hypotension disorder
4. chronic pulmonary thrombotic or embolic disease
- dirofilarias
- neoplasia
- thromboembolism
5. miscellaneous
- compression of pulmonary vessels
- lymphadenopathy
- granulomatous disease

Front 79

what are the two main causes of sustained volume overload of the heart?

Back 79

1) valvular insufficiency
2) congenital defect (shunt)

Front 80

what are the pathological changes associated with sustained volume overload?

Back 80

- eccentric chamber dilation and hypertrophy
- endocardial fibrosis (jet lesions)
- early systolic murmur due to increased vol of blood trying to be pumped into the ventricle (more severe types can be throughout all of systole)

Front 81

how do we get pulmonary oedema with mitral valve disease?

Back 81

due to LAV valvular insufficiency there is more blood remaining in the left atrium hence less being ejected by the aorta therefore we have decreased cardiac output and compensatory mechanisms may lead to pulmonary oedema over time

Front 82

you will hear a continuous murmur with Patent ductus arteriousus (PDA)
true or false?

Back 82

true. - continuous flow: LV-->aorta--> PDA-->PA-->RA

Front 83

what kind of hypertrophy occurs in RA and RV with atrial septal defect?

Back 83

eccentric (increased preload)

Front 84

what does a R-L shunt in the heart usually develop secondary to?

Back 84

severe pulmonary disease

Front 85

what are the two major causes of altered normal contractility?

Back 85

1) insufficient myocytes
2) dysfunctional myocytes

Front 86

hypertrophic cardiomyopathy is a disease of?
a) increased pressure overload
B) increased volume overload
c) altered normal contractility
d) altered normal compliance
e) altered normal rate and rhythm

Back 86

d) altered normal compliance

Front 87

name two heart conditions of altered compliance

Back 87

- HCM
- pericarditis

Front 88

how do we have decreased CO with tachyarrhythmias?

Back 88

because when there is tachycardia the heart is constantly beating at a rapid rate so there is reduced time for ventricular filling--> may be weaker than normal ventricular contraction-->decreased stroke volume= decreased CO

Front 89

name the causes of vagally-mediated bradycardia

Back 89

- chronic respiratory disease
- GIT disease
- hypothyroidism
- drugs: (digoxin, xylazine)
- ocular or retrobulbar disease
- central neurological disease

Front 90

list causes of non-vagally mediated bradycardia

Back 90

- feline DCM
- drug toxicities (carbamates/OP?)
- anaesthesia
- end stage heart failure

Front 91

what are the causes of atrial standstill/SA node failure?

Back 91

- excess vagal stimulation (suppresses SA node firing)
- drugs i.e. digitalis
- "sick sinus syndrome"/ bradytachy syndrome
-DCM (rare)
- SA node destruction i.e. neoplasia, atrial myocarditis

Front 92

what does clostridium chauvei cause?

Back 92

black leg, severe arrythmias

Front 93

what is mulberry heart disease caused by?

Back 93

Vit E/sel deficiency (arrhythmias of ventricular origin--> death

Front 94

what is the predilection site for haemangiosarcomas?

Back 94

right atrium

Front 95

list the components of Virchow's triad

Back 95

1. static blood
2. vessel wall injury
3. hypercoaguability

Front 96

how do cats with aortic (distal) thromboembolism present?

Back 96

- very painful initially
- nail beds cyanotic
- leg muscles hard (depletion ATP-rigor)
- cold hind limbs
- absent femoral pulses
- proprioceptive deficits

Front 97

what are the diseases that cause hypoalbuminaemia?

Back 97

- protein losing nephropathy
- protein losing gastropathy
- protein losing dermopathy
- liver failure

Front 98

what are the causes of oedema?

Back 98

1. decreased plasma oncotic pressure
2. increased hydrostatic pressure
3. increased intersitial osmotic pressure
4. increased vascular permeability
5. decreased lymphatic drainage

Front 99

what are some causes of increased IV hydrostatic pressure?

Back 99

- IV fluids- plasma expansion
- congestive heart failure
- venous obstruction i.e. torsion

Front 100

what are the factors for controlling haemorrhage

Back 100

1. platelets
2. coagulation cascade/clotting factors
3. vessel wall factors (vascular repair and return of vascular integrity)

Front 101

list some causes of vasculitis

Back 101

- Strongylus vulgaris- horses
- malignant catarrhal fever
- sterile- drugs i.e. antibiotics
- Erysipothrix rhusipathae--> arteritis leading to thrombisus and ischaemia

Front 102

what are the primary vascular causes of haemorrhage?

Back 102

1. large vessel rupture i.e. ruptured haemangiosarcoma, trauma
2. endothelial damage from systemic viral/ bacterial infections i.e. CAV1, hog cholera, gram -ves
3. coagulopathy

Front 103

what can happen to the liver +/- spleen if bone marrow is not functioning?

Back 103

extramedullary haemopoesis--> these organs enlarge and are producing cells because bone marrow cant

Front 104

what is the critical level for haemoglobin?

Back 104

30-40g/L

Front 105

what is the half life for neutrophils in circulation?

Back 105

6-8hrs (limits usefulness of transfusions for this)

Front 106

how long does it take to produce more neutrophils (bone marrow)

Back 106

6 days

Front 107

what is the WBC critical value?

Back 107

1 x 10^9/L

Front 108

what is the critical platelet value

Back 108

<50 x 10^9/L

Front 109

what are the 3 requirements for RBC production?

Back 109

1. stem cells- self replicate, migrate to spleen etc
2. regulators- cytokines
3. microenvironment i.e. need space in marrow, nutrients and oxygen

Front 110

androgens slightly increased RBC true or false?

Back 110

true i.e. sertoli cell tumour in the dog

Front 111

how can cytokines negatively regulate RBC production?

Back 111

- inflammatory mediators can suppress RBC production i.e. TFN, IL-1, IFN i.e. anaemia of inflammatory disease

Front 112

is an animal with hypothyroidism likely to have increased or decreased RBC production?

Back 112

decreased because dont have extra stimulation for RBC production

Front 113

proliferative white cell phases in the circulation are indicative of what condition?

Back 113

leukaemia

Front 114

when might we see regenerative anaemias w/o reticulocytes in the circulation?

Back 114

horses

Front 115

when might we see increased RBC regeneration without anaemia?

Back 115

- hypoxia- i.e. high altitude environment or respiratory disorder, or circulatory problem- poor perfusion to tissues
- compensated anaemia

Front 116

anaemia only occurs when RBC destruction exceeds RBC production true or false?

Back 116

true

Front 117

what is a key morphological clue for horses with anaemia

Back 117

anisocytosis

Front 118

what are the clinical findings of an anaemic animal?

Back 118

1. pale mm (critical sign but can be associated with CVS abnormalities)
2. increased HR (compensatory mechanism)
3. systolic murmur- lack of viscosity of blood causes rattle when heart contracts
4. increased RR (compensatory)
5. weakness, lethargy

Front 119

what are the PCV reference ranges for anaemic dogs?

Back 119

mild anaemia: 0.3-0.37L/L
moderate: 0.2-0.29L/L
marked: <0.2L/L

Front 120

What are the steps to assess pathogenesis of anaemia?

Back 120

1. look at lab data and clinical signs
2. check hydration status (haemoconcentration/haemodilution)
3. check protein
4. is it regenerative or non-regenerative?
5. What do the RBC indices suggest? (MCV, MCHC)
6. what clues from RBC morphology?
7. check platelets

Front 121

what are the causes of haemorrhagic anaemia?

Back 121

1. internal parasites (blood in faeces) or external parasites
2. GIT ulcer
3. coagulopathy
4. trauma
5. defect of platelet numbers or function (petechial haemorrhages)
6. ruptured neoplasm-->usually older animals
7. ruptured spleen, liver (trauma)

Front 122

what type of anaemia is more regenerative? haemolytic or haemorrhagic?

Back 122

haemolytic

Front 123

why are haemolytic anaemias more regenerative than haemorrhagic anaemias?

Back 123

iron delivery is the rate-limiting step of RBC production and delivery of iron is much quicker/greater in haemolytic anaemia so generally more regenerative

Front 124

what are the protective mechanisms by the liver in response to intravascular haemolysis?

Back 124

1) produces haptoglobin to complex with Hb then destruction occurs in hepatocyres
2) if exhaust haptoglobin some of the free iron oxidises to methaemaglobin and breaks down to haem and globin-->protective protein hemopexi binds with haem molecule and carries to liver

Front 125

what are the causes of haemolytic anaemia?

Back 125

genetic:
1. hereditary elliptocytosis - compensated anaemia, genetically abnormal RBC shapes- elliptical cells
2. hereditary stomatocytosis
- stomatocytes- slit of pallor
Acquired
1. Heinz bodies haemolytic anaemia
- exhaustion of G6PD
- Hb irreversible denaturation
- haemolysis is primarily extravascular
2. hypophosphataemia
3. IMHA
4. nitrate poisoning
5. mechanical damage
6. red cell parasitism
- Theileria and babesia= intravascular haemolysis
- Rickettsia (myco)- extravascular haemolysis
7. hypersplenism
- splenomegaly, haemangiosarcoma
- extravascular haemolysis
8. bacterial haemolysins
9. animal and plant haemolysins
10. chemical haemolysins
11. physical agents
- xs water ingestion esp juvenille goats and calves
- intravascular haemolysis

Front 126

what is the underlying pathogenesis of heinz body anaemia as a result of prolonged exposure to oxidant drugs?

Back 126

causes exhaustion of G6PD which is the rate limiting enzyme for producing NADPH which maintains glutathione in a reduced state so glutathione can protect Hb from oxidants = irreversible denaturation of Hb

Front 127

what can cause falsely elevated Hb levels?

Back 127

lipaemia, Heinz bodies (denatured Hb)

Front 128

what is the most common cause of Heinz body haemolytic anaemia in dogs?

Back 128

onions

Front 129

what types of anaemias cause pancytopenia?

Back 129

- aplastic anaemia
- myelopthisic anaemia

Front 130

with defects in nucleotide synthesis will RBCs be macrocytic or microcytic?

Back 130

macrocytic- dont have the nutrients to divide

Front 131

what is the common poikilocyte we see with iron deficiency anaemia?

Back 131

dacryocytes

Front 132

why might we see increased platelets with iron deficiency anaemia?

Back 132

may have thrombopoeisis with erythropoesis- bilinear stem cell line ?

Front 133

what are the diagnostic features for iron deficiency anaemia?

Back 133

serum iron <9mmol and TIBC>63mmol/L, iron saturation levels 16% (n.33%)
bone marrow shows absence of haemosiderin with Perls stain (compare to anaemia of inflammatory disease)

Front 134

what are the causes of iron deficiency anaemia?

Back 134

1. increased loss i.e. external haemorrhage
- parasites
2. reduced absorption or intake i.e. GIT neoplasia
3. neonates- have low due to low levels in mothers milk
- dietary deficiencies uncommon

Front 135

what can basophilic stippling indicate?

Back 135

ruminants- RBC regeneration
carnivores may indicate lead poisoning ( occurs only chronic anaemia in dogs)

Front 136

what is a spherocyte?

Back 136

a RBC with reduced surface area not volume. Commonly seen in IMHA when the RBC has anti-RBC-antibody on so as it passes through spleen or liver macrophages ingest the membrane

Front 137

do spherocytes have central pallor?

Back 137

no

Front 138

when do we most commonly see spur cells/ acanthocytes?

Back 138

when there is abnormal microenvironment in spleen--> enlarged splenic capsules- splenic sinuses with static blood, low oxygen, low glucose- most commonly haemangiosarcoma

Front 139

what are codocytes?

Back 139

RBCs with increased surface area per unit volume, look like targets. Due to cholesterol loading on the membrane-->any condition causing hypercholesterolaemia i.e. cholestasis

Front 140

what type of poikilocytes are common for renal failure?

Back 140

burr cells/echinocytes (renal toxins)

Front 141

when do we see more Howell-Jolly bodies on RBCs?

Back 141

- increased RBC production i.e. can indicate regeneration
- hypersplenism

Front 142

what do the presence of shift platelets indicate?

Back 142

increased thrombopoesis

Front 143

what is the normal refernce range for platelets in circulation, and is this the same for horses?

Back 143

approx 150-400 x 10^9/L but horses can be as low as 70 x 10^9/L

Front 144

when will see clinical signs of thrombocytopenia?

Back 144

when platelet count <50 x 10^9/L

Front 145

how many platelets should we normally see per oil immersion field?

Back 145

10-25

Front 146

can we do BMBT (buccal mucosal bleeding time test) for animals with low platelet counts?

Back 146

no only do on animals with normal platelet numbers (testing function)

Front 147

what type of tube do we used for measuring factors XI and XII?

Back 147

ACT (activated clotting time tube)

Front 148

what are the clinical signs of haemophilia A?

Back 148

-haematomas
- bleeding into major body cavities
- haemarthroses
- prolonged bleeding time

Front 149

we do we see poikilocytes such as keratocytes and schiztocytes in DIC?

Back 149

because the cells are mechanically injured by fibrin strands

Front 150

if we have reduced anti-thrombin III what does this tell us?

Back 150

we have consumption of anticoagulant factors i.e. plasminogen, Protein C and S

Front 151

when we take a blood sample we can assess:
a) circulating PMN pool
b) marginated PMN pool
c) both pools
d) none of the above

Back 151

a)circulating pool

Front 152

what is the life span of PMNs in tissues?

Back 152

2-3 days

Front 153

why do we have a sudden drop in neutrophils (and platelets) with endotoxaemia?

Back 153

causes neutrophils to marginate

Front 154

what do corticosteroids do to the marginating neutrophils?

Back 154

inhibits migration of marginated pool to tissues

Front 155

are vacouoles in the cytoplasm a reliable indicator of toxic change in neutrophils?

Back 155

not a reliable indicators because can get when left in EDTA for too long

Front 156

what are acquired causes of defects in phagocytic function?

Back 156

1. steroids
2. diabetes mellitus
3. uraemia
4. leukaemia (might have massive numbers but not functional)
5. some viral and bacterial infections

Front 157

if we see a marked neutrophilia in a cow what does this tell us about the duration of neutrophilia?

Back 157

cow has very minimal MGR and takes a long time to mount marked response so if we see marked neutrophilia know has been going on for at least 7-8 days

Front 158

when is lymphocytosis commonly seen?

Back 158

with viral infections

Front 159

do greyhounds have a lower or higher lymphocyte and neutrophil count compared to other dogs?

Back 159

lower

Front 160

does adrenaline cause an increase in the PMN circulating or marginated pool?

Back 160

circulating

Front 161

what are the features of a stress leukogram/physiological leukocytosis?

Back 161

- WBC <25 x 10^9/L
- lasts about 30min
- circulating pool >marginated
- also transient lymphocyte count in cat and horse
- splenic contraction in horse = increased PCV
- fear, stress, excitement
- adrenaline causes demargination

Front 162

why do we see lymphopaenia with a stress leukogram?

Back 162

due to lysis or redistribution of lymphocytes (depending on species)

Front 163

what does the return of eosinophils on haematology indicate?

Back 163

recovery

Front 164

what will stilboestrol do to the haematology?

Back 164

- dogs are particularly sensitive
- leukocytosis/paenia?
- thrombocytopaenia
- decreased PCV

Front 165

what do endotoxins and anaphylaxis do to WBCs and platelets?

Back 165

increased margination of WBCs and platelets--> neutropenia and thrombocytopenia
- may have lymphopenia
- transient
-often see severe neutropenia in horses with salmonella

Front 166

what are basophils often seen with?

Back 166

eosinophilia, lipaemia

Front 167

what count of lymphocytes in blood would be a strong indicator of lymphoid leukaemia?

Back 167

dog: >20 x 10^9/L

Front 168

what stain can we use to show up non-staining hyphae?

Back 168

periodic acid shift stain (PAS)

Front 169

when doing cytological evaluation what can the nuclear features tell us?

Back 169

- indicates state of growth
- look at for malignancy
- can look at sub-nuclear detail of chromatin to tell us about cell cycle
- nucleolus = rapid growth
- hyperchromasia in malignant cells (sometimes polyploidy and have more DNA)

Front 170

When doing cytological evaluation what can cytoplasmic detail tell us?

Back 170

- lineage of cell/functional differentiation
euplasia
proplasia
retroplasia- too much injury- shrivelled growth nuclear membrane
dyskarious- irregular nuclear margins= irregular nucleus- may be early sign malignancy

Front 171

define dyskariosis:

Back 171

irregular nuclear margins = irregular nucleus- may be an early sign of malignancy

Front 172

define retroplasia

Back 172

too much injury has occurred - degeneration of cell into more primitive type- shrivelled growth nuclear membrane

Front 173

define euplasia

Back 173

a cell with normal growth

Front 174

what tube do we collect cytology samples into?

Back 174

EDTA

Front 175

what can we use to encourage cell exfoliation for sampling?

Back 175

use saline wash- i.e. bronchial or prostatic wash, then sediment cells

Front 176

whats stain is good for identifying tumours?

Back 176

H & E- good for detecting nuclear detail by clearing cytoplasm- in tumours alot of change is in the nucleus

Front 177

what are the cytology requirements?

Back 177

1. adequately cellular
2. monolayer
3. intact cells
4. minimum blood contamination
5. several smears representative of entire lesion

Front 178

what are the three main features we observe in cytological smear?

Back 178

1. cell types (%)
2. subcellular detail
3. background

Front 179

what are the general cytological features of malignancy?

Back 179

- macrocytosis (use RBCs 4micron,to compare size)
- Hypercellularity
- pleomorphism
- nueclear changes

Front 180

what are the nuclear features of malignancy?

Back 180

- high N:C ratio
- anisokaryosis
- nuclear deformation by other nuclei
- enlarged nucleoli
- irregular shapes and angularity of nucleus/nucleoli
- marked variation in shape, size number of nucleoli
- chromatin
- mitotic figures; abnormal mitoses, stray chromosomes
- binucleate cells

Front 181

describe the cytological features of carcinomas?

Back 181

- tight desmosomes- cells cluster together
- large nuclei
- abundant cytoplasm
- nucleoli prominent
- in adenocarcinomas b/c secretory have nucleus pushed to one side= eccentric

Front 182

describe the cytological features of adenocarcinomas

Back 182

- eccentric nucleus
- signet shape with secretory product
- secretory inclusions
- cytoplasmic vacuolation

Front 183

describe the cytological features of sarcomas?

Back 183

- poor cellularity
- bipolar cytoplasm- characteristic feature
- indistinct cytoplasmic margins

Front 184

bipolar cytoplasm is a characteristic feature of what kind of malignancy?

Back 184

sarcomas (mesenchymal)

Front 185

what are the advantages of cytological evaluation?

Back 185

- quick diagnosis
- minimal equipment
- low cost
- simple
- no anaesthetic required

Front 186

what are the disadvantages of cytology?

Back 186

- does not include histopathology
- may be inconclusive
- requires skill in interpretation
- a negative finding does not rule out malignancy

Front 187

if we suspect bacterial infection when collecting cytology sample what should we do?

Back 187

- collect second sample into plain tube (EDTA can destroy bacteria)

Front 188

if our sample clots on exposure to air what does this tell us?

Back 188

increased clotting factors and fibrinogen

Front 189

what does the buffy coat layer contain?

Back 189

all nucleated cells including nucleated RBCs and tumour cells - important for detecting malignancy

Front 190

what tube do we use for body cavity fluids analysis?

Back 190

plain tube

Front 191

what are the features of chylous effusion?

Back 191

- triglycerides >1.13mmol/L (compare with blood- 3:1)
-well differentiated mature lymphocytes
- may have occasional plasma cell and occasional lymphoblast
- if chronic can cause irritation--> inflammatory cells and finely vacuolated macrophages

Front 192

what is pseudochylous effusion commonly seen with?

Back 192

cardiac abnormalities in cats

Front 193

what are the features of a body cavity fluid sample from cat with FIP

Back 193

- high protein- high globulin
- low cell count (0.03 x 10^9/L)
- dense protein background
- dont expect neutrophils with viral infections
- polycloncal lymphocytes produce many immunoglobulins but not effective in eliminating virus

Front 194

why do we see karyolytic neutrophils with bile peritonitis?

Back 194

bilirubin and bile are highly irritant causing karyolytic change

Front 195

what stain do we use to identify haemosiderin?

Back 195

Perl's Prussian

Front 196

what are common adenocarcinoma sources in animals?

Back 196

GIT, prostatic, sometimes respiratory

Front 197

what is the major cytokine produced by CD8 + T-cells and what is it required for?

Back 197

IL-2, major growth factor for T-cells, required to undergo clonal expansion

Front 198

what two interleukins do helper T-cells produce?

Back 198

IL-1, IL-6

Front 199

what are the four types of hypersensitivities?

Back 199

1. type I- IgE mediated
2. type II- cytotoxic hypersensitivity, IgG, IgM, complement mediated
3. Type III- immune complex disease, IgG, IgM, complement
4. Type IV- delayed type hypersensitivity- not mediated by antibody, mediated by sensitised T-cells

Front 200

what are the primary effector cells of Type I HS?

Back 200

basophils and mast cells

Front 201

what are the features of Type I HS?

Back 201

1. increased vascular permeability
2. oedema
3. infiltrate of eosinophils

Front 202

what happens when we have re-exposure to antigen stimulating IgE (anaphylaxis)?

Back 202

- degranulation of mast cells release histamine--> bronchoconstriction, increased vascular permeability
- basophils can respond in the same way
- synthesis and release of PGs, leukotrienes, bradykinins

Front 203

what do vasoactive mediators cause?

Back 203

- local inflammation
- systemic anaphylaxis
- vasodilation and oedema

Front 204

list some examples of type one hypersensitivities

Back 204

- atopic dermatitis
- allergic rhinitis
- FAD
- milk allergy
- acute bronchiolasthma
- anaphylaxis

Front 205

describe the pathogenesis of milk allergy in cows

Back 205

can be a problem if milking is delayed = increased intra-mammary pressure forcing casein into blood- casein recognised as foreign protein. Reaction varies depending where it occurs i.e. localised uticaria (hives), multifocal cutaneous oedema. Can precipitate anaphylazis and may lead to death upon re-exposure

Front 206

how does systemic anaphylaxis occur?

Back 206

occurs in sensitised animals --> have specific IgE circulating and are re-exposed to antigen
- mast cells in lung primary target

Front 207

type II hypersensitivities are mainly mediated by?
a) IgE
b) IgG
c) IgM
d) IgD
e) complement

Back 207

b) IgG

Front 208

what are the general responses to type II hypersensitivity?

Back 208

- fever
- cutaneous signs
- polyarthritis
- pain or joint swelling

Front 209

describe haematological disorders associated with type II hypersensitivity

Back 209

- haemolytic anaemia
- thrombocytopenia
- neutropenia
- lymphopenia

Front 210

give examples of conditions associated with type II hypersensitivity

Back 210

1. antibiotics or NSAIDs can cause haemolytic anaemia
2. infections can induce antibodies that cross react with host tissue i.e. streptococcus antigen can cross react with cardiac collagen in rheumatic heart disease
3. auto-immune- antibody to DNA i.e. systemic lupus erythematosis (SLE)
4. transfusion reactions- mismatched blood (not a problem for first transfusion)

Front 211

what type of hypersensitivity is associated with immune complexes?

Back 211

type III

Front 212

what is the big problem with immune complexes?

Back 212

they activate complement

Front 213

what are the clinical signs assoc with type III HS?

Back 213

- fever
- erythema
- polyarthritis, joint pain
- ataxia, behaviour changes (immune complexes in choroid plexus?)
- isosthenuria, PU/PD, proteinuria, abdominal pain

Front 214

where do immune complexes deposit?

Back 214

in locations with filtering functions:
- blood vessel walls
- synovial membranes
- choroid plexus
- glomeruli

Front 215

describe complex glomerulonephritis

Back 215

- immune complexes deposit in glomerulus
- antibodies leave circulation and complex with: glomerular self antigens and exogenous antigens planted in glomerulus
- brown staining with immune-histochemical stain
- can be caused by viral and chronic bacterial infections
- can lead to nephrotic syndrome: proteinuria, hypoalbuminaemia, azotemia, hypercholesterolaemia, +/- amyloidosis, hypercoaguability
- common in horses, rare other sp

Front 216

what are some examples of delayed type hypersensitivities?

Back 216

1. granulomatous infections i.e. Mycobacteria, coccidoides, Blastomycoses
2. Encephalitis- canine distemper virus
3. contact hypersensitivities i.e. drugs, plastics, canine contact allergic dermatitis
4. hypothyroidism (type II and IV)
5. autoimmune adrenalitis- dogs

Front 217

what may cause us to suspect B-cell and plasma cell immunodeficiency?

Back 217

recurrent bacterial or (especially) recurrent viral infections

Front 218

what is the major way in which B-cell/plasma cell IDs are acquired?

Back 218

through failure of passive transfer
- failure of neonate to feed
- early removal from milk
- colostrum deficiencies
- decreased GIT absorption

Front 219

what are the manifestations of congenital hypogammaglobulinaemia?

Back 219

- recurrent respiratory or skin bacterial infections
- excessive allergies--> inability to bind and remove allergens or may have over-reactive immune components

Front 220

what are the manifestations of deficiencies in phagocytosis?

Back 220

- increased bacterial infections of skin, RT, GIT
- may have neutropaenia
- decreased phagocytic number or function
- decreased opsonisation

Front 221

what are acquired causes of phagocytic immunodeficiency?

Back 221

- FeLV, FIV
- drug induced granulocytopaenia- cytotoxics, anti-convulsants, oestrogens

Front 222

name a marker for T-cells and B-cells

Back 222

CD3- T-cells
CD79a- B-cells

Front 223

list the main supporting neuroglial cells

Back 223

- astrocytes
- oligodendrocytes
- microglia
- ependymal cells lining ventricular system

Front 224

what cells are responsible for myelination in the CNS?

Back 224

oligodendrocytes

Front 225

what cells are responsible for myelination in PNS?

Back 225

Schwaan cells

Front 226

why is the CNS prone to oedema?

Back 226

no lymphatic drainage

Front 227

what forms the blood brain barrier and what is its purpose?

Back 227

formed by endothelial cell and astrocyte interactions. Prevents antibodies, certain drugs and infectious agents

Front 228

can activated lymphocytes enter the BBB?

Back 228

yes

Front 229

mannitol is contraindicated as diuretic in CNS disease
True or false?

Back 229

true

Front 230

what are the consequences of akabane virus at 3-4months gestation, 5-6 months gestation and near term (9 months) in cattle?

Back 230

- 3-4months: porencephaly (cavities and cysts in brain) and hydrancephaly
5-6 months: motor neurons of spinal cord ventral horn more susceptible= reduced or absent motor nerves-->arthrogyrposis
9 months: abortion or encephalomyelitis

Front 231

what nervous tissue is least susceptible to hypoxia?

Back 231

microglia

Front 232

what is the common sequele to hypoxia of neuronal cells?

Back 232

neuronophagia

Front 233

describe central chromatolysis/axonal reaction

Back 233

reaction of neuronal cell body to axonal damage in both CNS and PNS. neuron swells, nucleus becomes peripheral and the Nissyl substance disperses to give a pale colour to cell body= chromatolysis, nucleolous increases in size

Front 234

when do we see chromatolytic-like change?

Back 234

seen in some dysautonomias i.e. Equine grass sickness, Key-Gaskell syndrome of cats

Front 235

what are the clinical signs of equine dysautonomia (EGS)

Back 235

- anorexic with patchy sweating
- absent gut sounds
- dry faecal balls covered in mucus
+/- muscle tremors
- assume an 'elephant on tub' posture

Front 236

what is Wallerian degeneration?

Back 236

occurs when a nerve is severed or crushed and the part of the axon separated from the cell body degenerates distal to the site. After transection of the axon, the proximal and disal axonal stumps swell (24hr post injury), the myelin sheath overlying the degenerating portion of the neuron degenerates too (interdependence)

Front 237

what are the possible outcomes for Wallerian degeneration in the PNS and the CNS

Back 237

- in the PNS if supporting connective tissue is in tact the Schwann cells can proliferate and aid axonal regeneration or if there is compromise to surrounding connective tissue may have functional loss.
- In CNS likely to be permanent loss of axon

Front 238

what do we see accumulating in the neurons of older animals?

Back 238

lipofuscin accumulates due to oxidative damage to cell membranes

Front 239

what kind of diseases typically have neuronal vacuolation?

Back 239

spongiform encephalopathies i.e. bovine, feline, may also be seen in surrounding neurophil due to swelling of astrocyte processes

Front 240

cytoplasm of astrocytes ODCs often demonstrable in routine stains
true or false?

Back 240

false

Front 241

what are the microglia?

Back 241

bone marrow derivatives, smallest glia, phagocytose dead cells and lipids- essentially macrophages of the nervous system

Front 242

what are gitter cells?

Back 242

Lipid laden microglia

Front 243

list the various functions of astrocytes

Back 243

- formation BBB
- NT uptake esp glutamate
- metabolic buffering
- detoxification
- nutrient supply
- glucose transport
- electrical insulation
- antioxidant roles (high levels glutathione peroxidase)
- secretion growth factors and chemokines
- astrocytosis--> repair and scar formation

Front 244

oligodendrocytes sometimes accumulate around degenerating neurons in a process called...?

Back 244

satellitosis

Front 245

which type of oedema in the CNS cant be reduced by diuretics? vasogenic or cytotoxic?

Back 245

cytotoxic

Front 246

what are herniations in the CNS commonly a response to?

Back 246

increased intracranial pressure

Front 247

what are the types of CNS herniation?

Back 247

1. subfalcine herniation- movement of medial portion of cerebral hemisphere laterally under falx cerebri
2. transtentorial- movement of medial temporal lobe of cerebral hemisphere under tentorium cerebelli
3. Tonsillar/coning- protrusion of cerebellar tonsils caudally through foramen magnum

Front 248

what are the consequences of transtentorial herniation?

Back 248

* mid brain compression- possible coma, damage to oculomotor nerve= pupilary dilation
* compression of midbrain aqueduct= further increase ICP
* compression of cerebral artery = occipital infarction and arterial or venous tears = haemorrhage

Front 249

what are the consequences of cerebellar coning?

Back 249

- medulla compression= respiratory depression and death

Front 250

which nervous tissue is most susceptible to ischaemic damage:

Back 250

hippocampus, purkinje cells of cerebellum and neurocortical neurons

Front 251

why is the CNS prone to infarctions following ischaemia?

Back 251

because mainly supplied by end arteries

Front 252

what are the causes of arterial obstruction in the CNS?

Back 252

- thrombosis i.e. arteritis- equine herpesvirus
- embolism of cardiac thrombi- fibrocartilagenous embolism in dogs, occ cats- source of cartilage unknown but thought to be from IV disks
- tumour
- air
- fat
-arterial compression from masses i.e neoplasia
- herniation

Front 253

explain excitotoxicity in the CNS

Back 253

- imbalance in stimulatory neurotransmitters- important cause of death in prenumbral region of ischaemic lesions. Ischaemia causes release of glutamate and aspartate= excess neuron stimulation which causes reversible acute swelling of depolarised neurons + Na+, Cl- and H2O influx. Glutamate also opens NDMA channels= Ca2+ influx-->uncoupling of mitochondrial electron transport- activates NO sythetise and generates reactive o2 and nitrogen species

Front 254

how do astrocytes reduced excitotoxic damage?

Back 254

by converting glutamate to glutamine and neutralising free radicals

Front 255

what are common causes of excitotoxicity in CNS?

Back 255

- spinal cord damage
- epilepsy
- hypoglycaemia
- ischaemia
- trauma
- Kainic acid derived from red algae

Front 256

what aetiological agent causes microabscesses in the CNS and what is the route of infection?

Back 256

listeria, via oropharynx and up trigeminal nerve= multifocal small abscesses in midbrain

Front 257

what are the clinical signs of neuro-meningeal listeriosis?

Back 257

- typical circling- most characteristic sign
- torticollis
- aimless wandering
- uncoordination- paddling movements
- cranial nerve paralysis- strabismus, salivation

Front 258

what is the aetiological agent of thrombotic meningoencephalitis?

Back 258

Histophilus somni

Front 259

what type of animal do we most commonly see TME in? (thrombotic meningoencephalitis)

Back 259

- feedlot cattle

Front 260

what are the clinical signs of thrombotic meningoencephalitis?

Back 260

- multifocal infarcts in cerebrum at grey/whte junction
- circling
- ataxia
- head pressing
- blindness
- pyrexia
- neutropenia- left shift
- convulsions
- coma
- death
- affects other organs i.e. lungs

Front 261

how can FIP differ from normal viral infections in the CNS

Back 261

FIP coronavirus type III (wet) and IV (dry) may cause multifocal and random pyogranulomas in CNS, eye, liver, kidney, serosa and meninges, this pyogranulomatous inflammation is somewhat different to usual lymphocytic pattern of viral infections in CNS

Front 262

how does canine distemper virus (CDV) cause demyelination?

Back 262

immune destruction of oligodendrocytes

Front 263

what are the CNS manifestations of viral infection during
a) first third gestation
b) mid gestation

Back 263

a) may cause persistent infections with loss of cell function +/- hypomyelination
b) cell death and congenital defects i.e. cerebellar hypoplasia (akabane virus, feline parvo), arthrogryposis- Akabane virus

Front 264

lymphocytic perivascular cuffing is a hallmark of?

Back 264

viral infection in CNS

Front 265

what are the CNS features of Rabies?

Back 265

- lymphocytic perivascular cuffs
- negri bodies in hippocampus and purkinje cells of cerebellum
- +/- neuronal degeneration

Front 266

what disease do we see the 'nibble reaction' with in sheep

Back 266

scrapie

Front 267

what are the CNS features of prion diseases?

Back 267

- neuronal vacuolation
- neurophil vacuolation
- astrocytosis

Front 268

what is a prion?

Back 268

protease resistant variant of normal prion protein

Front 269

what are the features (CNS and clinical signs) of scrapie?

Back 269

- hindquarter pruritis
- nibble reaction
- recumbency
- neuronal vacuolation
- astrocytosis
- shrunken, angulated neurons

Front 270

what type of inflammation is seen with fungal infections in the CNS?

Back 270

granulomatous

Front 271

what cell type can protozoa replicate in in CNS?

Back 271

astrocytes

Front 272

list some protozoa that effect CNS

Back 272

- Toxoplasma Gondii
- Encephalitozoon
- Neospora caninum
-Neospora hughesi
- Trypanosoma

Front 273

describe manifestations of cauda equina neuritis (polyneuritis equi)

Back 273

- tail and anus sphincer paralysis
- sensory loss in perineal region--> faecal retention, croup muscle atrophy and hindlmb ataxia
gross pathology:
- enlargement and haemorrhagic discolouration of extradural nerve roots in lumbosacral and caudal regions of spinal cord
- granulomatous inflammation with demyelination and axon degeneration

Front 274

describe the lesions/manifestations of Horner's syndrome

Back 274

- unilateral, efferent, sympathetic degeneration to eye and surrounding structures causing:
- Ptosis (drooping upper eyelid)
- Misosis (pupillary constriction)
- aniscoria
- Enophthalmus (posterior displacement eyeball in orbit)
- sweating in horses
- third eyelid protrusion and sometimes conjunctival hyperaemia

Front 275

what are the pathogenic mechanisms for Horner's syndrome?

Back 275

1. First order neuron- in hypothalamus to T1-3 of spinal cord
2. Second order neuron-thoracic sympathetic trunk to cervical ganglion
3. Third order neuron- post ganglionic fibres arriving at cranial cervical ganglion
- T1-3 spinal trauma, disc disease, neoplasia, fibrocartilagenous embolism, brachial plexus avulsion, trauma or neoplasia affecting vagosympathetic trunk, middle ear disease or retrbulbar disease, thoracic neoplasia or mediastinal mass

Front 276

what are the symptoms in young puppies with protozoan polyradiculoneuritis?

Back 276

- acute paresis, limb extension, lose patellar and withdrawal reflexes but do not lose pain sensitisation
in brain, muscles and spinal cord- inflammation and necrosis esp in lumbosacral spinal cord

Front 277

how do we diagnose genetic CNS storage diseases?

Back 277

- clinical signs, histological findings, biochemical analysis, measuring enzyme activities, genetic tests i.e. PCR

Front 278

describe globoid cell leukodystrophy (Krabbe's disease)

Back 278

- autosomal recessive deficiency in lysosomal enzyme in dogs, cats, sheep, humans
- prominent CNS changes: astrocytosis, demyelination, PAS-positive globoid cell accumulations, neurons with karyolysis and vacuoles
- PNS signs: pelvic limb paralysis, reflex loss, muscle atrophy, globoid macrophages seen in peripheral nerves with myelin loss and axon swelling

Front 279

what is the pathogenesis of demyelination in Krabbes disease?

Back 279

- accumulation of lipid products toxic to oligodendroctes and Schwann cells

Front 280

define abiotrophy

Back 280

premature death of cells after differentiation

Front 281

what are the clinical CNS signs of hypocalcaemia in cattle?

Back 281

- ataxia
- hyperexcitability
- paresis
- coma and death

Front 282

what are the clinical signs of grass tetany (hypomagnesaemia) in cattle?

Back 282

- ataxia
- convulsions
-staggers
- muscular spasms
- respiratory distress
- collapse
- death

Front 283

what are the clinical signs of ketosis in ovine pregnancy toxaemia?

Back 283

- often with hypoglycaemia
- listlessness
- aimless walking
- opisthotonus
- bruxism (teeth grinding)
- blindness
- ataxia
- recumbence
- coma, death

Front 284

what change might we see in CNS with hepatic encephalopathy

Back 284

- enlarged astrocytes
- spongiform changes in CNS

Front 285

what are the manifestations of diabetic neuropathy in
a) cats
b) dogs

Back 285

- accompanies diabetes mellitus
a) hind limb weakness and classic plantigrade stance with muscle wasting and proprioceptive loss
b) progressive paraparesis, proprioceptive deficits, reduced spinal reflexes and muscle atrophy

Front 286

describe the manifestations of hypothyroid neuropathy

Back 286

- cranial and peripheral nerve dysfunction in hypothyroid dogs
- laryngeal paralysis, hindlimb ataxia, paresis and muscle wasting
- CN deficits may be seen (V trigeminal, VII facial, VIII vestibulocochlear)
* distal axonopathy has been proposed

Front 287

what is the causeof thiamine deficiency in cattle?

Back 287

overgrowth of thiaminase producing bacteria usually after change in diet i.e. bracken fern

Front 288

what are the roles of thiamine in the CNS

Back 288

-needed in various enzymes in energy metabolism, neurotransmitter synthesis and regulation of oxidative stress

Front 289

what are the causes of thiamine deficiency in carnivores?

Back 289

uncooked fish contains thiaminases, heated diets, poor diets

Front 290

what are the clinical signs of thiamine deficiency in
a) cattle
b) cats

Back 290

a) depression, stupor, ataxia, head pressing, cortical blindness, opisthotonus, paddling, death
b) anorexia, vomiting, base-wide stance, ataxia, circling seizures,opisthotonus, weakness, death

Front 291

which vitamin deficiency is associated with goose-stepping gait and hindlimb ataxia

Back 291

vitamin B5 pantothenic acid

Front 292

which vitamin deficiency causes retinal degeneration in pigs and cattle on deficient rations?

Back 292

vitamin A

Front 293

describe the manifestations of riboflavin (B2) deficiency in chickens

Back 293

- peripheral neuropathy
- chickens unable to extend distal limb and may have plantigrade stance- curly toe
- they become unable to stand and mortality after 3 wks
- demyelination due to poor energy supply to Schwann cells at time of high demand

Front 294

what is copper deficiency thought to affect in CNS?

Back 294

affect ability if axons to maintain myelin sheath in CNS

Front 295

how is delayed swayback (enzootic ataxia) acquired?

Back 295

- lambs and kids born to Cu deficient mothers or high Molybdenum/zinc-->antagonise
Cu absorption
- occurs shortly after to birth, up to 6 months

Front 296

what are the manifestations of enzootic ataxia?

Back 296

- hindlimb ataxia, chromatolysis of motor neurons in brain stem and spinal cord, wallerian degeneration in distal regions of long white matter tracts

Front 297

what may be involved in motor neuron disease in horses?

Back 297

vitamin E deficiency and high copper levels in spinal cord suggesting possible oxidative injury as underlying mechanism

Front 298

which is more common acute lead poisoning or chronic lead poisoning?

Back 298

acute

Front 299

what animal do we typically see chronic lead poisoning in?

Back 299

horses

Front 300

what are the clinical signs of acute lead poisoning?

Back 300

- CCN, encephalopathy-->seizures, blindness, hysteria

Front 301

what are the manifestations of chronic lead poisoning?

Back 301

- periperal neuropathy- cranial and peripheral nerve paresis with lip and anal sphincter paralysis
- larygneal hemiplegia, pharyngeal paresis with regurgitation
- segmental demyelination and remyelination
- Schwann cell damage seems to be primary insult

Front 302

what is the pathogenesis of strychnine poisoning?

Back 302

blocks glycine post-synaptically (inhibitory NT)
- very similar to tetanus except tetanus blocks glycine pre-synaptically
- resulting disinhibition = violent spasms, tetanic neuron activity

Front 303

what are the lclinical signs of OP/carbamate poisoning

Back 303

- SLUD (salivation, lacrimation, urination, defecation), miasis, muscle twitches +/- seizures

Front 304

what is the pathogenesis of OP/carbamate poisoning?

Back 304

inhibit AChesterase, therefore ACh is not inhibited and persists at muscarinic and nictotinic receptors= disruption of some central synapses, NMJs and autonomic nerve endings

Front 305

describe salt toxicity in pigs

Back 305

occurs when there is a high salt diet and water deprivation;
- when water intake is resumed, there is rapid rehydration of the brain= swelling and vascular compression-->CCN and eosinophilic meningitis
CS:
- inappetance, dehydration, head pressing, incoordination, blindness, circling, paddling, convulsions

Front 306

what is the pathogenesis of carbon monoxide toxicity?

Back 306

haemoglobin has strong affinity for carbon monoxide therefore binding more carbon monoxide and causing hypoxia
- ischaemic necrosis of most susceptible cells; purkinje cells, cortical laminae and hippocampus neurons

Front 307

there are often no microscopic lesions in CNS with tetanus poisoning,
True or false?

Back 307

true

Front 308

describe the pathogenesis of tetanus

Back 308

tetanus toxin may be acquired after colonisation of deep wound - reaches CNS via peripheral nerves- releases spinal motor neurons from inhibitory effects of renshaw cells by pre-synaptic blockade of glycine--> muscle spasms, predominant extensior tone due to greater strength in these muscles

Front 309

describes the pathogenesis of botulinum toxicity

Back 309

-pre formed toxin ingested or toxoinfectious aetiology where toxin elaborated after infection by clostridium ( horses)
- prevents ACh release pre-synaptically at NMJ - lower motor neuron dysfunction

Front 310

describe the pathogenesis of focal symmetrical encephalomalacia

Back 310

- chronic form of enterotoxaemia caused by Clostridium perfringens type D
- absorption of toxin from gut caan cause a symmetrical necrosis affecting areas of the thalamus, internal capsule, brainstem and white matter of cerebellum
- often no gross lesions, may have FSE, pulpy kidney, blindness
-

Front 311

what are the clinical signs of Key-Gaskell syndrome in cats?

Back 311

- anorexia, vomiting, depressed, third eyelid protrudes, mydriasis
- chromatolysis and neuron loss in enteric plexuses and autonomic ganglia, also brain stem nuclei and occ DRG and motor neurons

Front 312

what does yellow star thistle toxicity cause?

Back 312

nigropallidal malacia (like Parkinson's)- hypertonia of lips, tongue and facial muscles--> inability to eat, drink and have wooden expression

Front 313

what is the inheritence pattern of congenital myasthenia gravis?

Back 313

autosomal recessive

Front 314

describe the pathogenesis of acquired myasthenia gravis

Back 314

seems to be associated with thyoma in dogs and cats- the thymus contains cells with internal muscle component that present as antigen under aberrant immune system development or thyoma- therefore normal number of ACh end plate receptors blocked by circulating antibodies
- type II hypersensitivity
- animals are weak, voice change, may be fatal

Front 315

describe the pathogenesis of equine laryngeal hemiplegia

Back 315

- left dorsal cricoarytenoid muscle loss of innervation by left recurrent laryngeal nerve
- neurogenic muscle arophy with progressive distal loss of large myelinated fibres= distal axonopathy
- polyneuropathy- other long nerves of hindlimbs affected
- mediastinal lymphosarcoma can cause bilateral laryngeal hemiplegia
- RS may be caused by pervivascular injections in right jugular vein

Front 316

describe pathogenesis and manifestations of stringhalt

Back 316

-in Aus occurs in later summer, early autumn
- ingestion of certain plants, may involve mycotoxin
- abnormal gait with exaggerated hindlimb flexion and delayed extension
- peroneal and tibial nerve degeneration and neurogenic atrophy of hindlimb muscles- thought to be distal axonopathy
- sometimes laryngeal hemiplegia occurs concurrently

Front 317

describe feline ischaemic neuropathy

Back 317

-occurs secondary to thromboembolism (lodges in distal aorta i.e. due to HCM)
- distal limbs cool, femoral pulses absent, proprioceptive deficits
- degeneration of sciatic nerve and branches with demyelination and ischaemic axonal degeneration

Front 318

how can pituitary tumours cause clinical signs?

Back 318

- by being SOL in CNS= compression of overlying brain and optic pathways
- by abnormal hormone secretion- PU/PD, polyphagia, truncal hair loss (hyperadrenocorticism)

Front 319

name some common PNS neoplasias

Back 319

1. Schwannomas
2. neurofibromas
3. lymphoma (Marek's disease)

Front 320

where do dogs commonly have Schwannomas?

Back 320

brachial plexus, requiring limb amputation

Front 321

define contusion

Back 321

haemorrhage with integrity of parenchyma

Front 322

animals recovering from acute CNS trauma may develop what as a delayed complication?

Back 322

epilepsy

Front 323

what can severe spinal cord trauma with thoracolumbar disc extrusion lead to with hopeless prognosis?

Back 323

progressive ascending myelomalacia hopeless prognosis due to respiratory paralysis in 2-4 days if reaches cervical areas

Front 324

define neuropraxia

Back 324

least severe PNS injury- conduction interruption often due to segmental demyelination w/o severe axon involvment

Front 325

define axonomesis

Back 325

= separation and damage of axons - fair prognosis

Front 326

define neurotmesis

Back 326

- most severe injury= complete severence of all structures of the nerve- poor prognosis for regeneration

Front 327

how does calving paralysis occur?

Back 327

- thought to be through compression of obturator nerve along medial shaft of ilium affecting adductor, gracillis and pectineus muscles
- L6 root of sciatic may also be compressed
- once cow is down, secondary nerve compression damage may occur

Front 328

does the lung have a large functional reserve?

Back 328

yes

Front 329

what type of immunoglobulin is important in URT disease?

Back 329

IgA

Front 330

what can negatively affect cilia beating?

Back 330

- fever (>39oC), low body temp or low air temp (need air to be warmed and humidified- nasal cavity)
- drugs
- viruses (herpes, calici, adeno)
- hot dry air (inflammation) increases viscosity of the mucus and causes mucus to crust
- increased serous fluid- increases aqueous layer of mucus barrier and cilia rendered ineffective
- decreased serous fluid increases the viscosity of the mucus- mucus tears exposes epithelium

Front 331

what are the aetiologies of rhinitis/sinusitis?

Back 331

1. physical- heat, dryness, dust
2. chemical- H2S, NH3
3. viral- herpes, adeno, calici, parainfl, rhino
4. bacterial- Bordatella bronchisepta, Streptococcus equi- mucopurulent fibrinous exudate
- can be secondary to viral
5. fungal- aspergillus, cryptococcus
6. Parasitic- dictyocaulus (lungworm)
7. type I hypersensitivity- allergies

Front 332

what are the pathological changes associated with brachycephalic airway syndrome?

Back 332

- stenotic nares, soft palate hyperplasia, secondary nasal and laryngeal oedema

Front 333

are nasal neoplasias in dogs normally benign or malignant?

Back 333

usually malignant, respiratory adenocarcinomas followed by SCC, commonly mestastasise to brain, liver, lymph nodes

Front 334

what are the clinical signs of nasal neoplasia?

Back 334

- airflow obstruction
- nasal deformity
- discharge, irritation, pain
- epistaxis associated with nasal and sinus tumours in small animals

Front 335

what are the consequences of excessive division of type II pneumocytes?

Back 335

- alveolar hyperplasia, alveolar wall thickening- can be caused by toxic gases i.e. pure O2

Front 336

what comprises the alveolar diffusion barrier?

Back 336

1. endothelial cells of capillaries
2. basement membrane (capillaries?)
3. type 1 pneumocytes

Front 337

how much of air breathed in is dead space?

Back 337

1/3

Front 338

which gas is more soluble O2 or CO2?

Back 338

CO2

Front 339

When do we have respiratory failure?

Back 339

inability to maintain PP of O2 and CO2
- O2 <60-70mmhg
-CO2 >40-50mmHg

Front 340

what are the clinical signs of respiratory failure?

Back 340

- change to rate and depth of breathing --> cyanosis
- polypnoea- rapid rate of shallow breathing i.e. panting
-hyperapnoea- rapid rate deep breathing
- dyspnoea- laboured, difficult breathing
- oligopnoea- decreased resp rate
+/- changes in percussion, adventitious sounds- crackles/wheezes

Front 341

define hyperpnoea

Back 341

rapid, deep breathing

Front 342

define oligopnea

Back 342

- decreased RR

Front 343

define polypnoea

Back 343

- rapid rate of shallow breathing i.e. panting

Front 344

describe restrictive respiratory failures

Back 344

- intrapulmonary: alveolar fibrosis, thickening of diffusion barrier, pulmonary oedema, atelectasis, intersistial pneumonia/pneumonitis--> decreased compliance
- extrapulmonary: haemothorax, chylothorax, pyothorax, pneumothorax--> collapse of lung, SOL i.e. neoplasia, chest deformities
- manifests as respiratory dyspnoea (inspiratory dyspnoea), hypoxaemia, polypnoea, eucapnia or hypocapnia

Front 345

describe obstructive respiratory failures

Back 345

- obstruction- blocks conducting airways- prevents elastic recoil of lungs
- inflammatory diseases: bronchitis, bronchiolitis, emphysema (decreased elasticity)
- manifests as hypoxaemia
- hypercapnia due to difficulty removing Co2 in blood due to obstructive changes
- may have inspiratory or expiratory dyspnoea

Front 346

what are the causes of pulmonary oedema?

Back 346

1. hydrostatic oedemia
- LSHF, hypovolaemia i.e. after XS IV fluids
2. permeability oedema
- endotoxins, pure O2, drugs

Front 347

what kind of appearance do lungs with pulmonary oedema have?

Back 347

mottled appearance due to fluid accumulation +/- brown tinge due to accumulation of haemosiderin

Front 348

what is atelectasis?

Back 348

collapse of the lungs and failure to inflate, alveoli are deflated- results in reduced or absent gas exchange

Front 349

what are the causes of atelectasis?

Back 349

1. acquired
- compressive - abdominal viscera (i.e. tumour)- increased pleural air/fluid, reversible before fibrosis
- obstructive- bronchitis, bronchiolitis- alveoli distal to obstruction fill with fluid, reabsorption of fluid, problems with surfactants- may lead to fibrosis= collapse
2. congenital

Front 350

what is the main clinical outcome of atelectasis?

Back 350

ventilation-perfusion mismatch (Va/Q mismatch)= right to left shunt arising- can lead to hypoxia

Front 351

describe the pathogenesis of emphysema

Back 351

An obstructive respiratory disorder--> overdistension of alveoli or alveoli duct- air is forced from alveoli into intersitium= intersitial emphysema, intersitial air in CT around alveoli--> bullae due to large scale rupture- large areas of collapse where air gets trapped- dead air--> loss of elastic recoil = decreased gas exchange and V/Q mismatch

or can have emphysema due to inflammation- excessive proteases made by macrophages and PMNs and break down elastin--> decreased gas exchange

can be secondary to obstructive disease

Front 352

what are the clinical signs of emphysema?

Back 352

(V/Q mismatch)
- hypoxia, hypercapnia
- expiratory dyspnoea, soft breath sounds, wheeze

Front 353

what are the risk factors for bronchopneumonias?

Back 353

- innate defences compromised; environment, population, host factors--> overcrowding, stressed, dust, ammonia in air--> compromise to mucociliary and often cellular defences --> virus damage cilia--> opportunistic bacteria colonise--> bronchopneumonia

Front 354

which is the least severe pneumonia?

Back 354

bronchopneumonias

Front 355

what can you expect on PE of animal with bronchopneumonia

Back 355

1. half excited cough reflex when palpate trachea
2. +/- nasal discharge
3. respiratory pattern may be normal, obstructive or restrictive (very advanced disease- entered intersitium)
4. louder breath sounds because have exudate and sound transmit better through solids than air, increased intensity
5. can hear crackles as pressures change through respiratory cycle and air randomly pushes through exudate
6. +/- systemic signs, fever, malaise, ill-thrift

Front 356

what are features of chronic bronchopneumonia?

Back 356

- no more neutrophils sent to site and exudate reabsorbed--> consolidation
- may have fibrosis if gets into intersitium
- bronchiolar walls can adhere and become non-patent

Front 357

list some examples of bronchopneumonias?

Back 357

1. enzootic pneumonias
- pigs, calves, sheeps
- microbial complexes
2. neonatal- foals
3. recurrent-dog i.e. ciliary dyskinesia
4. stage 3 aspiration pneumonia

Front 358

what can be seen on PE of animals with fibrinous/lobar pneumonia?

Back 358

- presents as acute/peracute may present as sudden death
- soft cough
- nasal discharge
- halitosis (due to tissue necrosis)
- restrictive respiratory pattern b/c pulmonary parenchyma diseased and has lost compliance
- respiratory distress, expiratory grunt, pain
- often normal breath sounds but can have increased intensity and crackles b/c is exudative but nowhere near extent of bronchopneumonia
- cyanosis

Front 359

do patients with fibrinous pneumonia usually heal entirely?

Back 359

rarely, fibrosis

Front 360

describe pathology of fibrinous/lobar pneumonias

Back 360

- lobar pattern or diffuse if really bad
- consolidation
- fibrinous exudate in alveoli
- secondary pleuritis
- microvascular damage--> V/Q mismatch--> cyanosis, hypoxaemia coupled with widened alveolar diffusion barrier, necrosis
- +/- abscessation, +/- granulomatous
- pleural adhesions
commonly causes death

Front 361

what is pneumocystis carini/pneumonia

Back 361

- opportunistic fungal pathogen only occurs in some dogs of certain breeds i.e. mini daschunds due to immunodeficiency

Front 362

what do we see on PE of animals with proliferative/intersitial pneumonias?

Back 362

- restrictive pattern dyspnoea (lost compliance)
- normal breath sounds - can be increased (not fluid in airways)
- low pitch inspiratory crackles b/c airways collapsed in expiration- 'velcro sounds'
- no systemic signs- no cytokines, unless primary lung disease
- increased intra-thoracic pressure- if chronic transmitted into pulmonary artery= high PA pressure= cor pulmonale --> right side of heart not designed to work under high pressure = RS concentric hypertrophy

Front 363

what type of pneumonia do we see rib imprints with?

Back 363

intersitial pneumonia, due to loss of compliance and fibrous tissue present

Front 364

compare the pattern of lung damage in bronchopneumonias vs intersitial pneumonias

Back 364

- cranioventral in bronchopneumonia
- caudodorsal/diffuse in intersitial

Front 365

describe pathological features of intersitial pneumonias

Back 365

- rib imprints
- paucity of inflammatory cells, mild and secondary inflammation only
- poor lung expansion, poor lung compliance
- diffuse/caudodorsal
- type II pneumocytes replace type I pneumocytes- reasonably irreversible and permanently changes gas exchange
- expanded alveolar intersitium

Front 366

give examples of intersitial pneumonias

Back 366

1. intersitial pneumonia of WHWT
2. SIRS (systemic inflammatory response syndrome)- dogs
3. cattle- mouldy hay - ARDs
4. infections-
sheep- mycoplasma
distemper virus- dogs
5. toxins:
smoke
praquat
O2
crotileria- plant pastures

Front 367

what is the most common primary pulmonary tumour?

Back 367

bronchoalveloar carcinoma

Front 368

what are the most common secondary/metastatic tumours affecting lungs

Back 368

- mammary carcinoma
- osteosarcoma
- haemangiosarcoma

Front 369

what is a major clinical sign of pulmonary neoplasia?

Back 369

haemoptysis

Front 370

what might you see on PE of animal with pulmonary neoplasia?

Back 370

- restrictive pattern dyspnoea
- hypertrophic osteopathy--> occurs with lung masses, thought to be vagally mediated (changes in blood flow to periosteum)-->
- painful periostatic reaction to hindlimbs, soft tissue swelling (oedema), lame--> take radiograph- often will be mass in chest
- lameness in cats- often mestastasise to D3

Front 371

what are the functions of the urinary system

Back 371

1. excretion of waste products and toxins from the body
2. maintenance of plasma ECF volume and composition
3. recovery and recycling of potentially valuable metabolites i.e. glucose, amino acids
4. regulation of acid base and electrolyte balance
5. Ca2+and P homeostasis- regulated by PTH
6. hormone synthesis- epo, vit D
7. store and voluntarily discharge urine

Front 372

what controls the permeability of the DT and CD to water?

Back 372

AVP/ADH via V2 receptor
- AVP greatly increases permeability of the membrane to water and water moves passively into hypertonic intersitium

Front 373

what happens in the distal tubules and collecting duct when there is an absence of AVP i.e. CDI?

Back 373

the membranes are impermeable to water and dilute urine is excreted

Front 374

when will glucosuria occur?

Back 374

when glucose concentration in filtrate overwhelms tubular maxima or when there is tubular dysfunction

Front 375

what causes renal glucosuria?

Back 375

when the glucose transport mechanism is absent or defective i.e. fanconi syndrome in basenjis, true renal glucosuria is rare

Front 376

what causes increased Phosphorus reabsorption from tubules?

Back 376

hypophosphataemia and insulin= increased Na+PO4 cotransporter

Front 377

what causes increased phosphorus excretion?

Back 377

hyperphosphataemia and increased PTH = decreased Na+PO4 cotransporter= increased fractional clearance of phosphorus (FCR-P)

Front 378

what is azotaemia always associated with?

Back 378

,decreased GFR

Front 379

describe the aetiopathogenesis for failure to empty LUT disorders

Back 379

1. sacral spinal lesion- pelvic N
= secondary detrusor atony
- disc disease
- trauma i.e. car accident, tail pull

2. lumbar or more rostral lesion
- persistence of pudendal nerve = constriction striated urethral sphincter

Front 380

describe the features of a sacral lesion affecting the bladder

Back 380

- pelvic N = detrusor atony so bladder cant contract to urinate
- pudendal nerve - = relaxation of urethral striated sphincter so easy to express bladder
- big, expressible bladder
- concurrent storage and voiding disorder
- urine dribble

Front 381

describe the features of a lumbar lesion affecting the bladder

Back 381

- no hypogastric nerve function
- persistence of pudendal nerve = tonic striated urethral sphincter + no pelvic N function = no bladder contraction
- big, unexpressible bladder
= voiding failure

Front 382

describe the clinical presentation for failure to empty LUT disorders

Back 382

- big, full bladder
- oligouria/anuria
- stranguria/dysuria
- systemically unwell -->ARF(?)
- secondary detrusor atony (no pelvic nerve function)

Front 383

describe the clinical pathology assoc with failure to empty LUT disorders

Back 383

- abnormal urinalysis- prone to UTIs
- post-renal azotaemia (big full bladder = backs up on kidneys decreasing GFR)

Front 384

what are the clinical signs of cystitis?

Back 384

- failure to store
- stranguria, pollakiuria
- malodourous discoloured urine +/- WBCs, RBCs

Front 385

what are the causes of neurogenic bladder/urethral malfunction

Back 385

1. functional
- oestrogen increases alpha receptors on urethral smooth muscle and sphincter
- when females desexed = less oestrogen = less sensitive to hypogastric N= decreased sympathetic tone- internal smooth muscle sphincter can atrophy
less resistance = leaking

2. trauma
- IV disc
- motor vehicle accident
- neoplasia/inflammation

Front 386

what can sometimes occur in female animals following sterilisation in regards to bladder function

Back 386

- oestrogen increases alpha receptors for hypogastric nerve on urethral smooth muscle/sphincter
- with less oestrogen= less sensitive to hypogastric nerve= decreased sympathetic tone= flaccid urethral sphincter-->atrophy
- with less resistance to overcome can have urine leaking

Front 387

what are the factors influencing development of urinary crystals ?

Back 387

- urine pH
- diet (protein)
- decreased H2O intake
- UTI - especially predisposes to struvite - in dogs not cats
- genetics
- metabolism

Front 388

what are the common uroliths in dogs?

Back 388

1. struvite
2. calcium oxalate
3. cysteine
- irish setters, dachshunds
4. ammonium urate
- dalmations
- liver failure

Front 389

what type of urolith may we see in a dog with liver falure

Back 389

ammonium urate

Front 390

what are the common uroliths in cats?

Back 390

1. calcium oxalate
2. struvite

Front 391

what are the common uroliths in ruminants?

Back 391

1. calcium carbonate/oxalate
- diet- silic
- urine pH
2. struvite
- high diet PO4 or high grain
- phytooestrogens- sheep diet- water belly- lodge in distal urethra

Front 392

what is the major local problem associated with transitional cell carcinoma (of bladder)

Back 392

because in trigone obstructs the urethra
- surgical resection feasible but rapid relapse so not often done, tend to treat with chemotherapy or NSAIDs

Front 393

describe enzootic haematuria in cattle

Back 393

- carcinomas and sarcomas (epithelial and mesenchymal) of bladder
- associated with bracken fern
- haematuria and anaemia

Front 394

what tests can we use to test for liver disease

Back 394

1. CBC
2. biochemistry
3. tests of liver function
- bile acids
- ammonia in maltese
4. urinalysis
5. liver biopsy
6. abdominal imaging

Front 395

what can serum biochemistry tell us about liver disease?

Back 395

- helps identify presence or absence of liver disease
- indicates if acute or chronic
- indicates signs of systemic disease

Front 396

what may we see on CBC with animals with liver disease?

Back 396

1. mild, poorly, poorly-regenerative anaemia (anaemia of chronic inflammation)
2. microcytosis seen in dogs with P-S shunts
- due to alterations in iron metabolism
- microcytosis w/o anaemia in cats
3. poikilocytosis
- hypercholesterolaemia or mechanical damage
- schiztocytes, acanthocytes, leptocytes, codocytes (hypercholesterolaemia)
4. +/- leukocytosis and neutrophilia
5. impaired platelet aggregation and function

Front 397

what does increased induced hepatic enzymes suggest?

Back 397

made in response to changes in the liver i.e. increased pressure in bile duct
- commonly reflects cholestasis

Front 398

list the liver leakage enzymes

Back 398

1. ALT (alanine aminotransferase)
2. AST (aspartate aminotransferase)
3. SDH (sorbitol dehydrogenase)
4. GLDH (glutamate dehydrogenase)
5. OCT (ornithine carbamyltransferase)

Front 399

in what animal(s) is ALT considered to be specific for hepatic injury?

Back 399

cats and dogs

Front 400

other than liver injury, what else could cause an increase in serum ALT?

Back 400

muscle damage/necrosis i.e. snake bite

Front 401

what animal(s) does AST have high activity in?

Back 401

all domestic species

Front 402

what may interfere with measuring AST levels for liver disease and how can we overcome this interference?

Back 402

also high in skeletal muscle, no test to differentiate muscle and liver AST so measure CK

Front 403

why is it that we see milder increases in AST/ALT in chronic liver disease?

Back 403

because not many hepatocytes

Front 404

what is the best leakage liver enzyme to measure in the horse and why is it rarely used?

Back 404

SDH and rarely used because very short half life (clearance <12hrs) best sampled <4-6 post collection

Front 405

what species is SDH useful in?

Back 405

horse, sheep, goats and cows

Front 406

what species is GLDH is useful in?

Back 406

sheeps, goats, cattle
- good for detecting acute hepatocelluar damage in horses- if chronic GLDH will return

Front 407

what are the induced hepatic enzymes?

Back 407

1. ALP (alkaline phosphatase)
2. GGT (gamma glutamyltransferase)

Front 408

induced liver enzymes are typically membrane bound and not released in the serum with increased membrane permeability.
True or false?

Back 408

true.
usually due to cholestasis, drug or hormonal effects

Front 409

what animals is ALP not commonly included in serum biochem for?

Back 409

cattle, sheep and goats due to wide reference range for these species

Front 410

what are the isoenzymes of ALP of clinical use?

Back 410

i) hepatic
ii) bone (young animals)
iii) corticosteroid induced (dogs only)
iv) intestinal and placental forms

Front 411

is hepatic ALP elevated in acute or chronic liver disease?

Back 411

elevated in both

Front 412

what is the half life of ALP in the dog and the cat?

Back 412

cat 6h
dog 72h

Front 413

what conditions cause highest serum concentrations of ALP?

Back 413

i) cholangitis
ii) biliary cirrhosis
iii) extrahepatic bile duct obstruction i.e. pancreatitis

Front 414

when might you see increased intestinal/placental ALP?

Back 414

- colicy horses
-late term pregancy

Front 415

comment on the sensitivity and specificity of ALP and GGT for hepatobilliary disease

Back 415

ALP- high sensitivity but low specificty (many isoforms)
GGT - low sensitivity but high specificity except in cat

Front 416

what limits the usefulness of ALP in cats

Back 416

lower levels than in dogs and short half life (6hr)

Front 417

what enzyme is the preferred indicator of cholestasis in birds?

Back 417

GGT

Front 418

we do we see elevated bilirubin levels in the blood after hepatic insult has been removed?

Back 418

due to the long half life of bilirubin

Front 419

is it a problem to see bilirubin in cats urine?

Back 419

yes because cats have a much higher renal threshold for bilirubin than dogs- normal to see some in dogs urine

Front 420

what are the critical bile acid fasting and post-prandial values for cats and dogs

Back 420

fasting: >13umol/L can be the result of hepatobiliary disease
post-prandial: >30umol/L dogs and >25umol/L cats = high probability of hepatobiliary disease

Front 421

most animals with congenital or acquired PSS have marked increase in post-prandial bile acid concentrations.
True or false?

Back 421

true

Front 422

what conditions cause animals to have increased bile acids?

Back 422

1. PSS
2. liver failure
3. cholestasis
4. inappropriate contraction of gall bladder (anticipation of being fed)
5. small intestine bacterial overgrowth- mild increase

Front 423

why is the bile acids test unreliable in maltese and maltese X and what test can be done instead?

Back 423

unreliable because have lots of microhepatic shunts. Use ammonia instead

Front 424

are albumin levels affected by acute liver disease?

Back 424

no

Front 425

how much functional liver mass has to be lost before we see decreased albumin levels

Back 425

>75%

Front 426

list reasons for hypoalbuminaemia

Back 426

- starvation
- cachexia
- protein losing enteropathy, nephropathy, dermopathy
- liver failure
- whole blood loss
- inflammation
- burns
- parasitism
- body cavity effusions

Front 427

why do we see hypoglycaemia with liver failure?

Back 427

the liver is the major organ for gluconeogenesis and glycogenolysis and insulin clearance therefore with liver failure we have decreased gluconeogenesis and decreased insulin clearance = hypoglycaemia

Front 428

what can result in decreased cholesterol levels in the blood?

Back 428

- end stage liver failure
- PSS

Front 429

what must we always do before performing a liver biopsy?

Back 429

check clotting factors

Front 430

what are the functions of the liver?

Back 430

1. carbohydrate metabolism- gluconeogenesis, glycogenolysis
2. glycogen storage
3. protein metabolism/synthesis
4. urea synthesis
5. lipid metabolism
6. ketogenesis
7. bilirubin metabolism
8. bile acid production +metabolism
9. intermediary metabolism, detoxification and elimination of toxins
8. phagocytose particles/immune function

Front 431

what is the major cell type involved in liver fibrosis?

Back 431

stellate (ito) cells located in space of Disse

Front 432

what are hepatic pit cells?

Back 432

large granular lymphocytes

Front 433

what are the hepatic itinerant cells?

Back 433

leukocytes

Front 434

where does the portal vein carry blood from?

Back 434

carries deoxygenated blood from the GIT to the hepatocyte

Front 435

what is the main exocrine function of the liver?

Back 435

excretion of bile

Front 436

what is bile comprised of?

Back 436

water, cholesterol, bile acids, bilirubin, inorganic ions etc

Front 437

what are the 3 major purposes for bile synthesis?

Back 437

1. excretion of waste products i.e. cholesterol, bilirubin, metabolised xenobiotics
2. facilitate digestion- lipids
3. buffering- neutralises pH of ingesta

Front 438

what are the mechanisms of liver injury?

Back 438

- metabolic activation of chemicals via cytochrome P450 to reactive species
- stimulation of auto-immunity
- stimulation of apoptosis or necrosis if hepatocytes overwhelmed
- disruption of calcium homeostasis- surface blebbing and lysis
- canalicular injury
- mitochondrial injury

Front 439

what are the 3 major patterns of acute hepatocellular necrosis?

Back 439

1. random
2. zonal
3. submassive/massive

Front 440

describe zonal hepatocellular necrosis

Back 440

- affects hepatocytes within defined areas of hepatic lobules i.e. centrilobular
- degenerate hepatocytes swell- pallor- necrosis--> appears red due to dilation/congestion of sinusoids and haemorrhage
- pale, friable and slightly enlarged liver with rounded margins and enhanced lobular pattern

Front 441

describe massive/submassive hepatocellular necrosis

Back 441

necrosis of entire lobule(s)
- loss of hepatic architecture--> acutely enlarged with congestion
- histologically see blood filled spaces within connective tissue stroma
- may be fatal or may result in nodular regeneration following lobular collapse and replacement by fibrous scar tissue--> chronic small liver with wrinkled capsule
- massive toxin dose, infarct, torsion, porcine vit E/sel deficiency (hepatosis dieteca)

Front 442

describe the catgeories of zonal hepatocellular necrosis

Back 442

1. centrilobular/ periacinar
- most common
- zone 3
- area of greatest drug metabolising activity (MFOs)
- see pallor in centre of lobule
2. paracentral
- milder version of centrilobular
- reflects partitioning of lobular blood flow- wedge shape
- often early change that precedes centrilobular necrosis
3. midzonal necrosis
- rare
- CCl4, phenobarbitone, aflatoxins etc
4. periportal
- uncommon
- affects zone 1-->extensive change
- strong toxins or toxins that dont require metabolism i.e. phosphorus
5. bridging
- characterised by connection of areas of necrosis between different lobules

Front 443

what are the early CSs of acute liver failure

Back 443

- dullness, depression, hepatic encephalopathy
- vomiting
- weakness (hypoglycaemia)
- abdominal pain
- PU/PD
- bleeding tendencies
- bilirubinuria

Front 444

what are the late clinical signs of acute liver failure?

Back 444

- icterus
- seizures (ammonia)
- coma

Front 445

what are the manifestations of chronic liver failure?

Back 445

- hypoalbuminaemia
- portal hypertension--> ascites
- acquired PSS's
- cutaneous lesions: photosensitisation, hepatocutaneous syndrome in dogs
- impairment of immune function- endotoxaemia/systemic infection

Front 446

what are the routes of infection of abortigenic herpesviruses?

Back 446

1. transplacental
2. passage through birth canal
3. contact with infected siblings
4. contact with dam's oronasal secretions

Front 447

what tissues does canine adenovirus have predilection for?

Back 447

hepatic, endothelium and renal epithelium

Front 448

describe two types of reversible liver injury

Back 448

1. steroid hepatopathy
- corticosteroids, Cushings
- marked hepatic glycogen deposition--> hepatic swelling- midzonal (glycogen storage) necrosis and hydropic change
- common WHWTs
- only recorded in the dog
2. lipidosis/fatty liver
- most common cause is large scale fat mobilisation for energy
- secondary to diabetes mellitus in cats (insulin deficiency= cant mobilise glucose)
- hydropic change--> more fluid in hepatocytes--> ballooning
- in extreme cases cellular swelling may impede blood and bile flow
- severe detected by hepatomegaly

Front 449

what are the early clinical signs of chronic liver disease?

Back 449

- weight loss
- lethargy

Front 450

what are the late CSs of chronic liver disease?

Back 450

- ascites (most cases)
- poor growth/ill thrift/ poor body condition
- behavioural changes--> hepatoencephalopathy
- cutaneous lesions--> photosensitisation herbivores, hepatocutaneous syndrome in carnivores
- seizures
- coma
- icterus

Front 451

describe the MOA of pyrolizidine alkaloids in causing liver disease

Back 451

- cause necrosis of hepatocytes but also prevent regeneration by irreversibly blocking mitotic activity of dividing liver cells in prophase - the cells get bigger but dont divide and eventually die
- megalocytes important diagnostic indicator

Front 452

what is an important diagnostic featured shared by PA, phomopsin and aflatoxin poisoning of the liver?

Back 452

megalocytes

Front 453

describe the MOA of phomopsin mycotoxin in causing liver disease

Back 453

phomopsin causes arrest of hepatic mitosis in metaphase--> useful in diagnosis
- bind to tubulin and inhibit assembly of microtubules --> interfere with microtubule dependent intracellular transport and mitosis
- may see megalocytes

Front 454

describe the manifestations of chronic lupinosis in sheep

Back 454

- photosensitisation
- +/- skeletal muscle/cardiac muscle nutritional myopathy due to decreased Se metabolism
+/- hepatoencephalopathy
- livers are small, hard, cirrhotic
- microscopic evidence of arrested mitosis
- might present as lameness or death

Front 455

what is the difference between MOA of chronic copper toxicity in sheep vs bedlington terriers

Back 455

in bedlington terriers - have a recessive gene cant produce chaperone protein which excretes Cu via bile
sheep only have small amount of metallothionien responsible for storage, transport and detoxfication of Cu and cannot produce more in response to high Cu

Front 456

describe the stages of chronic copper poisoning in sheep

Back 456

1. lysosomal accumulation
- normal to slightly increased dietary Cu levels
- hepatocytes and kupffer cells accumulate Cu
2. hepatocyte damage
- subclinical, may have elevated leakage enzymes
- hepatocyte swelling- fat infiltration--> hydropic change
- slight increase in blood Cu
3. haemolytic crisis
- precipitated by stress i.e. shearing
- rapid lysis of hepatocytes = rapid release Cu
- Cu oxidises iron and lyses RBCs = acute intravascular haemolytic anaemia
- hypoxia and Hb= toxic to renal tubular cells = renal failure
- discolouration of urine and plasma (intravascular)
- centrilobular necrosis
- livers orange, kidneys deep red-black

Front 457

what are the clinical signs (and causes of clinical signs in brackets) of chronic copper poisoning in sheep

Back 457

1. icterus (haemolysis)
2. dyspnoea (hypoxia due to haemolysis and iron lysis)
3. haemoglobinaemia (haemolysis)
4. methaemaglobinaemia
5. shock (hypoxia + anaemia)

Front 458

why do we see mix of unconjugated and conjugated bilirubin when the cause of bilirubinaemia is hepatic?

Back 458

because some conjugated bilirubin leaks from damaged hepatocytes but also hepatocytes have impaired ability to conjugate incoming unconjugated bilirubin

Front 459

is ALP specific for cholestasis?

Back 459

no because many isoforms i.e. bone

Front 460

what are the CS of cholestasis?

Back 460

- icterus
- photosensitisation
- maldigestion (need bile acids for lipid digestion)

Front 461

what type of pastures are sporidesmin mycotoxins associated with?

Back 461

perenial rye grass

Front 462

what are the manifestations of sporidesmin toxicity?

Back 462

- absorbed from SI excreted unchanged from liver into bile and is directly toxic to epithelium of bile ducts (affects bile canaliculi) causing necrotising cholangitis--> obstructive jaundice
- retention of phyloerythrin= photosensitisation
- intrahepatic cholestasis
- diffuse necrosis of hepatocytes
- hepatic fibrosis- atrophy of left lobe = "boxing glove liver"

Front 463

does pre-hepatic portal hypertension cause ascites?

Back 463

no

Front 464

what toxins can cause secondary photosensitisation in ruminants?

Back 464

sporidesmin, PAs, lupinosis

Front 465

describe the causes of ascites/portal hypertension

Back 465

1. pre-hepatic
- usually caused by thrombosis in portal vein
- can also be caused by external pressure i.e. neoplasia
- promotes vascular hyperplasia and PSS and congestion but will not cause ascites
- uncommon

2. hepatic
- most common
- PSS and ascites
- extensive fibrosis and atrophy of liver is most common cause (liver failure)
- the increased pressure in sinusoids causes generation of oedema in space of Disse which overwhelms lymphtic system and seeps through Glisson's capsule into peritoneum

3. post-hepatic
- blood flow impeded through hepatic vein or caudal vena cava = increased pressure and increased resistance to venous outflow
- most commonly RS-CHF, can be thrombi
- nutmeg liver- chronic pooling of blood + replacement by fibrosis

Front 466

what is portosystemic shunting?

Back 466

- can be congenital or acquired
- occurs when blood from the portal vein bypasses the hepatic sinusoids and finds a way directly to caudal vena cava i.e. not supplying hepatocytes
- can be intrahepatic PSS (congenital or acquirec) or extrahepatic PSS (acquired)

Front 467

what are the clinical signs of congenital PSS?

Back 467

- small for age
- bizarre behaviour esp after eating (post-prandial hyperammonaemia)
- small but symmetrical liver
- bilaterally enlarged kidneys

Front 468

describe the pathological features of acute cholangiohepatitis

Back 468

- acute cholestasis with icterus and acute hepatocellular necrosis
- will have increase leakage and induced enzymes
- liver is swollen and yellow-green

Front 469

describe the pathological features of chronic cholangiohepatitis

Back 469

- progressive destruction of bile ducts and adjacent hepatocytes
- portal fibrosis and biliary hyperplasia
- massive fibrosis but liver usually not reduced in size
- causes; Fasciola hepatica, immune-mediated

Front 470

what are the primary hepatic neoplasias?

Back 470

- hepatocellular carcinoma
- bile ductular carcinoma
- hepatic carcinoid (arises from neuroendocrine cells of bile ducts)

Front 471

what are the causes of pancreatic insufficiency?

Back 471

1. primary pancreatic atrophy
- juvenile pancreatic acinar atrophy of german shepherds and rough coated collues
2. secondary pancreatic atrophy
- pancreatic duct obstruction
- recurrent necrotising pancreatitis
3. pancreatic hypoplasia- calves
- also dogs <12m
4. pancreatic agenesis

Front 472

what are the consequences of pancreatic insufficiency?

Back 472

when inadequate pancreatic enzymes for digestion esp of protein and fat in SI patient begins to starve because foodstuff not being digested therefore nutrients not absorbed
- maldigestion-->cachexia, debility with dull hair coat and dry skin
- steatorrhea- protein and fat in faeces, large voluminous faeces

Front 473

what are the most likely causes of pancreatic insufficiency in a) the dog and b) the cat?

Back 473

a) dogs- usually recurrent necrotising pancreatitis
b) cats- progressive chronic idiopathic pancreatitis, possibly immune mediated

Front 474

define maldigestion

Back 474

- failure to break down ingesta

Front 475

define malabsorption

Back 475

failure to absorb nutrients

Front 476

how do we diagnose pancreatic insufficiency?

Back 476

- by using tests to detect both maldigestion and deficit in enzyme delivery
1. microscopy- faecal analysis
- most useful
- fat and muscle fibres in faeces
2. TLI (trypsin-like immunoreactivity)
- reliable but expensive
- in normal animal high trypsin activity but in pancreatic insufficiency low or absent trypsin
3. assay fresh faeces for trypsin activity
- cheaper than TLI
- quite unreliable

Front 477

how does acute pancreatitis present?

Back 477

sudden onset of dramatic abdominal pain and shock
+/- vomiting

Front 478

describe the pathogenesis of pancreatitis

Back 478

-trigger unknown but pathogenesis dependent on activation and release of pancreatic enzymes into and nearby to pancreas--> affected tissues undergo autodigestion and fulminating acute inflammation
- liquefactive necrosis and inflammation- white opaque masses surrounded by haemorrhagic inflammation in interlobular septa
- swelling can extend to wall of duodenum and obstruct common bile duct= cholestasis
- serosanguinous exudate into peritoneal cavity

Front 479

what are the symptoms of pancreatitis?

Back 479

- intense abdominal pain
- vomiting
- some cases death from shock
- diarrhoea
- jaundice (cholestasis)
- fever (inflammatory mediators)

Front 480

describe the diagnostic tests for pancreatitis

Back 480

1. cPLI (canine pancreatic lipase immunoreactivity)
- gold standard dogs
- least affected by GIT, corticosteroids, renal disease
>80% sensitvity
2. serum amylase
- only useful in dogs
- low specificity- can also be elevated by pancreatic neoplasia and decreased renal clearance
3. serum lipase
- useful in dogs +/- cats
- may increase slower and remain higher than amylase
- more specific than amylase
4. biochemistry
- only detects non-specific changes associated with pancreatitis
- increased leakage and induced enzymes
- hyperbilirubinaemia (cholestasis)
- urea and creatinine due to dehydration-vomiting (pre-renal azotaemia)
- hyperlipidaemia (cholesterol and TAGs)
5. CBC
- not specific
- elevated PCV and TP= dehydration
- neutrophilia with left shift and toxic changes
- thrombocytopaenia with DIC
6. abdominal US
7. peritoneal fluid amylase and total lipase
8. TLI
- not useful for pancreatitis except in cats

Front 481

what tube do we collect amylase and lipase into?

Back 481

heparin (needs Ca)

Front 482

what animals is serum amylase a useful test in?

Back 482

dogs

Front 483

what animals is serum lipase a useful test in?

Back 483

dogs +/- cats

Front 484

what sample tube do we use for PT and APTT ?

Back 484

sodium citrate

Front 485

what are the clinical signs of dysphagia?

Back 485

- inappetance/anorexia
- pytalism (excess salivation)
- retching
- halitosis

Front 486

list the phases of deglutition and whether they are voluntary or involuntary

Back 486

1. oral - voluntary
involuntary phases:
2. pharyngeal-
3. cricopharyngeal
4. oesophageal
5. gastro-oesophageal

Front 487

what may be an important implication in dogs and cattle with the oesophageal muscularis being completely striated muscle?

Back 487

important for myasthenia gravis, snake envenomation etc because NMJ targeted= flaccid paralysis of oeseophagus--> oesophageal dysphagia

Front 488

what is the funtion of the lower oesophageal sphincter?

Back 488

usually tonically constricted to prevent stomach acid from eroding oesophageal mucosa (gastric reflux). Stomach has protective mechanisms against acid but oesophagus doesnt

Front 489

what are the two things the oesophageal stage of deglutition depends on?

Back 489

1. normal oesophageal musculature
2. intact vagal innervation

Front 490

what are 2 indications of failure of pharyngeal stage of deglutition?

Back 490

- nasal regurgitation of feed or water
- aspiration pneumonia

Front 491

what are the aetiologies of oesophageal disease?

Back 491

1. infectious i.e. BVD
2. toxic i.e. corrosive agents
3. trauma i.e. foreign bodies, iatrogenic
4. neoplastic- i.e. lymphosarcoma
5. developmental/degenerative
i.e. vascular ring anomolies
6. intraluminal obstruction i.e. choke in a horse
7. extraluminal obstruction i.e. persistent right aortic arch, neoplasia

Front 492

what are the two functional regions of monogastric motility in the stomach?

Back 492

1. pyloric (antral region)acts like a pump regulated by a pacemaker in greater curvature, grinds digesta and moves small particles in duodenum, larger particles retained.
2. the fundic region under influence of vagus nerve and gastrin is a reservoir for undigested food- slow phasic contractions move digesta into pyloric region

Front 493

what are the 3 agents that regulate stomach acid secretion?

Back 493

1. histamine
2. ACh
3. hormone gastrin

Front 494

define regurgitation

Back 494

passive retrograde expulsion of oesophageal or gastric contents, most commonly associated with oesophageal disease i.e. megaoesophagus

Front 495

how can we differentiate regurgitation from vomiting

Back 495

in vomiting expect to see (and dont see in regurgitation)
1. nausea
2. abdominal contraction
3. conscious effort
4. bile staining

Front 496

define retching

Back 496

forceful contractions of abdominal muscles and diaphragm against closed glottis, increases pressure in GIT and usually preceedes vomiting

Front 497

define vomiting

Back 497

= reflex act under control of medullary emetic centre that occurs when gastric contents are forcefully expelled (associated with RGC) from the mouth

Front 498

what are the fluid/electrolytes consequences associated with vomiting?

Back 498

- dehydration/hypovolaemia
- malnutrition
- hyponatraemia
- hypochloraemia(loss of HCl)
- metabolic alkalosis (loss of H+ ions)
+/- hypokalaemia due to direct loss in vomitus and loss via urine (compensatory)
- urine generally alkaline but may have paradoxical aciduria in dogs and cattle

Front 499

describe the vomiting process:

Back 499

- prodromal events: hypersalivation, cardiac rhythm changes- tachycardia, defecation
- starts with retrograde giant contraction in proximal duodenum (why we see bile contents in vomitus)
- immediately after RGC, duodenal motor activity is inhibted
- retching is associated with onset of RGC
- accumulation of digesta in proximal stomach followed by retrograde antral contractions and relaxation of corpus, lower oesophageal sphincter, oesophagus and upper oesophageal sphincter
- vagally mediated contraction of oesophageal longitudinal muscle moves intra-abdomonal oesophagus into thorax facilitating entry of gastric contents
- gastric contents are forcefully expelled by contraction of abdominal muscles and diaphragm
- as vomiting passes through, pharynx, glottis and nasopharyngeal openings close preventing aspiration pneumonia

Front 500

describe how the cell function changes as new enterocytes mature

Back 500

- new cells (crypt cells) largely secretory function, as they mature (become villous cells) they have absorptive function and play a major role in digestion

Front 501

GIT plays major role in water electrolyte balance. True or false?

Back 501

true

Front 502

compare epithelial replacement time (In GIT) of adults to neonates and explain the implication of this

Back 502

adults turnover 3-5 days
neonates 7-10 days - implication of slower turnover is that cells damaged by pathogens take longer to be replaced and a longer duration of treatment may be needed

Front 503

the permeability of the intestinal epithelium increases from the duodenum to the distal colon.
True or false?

Back 503

true

Front 504

describe the sodium channels in the SI and LI

Back 504

1. apical sodium channel: in the distal colon sodium is reabsorbed in response to aldosterone
2. Nutrient coupled transport: in SI apical SGLT1 transporter driven by low intracellular sodium generated by Na+/K+ pump and K+ channel. GLUT2 transporter on basolateral surface, both of these channels-sodium reabsorption coupled to glucose reabsorption
3. Sodium hydrogen exchangers: NHE3 channels in SI and LI- extracellular Na+ is exchanged for intracellular H+ (Na+ reabsorbed and H+ secreted into lumen) driven by Na+ gradient generated by basolateral Na+/K+ pump and pH gradient. NHE3 is inhibited by cAMP and cGMP
4. in ileum and proximal colon- coupling of NHE3 transporter- Na+ absorption is coupled to movement of Cl through a Cl HCO3 exchanger - alkalinisation of the cell by NHE drives the exit of HCO3 in exchange for Cl- resulting in electroneutral Cl and Na+ reabsorption

Front 505

what is the major anion in clinically significant diarrhoeal fluid?

Back 505

HCO3 (metabolic acidosis)

Front 506

pathologic diarrhoea is associated with an increase in the rate of____ of faecal____ and_____and in extreme cases faecal electrolyte content may approach that of_____

Back 506

loss
water
electrolytes
plasma

Front 507

what are the consequences of severe diarrhoea?

Back 507

- acidosis
- shock
- dehydration
- renal failure
- death

Front 508

what are the main pathological mechanisms of diarrhoea?

Back 508

1. malassimilation- increased loss of surface area (villous atrophy)-->increased osmotic pressure in lumen
2. secretory diarrhoea- stimulation of active ion transport --> increased osmotic pressure of luminal contents
3. changes in intestinal permeability- inflammation-enteroinvasive bacteria- water moves intointestinal lumen= increased osmotic pressure
4. changes in intestinal motility- never causes diarrhoea by itself

Front 509

list examples of diseases that cause a protein losing enteropathy or gastroenteropathy

Back 509

- paratuberculosis in ruminants
- equine granulomatous and eosinophilic enteritis
- histiocytic ulcerative colitis of boxers
all these are chronic inflammatory diseases in which lamina propria is heavily infiltrated by inflammatory cells
- lymphangiectasia

Front 510

what causes villous atrophy (pathogenesis)?

Back 510

either excessive loss of mature enterocytes from villi (i.e. enteroinvasive bacteria) or from destruction of progenitor cells in crypts of leiberkuhn.
if due to excessie cells loss, bridging or fusion of adjacent villi can occur further reducing SA

Front 511

describe pathogenesis of malissimilation diarrhoeas

Back 511

1. maldigestion
intestinal absorptive capacity is intact but there is incomplete breakdown of digestive molecules accumulating in lumen elevating intraluminal osmotic pressure--> water moves into lumen from blood. In the LI the large quantities of undigested material is fermented by bacteria and in case of carbohydrates produces lactate further increasing luminal osmolality. HCO3 buffer is overwhelmed and pH falls (decreased pH probably further interferes with absorption). Water moves into LI lumen= diarrhoea (osmotic)
eg saline laxitives, lactose intolerant dogs,exocrine pancreatic or hepatic insufficiency (bile)
2. malabsorption
precedes maldigestion and is associated with loss of SA (villous atrophy) clumped and fused villi--> increased luminal osmolality- osmotic diarrhoea
- coronavirus, coccidia, cryptosporidium, enteroinvasive bacteria

Front 512

list aetiological agents of villous atrophy (GIT)

Back 512

- coronavirus
- rotavirus
- invasive bacteria
- Trichostrongylus colubriformis
- cryptosporidium
- coccidiosis

Front 513

destruction of crypt (progenitor) epithelial cells is characteristic of what viruses?

Back 513

canine and feline parvovirus and bovine pestivirus (BVDV)
it can also occur from radiation injury and cytotoxic drugs

Front 514

what are the most common clinical signs of malassimilation syndromes?

Back 514

- diarrhoea
- weight loss
- ravenous appetite
+/- stearrhoea in carnivores
in horse may be no diarrhoea if only SI involved

Front 515

describe the composition of diarrhoeal fluid of secretory diarrhoeas

Back 515

isotonic to plasma, alkaline, low in calcium, magnesium and protein, high in sodium, bicarbonate and chloride

Front 516

what agents can cause secretory diarrhoeas?

Back 516

- enterotoxigenic E.coli
- Salmonella Typhimurium
- Vibrio cholerae
- prostaglandins
- intestinal hormones such as vasoactive intestinal polypeptide

Front 517

describe the pathogenesis of diarrhoea caused by enterotoxigenic E.coli

Back 517

secretory diarrhoea
Enterotoxigenic E.coli is non-invasive, stays in the lumen and turns on cAMP (heat labile toxin) and gCMP (heat stable toxin) both of which inhibit NHE3 (inhibits Na+ reabsorption), Cl secretion most important increased. (SGLT1 and GLUT transporters not affected) Going to have pre-renal azotaemia assoc with dehydration and metabolic acidosis (HCO3 lost in diarrhoea)

Front 518

describe the pathogenesis of increased intestinal permeability diarrhoeas

Back 518

factors associated with increased capillary permeability i.e. inflammation are capable of raising effective tissue pressure in lamina propria - this changes the normal osmotic and hydrostatic gradients so that water moves from blood to intestinal lumen= increased intestinal permeability and probably widens tight junctions. Increased permeability permits loss of proteins and can have a protein losing enteropathy (can cause oedema)
eg acute Salmonellosis (enteroinvasive), enteroinvasive E.coli Johne's disease (chronic inflammation)

Front 519

what are the clinical signs of enteroinvasive acute salmonellosis

Back 519

- fever
- shock
- watery diarrhoea
- hypochloraemia
- hypokalaemia
- hypoalbuminaemia if very leaky
- metabolic acidosis

Front 520

what diagnostic features are common of enteritis?

Back 520

in acute enteritis catarrhal, haemorrhagic and fibrinous reactions may occur, in all types there is exudation of fluid and cells and in some cases necrosis of enteroytes to varying degrees

Front 521

what is the causative agent of a severe necrotising enteritis in chickens, pigs and foals?

Back 521

Clostridium perfringens type C

Front 522

what are the consequences of chronic enteritis?

Back 522

- altered permeability and protein loss (oedema)
- likely to have maldigestion/malabsorption due to villous atrophy
most normally granulomatous in nature, accumulation of macrophages and thickening of intestinal wall

Front 523

pain signals from abdomen are mostly carried by which nerve ?

Back 523

splanchnic nerve via spinothalamic tract

Front 524

slowly conducting C-fibres generally respond to

Back 524

extreme stretch or nociceptors

Front 525

where are the abdominal stretch receptors located?

Back 525

- in muscular layers of hollow viscera esp between muscularis mucosa and submucosa
- also in serosa of solid organs - pancreatitis, renal disease
- mesentery- esp adjacent large vessels

Front 526

where are the abdominal chemoreceptors located?

Back 526

- mainly within mucosa and submucosa of hollow viscera

Front 527

what can activate the
intestinal chemoreceptors?

Back 527

1. inflammation
- peritonitis-primary, or secondary to ruptured viscus
- pancreatitis, hepatitis
- abscess
-GIT infection and ulceration
2. tissue ischaemia or necrosis
- intestinal volvulus or incarceration
- gastric dilatation volvulus- small animals
- abomasal torsion- ruminant
- intestinal infarct--> downstream necrosis activates chemoreceptors
- splenic torsion-inflammatory mediators activate chemorecetors, swelling may activate stretch receptors

Front 528

describe the 3 basic types of intestinal obstruction

Back 528

1. simple obstruction- only problem is interference of aboral passage of gut contents i.e. phytobezoars, trichobezoars
2. closed loop obstruction- a segment of gut is isolated by occlusion at two points i.e. herniation of a loop of bowel through a restricted opening such as the epiploic foramen - veins collapse easily and can become oedematous exacerbating problem
3. strangulation obstruction- interference of venous and arterial blood flow from a closed loop obstruction - onset of clinical signs quicker i.e. GDV

Front 529

sand impaction in a horse is an example of what type of intestinal obstruction?

Back 529

simple obstruction although sand may pull down on mesenteric vessels so may be some activation of chemoreceptors

Front 530

describe paralytic ileus

Back 530

= failure of peristalsis. A functional obstruction where there is failure of contents to be propelled aborally, believed to be associated with electrolyte imbalances (potassium depletion) +/- excessive sympathetic stimulation
may occur following abdominal surgery and in peritonitis, toxaemia and electrolyte imbalance

Front 531

describe vascular bowel disease

Back 531

usu horses. Compromised blood supply to a segment of bowel due to thrombosis/embolism in mesenteric vessel i.e. equine parasitic arteritis, commonly aassoc with Strongylus vulgaris- larvae migrate through mesenteric artery= thrombis. Also see downstream lesions probably also assoc with migrating larvae i.e. segmental infarcts.
Severe abdominal pain, mainly chemoreceptors +/- stretch due to fluid gathering proximal to site

Front 532

what are the general clinical signs of abdominal obstruction/pain?

Back 532

- failure to pass faeces and gas - distal to obstruction bowel is empty
- vomiting due to reflux into stomach
- dehydration
- tachycardia, hypovolaemia
- increased CRT >2sec, can be up to 8 due to dehydration or endotoxic shock
- reduced or absent borborygmi
- abdominal distension (fluid and gas accumulation proximal to site)

Front 533

what are the signs of abdominal pain in dogs

Back 533

- range from obvious discomfort- whine, growl, may snap, tense abdomen, grunts or tries to get away from you

Front 534

what are the signs of abdominal pain in cattle?

Back 534

- anorexia, depression, kicking at abdomen, getting up and down constantly, bruxism, may grunt when they move, may be recumbant

Front 535

what are the clinical signs of abdominal pain in horses?

Back 535

- looking at flank, bruxism, sweating,stretching out as if to urinate, getting up and down constantly, rolling, lateral recumbency +/- groaning, foals may throw themselves on ground and exhibit dog sitting

Front 536

what are the causes of reduced or absent intestinal borborygmi with intestinal obstruction?

Back 536

- distenstion of proximal intestine (to site) with fluid and gas
- reflex neural inhibition of intestinal motility
- reduced blood supply, hypovolaemia, acid base and electrolyte disturbances
- endotoxaemia

Front 537

what is abominal distension associated with in regards to intestinal obstruction?

Back 537

- fluid and gas accumulation proximal to site
- if have reflex neural shutdown of intestinal motility- large intestine is still fermenting producing tympany (becomes slightly larger) esp horses
in horses often able to detect caecal gas cap (high pitch noise due to gas accumulation in caecum)

Front 538

how can a strangulation obstruction lead to peritonitis?

Back 538

intestinal bacteria multiply rapidly in a closed loop of intestine due to absence of HCl. The bacteria , their toxins and by-products of tissue necrosis leak through damaged/degenerate intestinal wall- this "strangulation fluid" in the peritoneal cavity causes peritonitis and toxaemia

Front 539

describe the features of large intestinal obstruction in
a) non ruminants
b) ruminants
c) horses

Back 539

a) abdominal tympany, dehydration and mild metabolic acidosis, electrolyte disturbances are minimal
b) ruminants tend to develop hypochloraemia, hypokalaemia and metabolic alkalosis
c) severe colic, metabolic acidosis and hypovolaemic shock (similar signs and metabolic disturbances in cattle with mesenteric torsion)

Front 540

D-lactic acid is produced by fermentation by Lactobacilli species in ruminal acidosis. Can D-lactic acid be used by the host?

Back 540

no

Front 541

what is the normal rumen pH?

Back 541

6.5

Front 542

what type of microbes predominate in the normal rumen?

Back 542

gram -ve bacteria and many protozoa

Front 543

what causes the diarrhoea associated with ruminal acidosis?

Back 543

the accumulation of lactate in the rumen pulls water into the rumen (osmotic drag) also causing dehydration/hypovolaemia
the diarrhoea exacerbates the metabolic acidosis

Front 544

what may be the sequale to animals with rumen acidosis?

Back 544

- death in 1-3 days usu if acute
- hypocalcaemia due to calcium malabsorption caused by the low pH of the ingesta entering the duodenum during acute stages of disease
- laminitis due to histamine and endotoxin release into circulation
- polioencephalomalacia caused by thiamine deficiency (induced by destruction of thiamine producing organisms by overgrowth of gram positive organisms and by production of thiaminases in ruminal fluid
- rumenitis and scarring of ruminal epithelium
- secondary invasions by organisms particularly fungi
- liver abscesses- ruminal bacteria esp Fusobacterium necrophorum and corynebacterium spp cause multiple liver abscesses

Front 545

what causes ruminal stasis associated with ruminal acidosis?

Back 545

- initially at stage of Strep bovis overgrowth, thought to be due to increased ruminal absorption of SCFA esp butyrate, later due to histamine and endotoxins causing wall damage and systemic toxaemia, hypovolaemia, metabolic acidosis

Front 546

how can we diagnose rumen acidosis?

Back 546

> clinical signs
> rumen fluid collection- put stomach tube down or rumenocentesis
- dipstick- pH etc
> gram stain

Front 547

when does bloat/ruminal tympany occur?

Back 547

when the eructation mehanism fails to expel gases produced by ruminal fermentation

Front 548

describe the pathogenesis of frothy bloat in comparison to free gas bloat

Back 548

- Frothy bloat occurs in association with legume (lush) pastures such as lucerne and clover. Normally gas bubbles coalesce, expand, burst and are eructated. These pastures are high in chloroplast membrane fragments and soluble protein forming a stable foam that traps gas preventing eructation. Ruminal distension can lead to compression of thorax, cardiopulmonary failure, recumbency
free gas bloat is due to an obstruction i.e. abscess, oesophageal occlusion- tumour etc (fermentation is normal)

Front 549

presents with distended left paralumbar fossa
a) free gas bloat
b) frothy bloat
c) both
d) neither

Back 549

c) both

Front 550

highly auscutable ping is associated with
a) free gas bloat
b) frothy bloat
c) both
d) neither

Back 550

a) free gas bloat only

Front 551

bloat is less likely to occur in animals with high salivary flow rates.
True or false and why?

Back 551

true because saliva is high in HCO3 and the cytoplasmic proteins of the legumes decrease pH making foam more stable therefore with HCO3 there is more buffering preventing the decline in pH. bloating is also less likely in animals with inherently high concentrations of salivary mucin due to its antifoaming properties

Front 552

the reticulorumen is almost completely dependent on neural activation for it's primary and secondary sequences of contraction.
True or false

Back 552

true

Front 553

what nerve is responsible for innervation (afferent and efferent) of rumen and reticulum

Back 553

vagus

Front 554

what are the 4 mechanisms of rumen motility abnormalities?

Back 554

1.depression of gastric centres in the medulla i.e. anaesthetics, pain, drugs i.e. xylazine, pyrexia, toxaemia
2. lack of excitatory inputs fromtension receptors in forestomachs i.e. anorexia, vagus indigestion
3. increased inhibitory reflex inputs from epithelial receptors in reticulum and cranial rumen sac - sustained response is more likely to be an important factor in ruminal stasis that occurs in severe bloat or hyperacidity (grain overload)
4. blockade of motor pathways - least commo cause, usu secondary to other conditions i.e. drugs such as atropine or hypocalcaemia

Front 555

describe vagus indigestion

Back 555

A cause of dysfunctional rumen motility due to lack of excitatory inputs; relatively common and usually irreversible ruminal stasis. It is usually a sequale to traumatic reticuloperitonitis (hardware disease) in cattle. It is likely that the signs attributable to vagus indigestion arise b/c the inflammatory process around the reticulum reduces the distensibility and intrinsic contractility of the smooth muscle of the wall hence the excitatory tension receptor drive to the gastric centres would be reduced, rather than due to vagal nerve damage itself

Front 556

what are the clinical signs of traumatic reticuloperitonitis (hardware disease)?

Back 556

- sudden drop in milk production
- cranial abdominal pain, +ve grunt test or withers pinch test, abducted elbows, arched stance
- anorexia
- depression
- fever
- increased HR and RR
- sounds like washing machine, can have RSHF secondary to pericarditis
clinical signs are reduced after 3 days- so may miss them

Front 557

what are the chronic clinical signs of traumatic reticuloperitonitis?

Back 557

- weight loss
- poor lactation
- rough hair coat
+/- vagal indigestion

Front 558

with what condition do we see cattle with the classic 'papple' appearance?

Back 558

vagal indigestion
left ventral and dorsal distension= apple
right ventral distension = pear

Front 559

what are the clinical signs of an oropharyngeal disease?

Back 559

- inappetance/anorexia
- pytalism
- difficulty in prehension/mastication
- dysphagia
- retching
- halitosis
- pain on eating or examination
- bleeding
- visible lesions- erosions, ulcers, dentition lesions etc

Front 560

what is the difference between an erosion and an ulceration?

Back 560

erosion= loss of epithelium but basement membrane still intact, heals quickly by re-epithelialisation and returns to normal
ulcer- loss of epithelium and basement membrane, heals by secondary intention with scarring (fibrosis)

Front 561

what are the defence mechanisms of the GIT?

Back 561

- saliva and mucus- IgA, IgG and antimicrobial lysozyme
- mucosal blood supply
- resident flora/fauna
- gastric pH
- vomiting
- extraintestinal secretions from liver and pancreas
- intestinal proteolytic enzymes
- phagocytes and other effector cells in submucosa
- high rate epithelial turnover
- increased peristalsis assoc with certain causes of diarrhoea
- paneth cells
- adaptive immune system

Front 562

what are the possible routes of entry of pathogens into GIT?

Back 562

1. ingestion- across mucosa
- alot viruses, bacteria
2. expectorated from URT/lungs and swallowed
- Rhodococcus equi
3. systemic haematogenous infections
4. parasite migration
5. direct extension

Front 563

list the 4 viral vesicular stomatitides

Back 563

1. FMD (picornavirus)
2. swine vesicular disease (picornavirus))
3. vesicular stomatitis (rhabdoviridae)
4. vesicular (calicivirus)

Front 564

list the viral ulcerative and erosive stomatitides

Back 564

- BVD- pestivirus
- blue tongue, epizootic haemorrhagic disease- orbiviruses
- malignant catarrhal fever - herpesvirus
- equine viral rhinotracheitis- herpes virus
- feline calicivirus
-rinderpest- morbillivirus

Front 565

what viral ulcerative and erosive stomatitides are not present in Australia?

Back 565

- blue tongue - we have the virus but do not keep small ruminants in northern Australia ]
- rinderpest- techinally eradicated (13 months))

Front 566

what are the two important viral causes of feline respiratory disese?

Back 566

- feline calicivirus and herpesvirus

Front 567

describe the pathogenesis of viral vesicular stomatitides

Back 567

virus causes vesicle by being epitheliotrophic--> binds to epithelium receptors and layers of epithelium separate to form a cleft and fills with serum and inflammatory exudate- they can coalesce becoming bullae--> become abraded and erosion or ulceration. They granulate to heal rapidly (<2wks) if there is no secondary bacterial/mycotic infection
vesicles are fragile and rupture rapidly

Front 568

describe the pathogenesis of erosive and ulcerative stomatitides

Back 568

endothelial damage to vessels within the mucosa causing microvascular thrombis--> increases vascular permeability- vasculitis leading to ischaemic necrosis, oedema and inflammation w/o vesicle formation

Front 569

what is an important differential to rule out for BVD (bovine viral diarrhoea) and how would you do so?

Back 569

FMD- BVD can cause coronary band lesions like FMD, but only FMD causes vesicles
do serology (can be difficult and takes time)
- sample ulcer and take multiple samples for histology
- can do a viral swab (of vesicle)- but most labs dont have

Front 570

what are some non-infectious causes of erosive and ulcerative stomatitides?

Back 570

- uraemia (renal)
- foreign bodies
- feline idiopathic erosive/ulcerative stomatitides

Front 571

describe the two histological types of feline idiopathic erosive and ulcerative stomatitides

Back 571

both types originally cause hyperaemic, swollen mass which gets obliterated easily- lips, tongue often inside surface of teeth etc
lymphoplasmacytic gingivitis/pharyngitis linked to calicivirus with secondary infection by spirochaetes

1) eosinophilic
- may have neutrophilic infiltration too, probably immune mediated. Often associated with eosinophilic skin disease (?)
2) lymphplasmocytic
-

Front 572

name the viral papular stomatitides

Back 572

parapoxviruses:
1) contagious ecthyma (scabby mouth)- orf virus
2) bovine papular stomatitis (milkers nodule)

both zoonotic

Front 573

describe the pathogenesis of viral papular stomatitides

Back 573

- cause epithelial degeneration, inflammation and hyperplasia- papules are proliferative lesions (1cm or less), intially thickening then ulceration and erosion slow to heal- crusting etc

Front 574

how can we tell the difference between gingival hyperplasia and oral neoplasia?

Back 574

only way to tell the difference is to biopsy and try get transitional zone to check invasiveness

Front 575

what is the most common oral neoplasm of
a) cats
b) dogs

Back 575

a) SCC
b) malignant melanoma

Front 576

what is the typical difference between melanomas on skin and melanoma on mucosa?

Back 576

generally melanomas of skin are benign whereas melabomas on mucosa are mostly malignant (90%)

Front 577

describe the aetiopathogenesis of "wooden tongue"

Back 577

caused by normal inhabitant of oral cavity in herbivores that becomes opportunistic invader- Actinobacillus lignieresii--> pyogranulomas, swollen tongue, draining sinus- healing by fibrosis

Front 578

what are the implications of having serosa (instead of adventitia) in the abdominal portion?

Back 578

injury here takes longer to heal and more prone to healing problems

Front 579

what is a good indicator for differentiating PM change and bloat?

Back 579

if lucky might see bloat/white line in oesophagus- due to blanching of distal oesophagus due to pressure and get congestion- if see this can be pretty sure is a pre-mortem change
bloat will always occur as a PM change

Front 580

what are the aetiologies of rumenitis?

Back 580

1) erosive
- BVD, MCF, blue tongue
2) chemical
- kikuyu grass, uraemia
3) bacteria
- can be sequale of lactic acidosis- spread by portal vein to liver- Arcanobacterium pyogenes, Fusobacterium necrophorum (multiple abscess)
4) fungal- tends to be secondary, fungi and bacteria can spread haemotogenously

Front 581

what is haematokesia

Back 581

- fresh blood in faeces- indicates lower GIT bleeding

Front 582

massive fatal haemorrhage from deep ulcers in cardiac zone is a common occurrence in pigs.
True or false?

Back 582

true, in pigs ulceration has been linked to dietary and genetic factors

Front 583

what are the common causes of gastric ulceration in
a) pigs
b) dogs
c) horses
d) ruminants

Back 583

a) dietary (grain) or genetic related
b) NSAIDs, mast cell tumours
c) NSAIDS, EGUS- usu subclinical- still not completely understood, stress?
d) calves usu assoc with dietary changes, mechanical irritation of abomasum by poor quality roughage, stress (weaning), in cattle may be mycotic, viral i.e. BVD, MCF, or due to local anaesthetics

Front 584

differentiate between the two types of osteotargiasis

Back 584

type I- seen in younger animals (lambs, calves) summer- autumn, all arise on pasture rapidly
type II- in older animals (>yearlings) infected with different stages of larvae that undergo hypobiosis then all come out at once - haemorrhage, ill thrift etc

Front 585

describe gastric retention

Back 585

a chronic condition resulting from obstruction of the pyloris. After eating there is dilation of the stomach and vomiting or regurgitation (in species that can) - the vomitous consists of scarcely digested food and no bile (doesnt reach duodenum)

Front 586

list causes of gastric retention

Back 586

> intraluminal/obturation- foreign bodies, mucosal polyps
> external compression- neoplasia
> intramural lesions- chronic ulceration, fibrosis
> congenital pyloric stenosis- puppies

Front 587

what disease do gastric neoplasias mimic clinically?

Back 587

chronic gastritis

Front 588

does enterotoxaemic colibacillosis (oedema disease) in pigs, cause diarrhoea?

Back 588

no, it is a neurological disease, the E.coli shiga-like toxin causes inreased permeability but not hypersecretion or diarrhoea

Front 589

why is it important we educate cat owners in regards to chronic lymphocytic enteritis?

Back 589

b/c can lead to lymphoma

Front 590

hypermotility rarely causes diarrhoea
true or false?

Back 590

true, usually most concerned about hypomotility (bacterial overgrowth etc)

Front 591

describe the pathogenesis of equine grass sickness

Back 591

neurological disease- adults get progressive loss of neurons in myenteric plexus and submucosal plexuses= hypomotility/gut stasis and also loss of autonomic ganglia neurons elsewhere- degenerative changes.
oesophageal ulceration- classic sign, patchy sweating, anorexia, tucked up stance, colic, absence of borborygmi +/- muscle tremors, faecal balls covered in mucus, losing weight, ill thrift etc

Front 592

what are the common intestinal neoplasias of cats, dogs, sheep, cattle and horses?

Back 592

- cats: benign : adenomas, malignant: lymphoma, adenocarcinoms, mastocytoma
- dogs: benign: adenomas or polyps, leiomyomas, malignant: adenocarcinomas, leiomyosarcomas, lymphoma
- sheep- adenocarcinomas
- cattle- lymphoas
- horses rarely get GIT neoplasia

Front 593

most dogs withe exocrine pancreatic insufficiency do not have faecal starch
True or false?

Back 593

true

Front 594

what is the purpose of doing TLI ( trypsin like immunoreactivity) test in diagnosing a GIT disease?

Back 594

to rule out exocrine pancreatic insufficiency as a cause of malassimilation (causes osmotic diarrhoea) TLI <2.5ug/L = EPI

Front 595

what is the diagnostic value of TLI test for exocrine pancreatic insufficiency

Back 595

<2.5ug/L = EPI
2.5-5 = gray zone (rarely EPI)

Front 596

low concentrations of vitamin B12 and folate in serum in absence of exocrine pancreatic insufficiency indicate what?

Back 596

severe small intestinal disease

Front 597

what is the purpose of the faecal alpha 1 proteinase inhibitor test?

Back 597

indirectly measures albumin concentration in blood so can diagnose protein losing enteropathy. MW is similar albumin therefore if this is lost indicates so to is albumin, but albumin cannot be measured b/c rapidly hydrolysed. Significant GIT protein loss is assoc with high faecal alpha-1 proteinase inhibitor concentration
(need to rule out haemorrhage, liver failure, protein losing nephropathy)
- can be an early indication of PLE before onset of CSs in dogs

Front 598

what is plasma pepsinogen as a diagnostic test used for?

Back 598

used predominately in ruminants and indicates damage to abomasum.
Increased with osteotargiasis esp type II
- may also increase with azotaemia

Front 599

what happens to proteins when there is a change in H+ concentration?

Back 599

proteins gain or lose H+ resulting in alterations in charge distribution, molecular configuration and consequently function- this applies to particular enzymes, enzyme functions may be totally inhibited with minor changes in proton concentration

Front 600

describe the major defense mechanisms against AB disturbances

Back 600

1. blood and tissue buffers (immediate but not long term)
- ECF- bicarbonate
- binding or release of H+ substances i.e. Hb from RBCs, phosphates from ICF, phosphate and ammonia from unrine
- release of calcium from bone (prolonged metabolic acidosis)

2. respiratory (mins to hrs)
- lungs are second line of defence - adjusts rate at which CO2 is cleared from blood i.e. hypo or hyperventilation
- hyperventilation removes more CO2 so compensates for metabolic acidosis
- hypoventilation to compensate for metabolic alkalosis but limited b/c decreasing O2 in blood (cant stop breathing)

3. renal (hrs to days)
- takes longer but advantage of being able to compensate for acidosis and alkalosis
- increases H+ secretion during metabolic acidosis, in alkalosis have decreased HCO3 reabsorption

Front 601

where is bicarbonate produced?

Back 601

- in cells that produce carbonic anhydrase from H2O and CO2
- proximal tubule cells, parietal cells, RBCs and intercalated cells of collecting tubules

Front 602

reabsorption of HCO3 is coupled to H+ secretion and occurs in all parts of the nephron except descending and thin ascending LOH.
True or false?

Back 602

true

Front 603

is there some excretion of HCO3 in animals with normal AB status?

Back 603

no, only excreted when compensating for alkalosis

Front 604

how do we collect samples to measure blood gas parameters?

Back 604

use lithium heparinised plasma- preferred sample, or heparinised whole blood
- lithium heparinised syringe or specialised heparinised capillary tube
- the sample tube must not be exposed to air as HCO3 would diffuse into air as CO2

Front 605

what indices are calculated for blood gas analysis

Back 605

- HCO3 (from PCO2 and pH)
- base excess
- anion gap

Front 606

what is the normal physiological ratio of bicarbonate to carbonic acid?

Back 606

20:1

Front 607

describe base excess

Back 607

= excess of base or deviation of bicarbonate from normal (deficit to replace to return to normal pH)
increased in metabolic alkalosis and decreased in metabolic acidosis
- calculated using pH, CO2 and Hct/Hb

Front 608

what are the causes of metabolic alkalosis (hyperbicarbonataemia)?

Back 608

1. gastric loss of H+
- vomiting, abomasal displacement in ruminants
2. renal loss of H+
- diuretics, compensation for metabolic acidosis, nitrogen overload in cattle
3) fluid shift of H+ from ECF to ICF
- hypokalaemia
4) administration of HCO3
- overdose of NaHCO3 infusion

Front 609

what are the causes of hypobicarbonataemia?

Back 609

1) increased generation of H+
-endogenous acid overload; ketoacidosis, lactic acidosis
- ingestion of certain substances that produce protons during their metabolism (ethylene glycol, methanol)
- fever, anorexia in horses
2) decreased renal excretion of H+
- renal failure
- distal tubular acidosis (type I RTA)
- hypoaldosteronism
3) increased loss of HCO3
- type II RTA (proximal tubule acidosis)
- gastric loss- diarrhoea, vomiting of pancreatic secretions
4) administration of acidifying compounds
- even rapid infusion of physiological saline (pH 5)

Front 610

why are mixed acid-base imbalances with the same tendency dangerous? and give an example

Back 610

i.e. metabolic and respiratory acidosis - dangerous b/c no compensation- no way to buffer the abmormality:
example: diabetic ketoacidosis- metabolic acidosis with secondary drop in HCO3 connected with acidotic coma = hypoventilation= increased PCO2

Front 611

give an example of a mixed metabolic acid base imbalance with opposite tendencies

Back 611

diarrhoea and vomiting in same patient (parvo)- loss of HCO3 from diarrhoea= metabolic acidosis and loss of HCl from vomiting = metabolic alkalosis
can be life threatening not due to AB abnormality but due to hypovolaemia

Front 612

define base excess

Back 612

the amount of strong acid required to titrate 1L of blood to pH 7.4 at 37oC while PCO2 is held constant at 40Hgmm

a base deficit is the amount of strong base that must be added (i.e. in metabolic acidosis)

Front 613

what is the physiological base excess range?

Back 613

usu around 0 (0-3.5)

Front 614

what is anion gap useful for?

Back 614

useful for evaluating metabolic acidosis and for distinguishing between the two types of metabolic acidosis (high anion gap metabolic acidosis and normal anion gap acidosis)
- it is important to know the origin of metabolic acidosis as the treatment is not necessarily the same for the two forms

Front 615

what is the anion gap equation?

Back 615

AG= (Na+K)- (Cl+ HCO3)

Front 616

what are the common substances that cause an increased anion gap?/

Back 616

MUDPILES
M- methanol
U- uraemia
D- diabetic ketoacidosis
P- paraldehyde, paracetamol, propylene glycole
I- infection
L- lactic acidosis
E- ethylene glycol
S- salicylates

Front 617

describe increased anion gap metabolic acidosis (IAMA)

Back 617

due to primary increase in acids/ acid overload. Associated with unmeasured (often unknown) acids in the blood, There is a secondary drop in HC03 as it is utilised for buffering the unmeasured acids i.e. ketones, lactate, uraemia

Front 618

what are the most common causes of increased anion gap metabolic acidosis

Back 618

1. lactic acidosis due to hypoxaemia in any species or grain overload in cattle (lactate)
2. ketoacidosis- diabetes mellitus, ketosis in ruminants (ketones)
3. non-metabolisable acids in uraemic acidosis or in some toxicoses (salicylate, ethylene glycol,methanol)
3

Front 619

describe normal anion gap metabolic acidosis

Back 619

occurs due to primary loss in HCO3
- renal loss due to proximal tubular acidosis (type II RTA) and gastric loss due to diarrhoea - most common causes

Front 620

what are the most commonly measured electrolytes in clinical pathology?

Back 620

the monovalent ions; sodium, chloride, potassium and bicarbonate

Front 621

osmotic properties of a solute in solution are conferred by:
a) number
b) molecular weight
c) charge

Back 621

a) number of particles

Front 622

90% of plasma osmolarity is provided by which 3 electrolytes

Back 622

Na+, HCO3 and Cl-

Front 623

how do we measure electrolytes?

Back 623

> ion selective electrodes dominate in clinical pathology, best and most reliable method
> dry chemistry reagent
- affected by haemolysis, lipaemia and high protein levels
> serum samples are usually used for quantifying of electrolytes - use plain tube, can use lithium heparin but do not use EDTA

Front 624

What two factors seriously affect electrolyte results?

Back 624

haemolysis and lipaemia

Front 625

how much sodium is excreted in urine of healthy animals?

Back 625

only 8% due to massive tubular reabsorption (PT)

Front 626

describe the causes of hypernatraemia

Back 626

1. conditions with primary Na+ excess
> primary salt excess (salt toxicosis) uncommon b/c hyperosmolality increases thirst hence water intake
> iatrogenic hypernatraemia- administration of hypertonic saline solutions or NaHCO3= immediate hyperosmotic hypervolaemia
> primary hyperadosteronism (Conn's syndrome) increased reabsorption of Na+ /decreased excretion of Na+ and primary hypernatraemia and hypokalaemia develop

2. conditions associated with primary water loss
> decreased thirst related hypodipsia can occur with some hypothalamic lesions
> vomiting/diarrhoea- loss of water and less severe loss of electrolytes may lead to hypernatraemia
> osmotic diuretics i.e. mannitol or glucose - hyperosmolar compounds in tubules draw water in from surrounding tissues. Urea can have similar effect
> phosphate enema in horses
> osmotic diarrhoea in ruminal acidosis- transient hypernatraemia
> panting in dogs (transcutaneous water oss)
> diabetes insipidus both NDI and CDI

3. other
> fluid shifts of EC

Front 627

what is the composition of the ECF usually with hyponatraemia?

Back 627

usually hypotonic (usu relative water excess)

Front 628

describe the causes of hyponatraemia

Back 628

1. primary sodium loss
a) poor sodium intake is rare (hypotonic normovolaemia)
b) urinary loss (hypovolaemic hyponatraemia)
- tubulopathy (Fanconi)
- furosemide, thiazide- decreased sodium reabsorption (diuresis)
- hypoadosteronism (Addison's)--> hyponatraemia and hyperkalaemia
- non reasorbable anions such as ketones in filtrate- can pull Na+ and cations in = hyponatraemia
c) GIT loss
- vomiting, diarrhoea, excess salivation
d) others:
- third space issues- peritoneal/pleural effusions or ruptured bladder (uroperitoneum)
- increased transcutaneous loss- sweating in horses
- both cases cause compensatory polydipsia and renal water retention--> hyponatraemia
- hyperglycaemia pulls water into tubules

2. primary water excess
a) excessive water intake
- psychogenic polydipsia (dogs)- rare
b) increased renal absorption of water
- increased AVP i.e. neoplasia with AVP-like substances, CNS lesions or hyperthryroidism or secondary increases in AVP due to CHF, chronic liver failure and nephriti

Front 629

give examples of normonatraemia hypovolaemia

Back 629

- patient with diarrhoea or vomiting (normonatraemic hypovolaemia- more water loss than electrolytes) then given IV fluids = haemodilution (secondary hyponatraemia)
- osmotic diuretics = normonatraemic hypovolaemia
- polyuric renal disease with tubular defects (PU/PD)
- early phase of sweating in horses

Front 630

give examples of normonatraemic hypervolaemia

Back 630

- retention of isotonic fluids i.e. oedema disorders such as CHF, chronic liver failure (ascites), nephritic syndrome, nephrotic syndrome
- overdosing with physiological saline solutions

Front 631

urea and glucose have stronger affects on serum osmolality than K+
True or false?

Back 631

true

Front 632

what can affect fluid shifts of K+ between ECF and ICF

Back 632

- insulin
- adrenaline
- AB status

haemolysis can cause false hyperkalaemia (release into ECF)

Front 633

does haemolysis cause a false hyperkalaemia in dogs?

Back 633

no, except for japanese breeds (also cattle and horses it does)

Front 634

describe the 5 aetiologies of hyperkalaemia

Back 634

1. pseudohyperkalaemia
- haemolysis in horses, cattle and japanese breed dogs
- leakage from leukaemic cells
- leakage from platelets
2. increased total body K
> decreased renal excretion, can be pre-renal, renal (esp ARF) or post-renal (dangerous for heart)
> hypoaldosteronism- decreased activity of Na+/K+ pump
> ACE drugs i.e enalapril, ramipril etc
> metabolic acidosis- uraemic acids
> increased dietary intake (common)- fresh lush grass or administration of K+ fluids
> trimethoprim (rare)- acts as a K+ sparing diuretic
3. shift of K+ from ICF to ECF
- most commonly with metabolic acidosis, exchange with H+
- massive tissue necrosis i.e. rhabdomyolysis, nutritional myopathies
4. congenital anomolies
- hyperkalaemic periodic paralysis in quarter horses
- stress induced release of potassium in dystrophin deficient (autosomal recessive X-linked- males)
5) repeated drainage of chylous effusions and peritoneal effusions in cats

Front 635

what is the most common cause of neck ventroflexion in cats?

Back 635

hypokalaemia. Hyperthyroidism is an important differential

Front 636

what concentration of K+ in the blood may be associated with muscle weakness and decreased cardiac function (bradycardia)?

Back 636

<3mmol/L

Front 637

describe the 3 aetiologies of hypokalaemia

Back 637

1. decreased total body K+
>
decreased intake due to anorexia or starvation (can cause significant loss as K+ not stored in body)
> decreased renal excretion
- hyperaldosteronism (Conn's)
- PU/PD - increased flow = increased excretion, osmotic diuresis i.e. glucosuria
- when ultrafiltrate contains large numbers of anions i.e. lactate, ketones (hypokalaemia and hyponatraemia)
- some diuretics i.e. loop diuretics such as furosemide, and thiazide diuretics (not K+ sparing)
- for unknown reasons hypokalaemia common in CRF in cats
2. K+ shifts from ECF to ICF
- acute metabolic alkalosis-exchange with H+
- increased insulin and adrenaline activity- promotes movement of K+ into cells due to cotransport with glucose
3. congenital
- hypokalaemic myopathy of burmese kittens

Front 638

what is considered a low Na/K ratio in dogs?

Back 638

<27

Front 639

what are the causes of low Na/K ratio?

Back 639

1. hypoadrenocorticism
2. diarrhoea
3. renal failure
4. lower UT obstruction or uroperitoneum
5. diabetes mellitus
- osmotic diuresis
6. third space loss- peritoneal/pleural effusions
- repeated drainage of effusions
7. any other disorders that cause hyponatraemia or hyperkalaemia

Front 640

changes in hydration status are associated with proportional changes in Na+ and Cl and acid-base alterations are associated with disproportional changes in Na+ and Cl.
true or false?

Back 640

true

Front 641

what are the causes of hyperchloraemia?

Back 641

1. false hyperchloraemia
- evaporation in vitro
-K+ bromide treatment (chloride sensitive electrodes cannot distinguish between chloride and bromide)
2. hypernatramic conditions
- dehydration
- salt toxicosis
- decreased renal excretion i.e. hyperaldosteronism
3. non-hypernatraemic conditions with Cl- excess
- diarrhoea can cause alimentary loss of HCO3 with secondary Cl- compensation
- renal loss of bicarbonate (due to proximal tubular acidosis)
- chronic respiratory alkalosis- prolonged hyperventilation- hypocapnia compensated by renal retention of protons and decreased reabsorption of HCO3 (uncommon)

Front 642

what are the causes of hypochloraemia?

Back 642

1. hyponatraemic conditions
- GIT, urinary, cutaneous loss of Na+ and Cl
- haemodilution/hyperhydration
- shift of Cl from plasma to extravascular ECF i.e. uroperitoneum
2. normonatraemic conditions
- metabolic alkalosis with increased HCO3 i.e. vomiting, abomasal displacement, gastric reflux in horses
- metabolic acidosis with increased anion gap
- bovine renal failure
- furosemide, thiazide diuretics inhibit Cl- reabsorption

Front 643

what is the consequence if HCO3 is not preserved in the proximal renal tubules?

Back 643

RTA type II a proximal tubular acidosis (part of Fanconi's)

Front 644

is articular cartilage innervated and/or vascularised?

Back 644

no it is not innervated and is avascular yet joint disease is very painful because stretch receptors in lining of joint

Front 645

can we see cartilage on radiograph?

Back 645

no

Front 646

in OCD (osteochondritis dissicans) at what stage of the disease would lameness be present

Back 646

not until there is a full cartilage defect and synovial fluid contacts richly vascularised subchondral bone and becomes bone defect (cartilage not innervated)

Front 647

what are the causes of delayed fracture healing?

Back 647

- excessive movement
- reduced blood supply/poor nutrition (cartllage instead-->endochondral ossification)
- tissue necrosis
- infection (secondary)
- pathological fracture i.e. neoplasia (rare in animals)
- metallic implants (damage blood supply and may cause inflammatory reaction--> bone resorption)

Front 648

how can we differentiate between sterile and septic infectious (or neoplasia) osteomyelitis?

Back 648

take a biopsy and do a culture

Front 649

list 3 diseases/syndromes that can decrease osteoclast activity

Back 649

- BVD
- osteopetrosis
- CDV

Front 650

what is rickets?

Back 650

failure of mineralisation of bone (young animals)-softening of bones in immature animals due to vitamin D deficiency or impaired metabolism of Vit D (osteomalacia in adults)

Front 651

what is the most common cause of septic joint infections?

Back 651

iatrogenic- surgeon , non-aseptic technique

Front 652

how does bone respond to inflammation and necrosis?

Back 652

by attempting to remove bone by inflammation and osteoclasis but if amount of bone is too great it is isolated by the production of new bone=involcrum

Front 653

chronic osteomyelitis invades joint.
True or false?

Back 653

false

Front 654

what is the prime site for osteosarcoma in dogs?

Back 654

proximal humerous and distal radius

Front 655

provide and describe two examples of sterile osteomyelitis

Back 655

1. panoesteitis
- adolescent large breed dogs, increased density in medullary bone, usu self resolving
- shifting lameness, pyrexia
2. metaphyseal osteopathy (hypertrophic oesteodystrophy)
- young adolescent large breed dogs- abnormalitity in growth/formation of physis--> metaphyseal inflammation leads to extra periosteal bone formation, self resolving
- painful swollen limbs

Front 656

what are synovial fossa?

Back 656

bilateral depressions not covered by cartilage. The function of synovial fossae is unknown but may be involved in joint lubrication. Not present at birth, synovial fossae appear in first few months of life, inexperienced persons may mistake synovial fossa as an articular lesion

Front 657

what is the most common joint disease in dogs?

Back 657

secondary osteoarthritis (degenerative, non-inflammatory)

Front 658

give an example of a polyarticular non-erosive joint disease

Back 658

systemic lupus erythemous

Front 659

degenerative joint disease is a synonym for

Back 659

osteoarthritis

Front 660

what factors is muscle function dependent on?

Back 660

1. integrity of skeletal elements (joints)
2. nervous system- motor nerves
3. structures such as skin

Front 661

what can myoglobinuria cause?

Back 661

directly nephrotoxic to tubules and also the accumulation of myoglobin here blocks reabsorption = tubulopathy = acquired fanconi syndrome

Front 662

what is the significance of a CK that has returned to normal but and elevated AST when suspecting/diagnosing myolysis?

Back 662

CK has a short half life (6hrs) whereas AST half life is twice as long (12hrs) so indicates this is not an active/ongoing myonecrosis

Front 663

what process can cause false positives of CK and AST?

Back 663

haemolysis

Front 664

why cant ALT be used to diagnose hepatopathies in horses and ruminants?

Back 664

because more muscle specific in these animals (more liver specific in dogs)

Front 665

what is the half life of ALT

Back 665

2.5 days

Front 666

what are the clinical/pathological changes associated with acute myonecrosis?

Back 666

- increased CK and AST in all species
+/- lactic acidaemia (depends on oxygen supply)
+/- hyperkalaemia (leakage from cells)
+/- myoglobinuria - myoglobin can be easily oxidised to metmmyoglobin = coffee colour urine
- site swollen, hard or soft, heat etc

Front 667

what are the causes of acute myonecrosis?

Back 667

1. ischaemic myopathy
- large animals i.e. downer cows, lateral recumbency, anaesthesia
2. exertional myopathy
if duration or level of exercise> fitness body cannot meet oxygen demand--> anaerobic metabolism-->lactate- lactic acidosis, pain and stiffness
- anoxia plus glycogen sepletion = myonecrosis
- greyhounds, racehorses
3. toxic
- most severe and fastest changes
- no characteristic gross lesions
- pain, muscle weakness, sudden death
- snake envenomation, ionophores i.e. monensin, narosin
4. physical trauma
- surgery, injection
- dying cells pick up calcium- dystrophic calcification
5. inflammatory
- most important is C.chauveoi- black leg
- Neospora- most common infectious myositis in dogs
- Pasteurella, Corynebacterium
CK, AST, ALT increased
- masticatory mastitis in dogs- rare, immune mediated, painful cannot eat

Front 668

what are the causes of subacute- chronic muscle disorders?

Back 668

1. genetic
- uncommon
- muscle degeneration and loss, pale, shrunken +/- fibrosis +/- hypertrophy +/- dystrophic calcification
- feline muscular dystrophy
2. metabolic
a) endocrine
- not commonly serious myopathies
- hypothyroidism, hyperadrenocorticism
- may be muscle atrophy
b) nutritional
- nutritional myopathy in sheep/lambs - Se, vit E deficiency
- blotchy muscles

Front 669

what disease does equine atypical myopathy resemble?

Back 669

seasonal pasture myopathy (due to toxin from maple trees)

Front 670

what conditions lead to depletion of glycogen stores?

Back 670

- with nutritional carbohydrate deficiency or increased carbohydrate use i.e. diabetes mellitus, starvation, bovine ketosis, ovine pregnancy toxaemia

Front 671

name the four insulin antagonists

Back 671

- adrenaline
- glucagon
- cortisol (glucocorticoids)
- growth hormone

Front 672

what are the actions of glucagon?

Back 672

- glycogenolysis
- gluconeogenesis
- lipolysis
- insulin antagonist
- ketogenesis

Front 673

what are the actions of insulin?

Back 673

- anabolic hormone
- promotes glucose uptake by peripheral cells esp muscle and adipose tissue
- enhances glucose utilisation in hepatocytes
- promotes glycogenesis in liver and muscle
- promotes lipogenesis in adipose tissue
- increases amino acid uptake by cells and conversion to protein
- inhibits proteolysis

Front 674

how does adrenaline cause hyperglycaemia?

Back 674

promotes glycogenolysis in liver and muscle (stress, fear- important in cats)

Front 675

what effects do glucocorticoids have on blood glucose?

Back 675

- promote glycogen storage (glycogenesis) but increase blood glucose by
i) gluconeogenesis
ii) decreased glucose utilisation by cells
iii) insulin antagonism

Front 676

cortisol increases blood glucose by promoting glycogenolysis in the liver.
True or false

Back 676

false. promotes glycogenesis but increases blood glucose by other methods such as gluconeogenesis and insulin antagonism

Front 677

ketogenesis is always associated with increased rates of____________?

Back 677

gluconeogenesis. Gluconeogenesis depletes oxalate and therefore the acetyl CoA produced from mobilisation of fatty acids is diverted to ketone bodies and cannot enter TCA cycle

Front 678

what are the causes of hyperglycaemia?

Back 678

1. post prandial
2. diabetes mellitus
3. growth hormone excess i.e. acromegaly (insulin antagonist)
4. catecholamine induced
- fear, excitement, pain, stress
- important in cats (can increase >20mmol/L)
5. glucocorticoids
- stress, Hyperadrenocorticism, exogenous corticosteroids
- not usu severe enough to cause glucosuria
5. multi-endocrine
- i.e. cortisol and adrenaline
- shock, sepsis, moribund animals esp cattle
7. iatrogenic
- infusion of glucose containg fluids
- corticosteroids
- megoestrol acetate (cats)
- ketamine, xylazine, halothane, detomidine

Front 679

what are the causes of hypoglycaemia?

Back 679

1. artefactual
- in vitro glycolysis by blood cells decreases 10% per hr at room temp
- avoid immediate separation of serum/plasma or collect into fluoride anti-coagulant to inhibit glycolysis
2. excess insulin
> iatrogenic OD (caninsulin)
> functional tumour of beta cells--> insulinoma
> paraneoplastic syndrome secretion of insulin like growth factor (IGF)- haemangiosarcoma, leiomyoma/sarcoma, melanoa, renal carcinoma
3. reduction of hormones that maintain glucose homeostasis
- i.e. hypoadrenocorticism (Addison's)
4. increased glucose use
- extreme leukocytosis
- sepsis (demargination)
- extreme physical exertion
- paraneoplastic syndromes
- pregnancy toxaemia and bovine ketosis (increased demand)
5.reduced glucose intake, decreased gluconeogenesis or both
- starvation
- malassimilation syndromes i.e. pancreatitis
- neonatal hypoglycaemia (piglets) glucose <2.2mmol/L will cause death
- bovine ketosis
6. reduced glycogen storage
- advanced liver disease/failure
- fat cow syndrome
- h

Front 680

list examples of neoplasias that may cause IGF secretion causing paraneoplastic hypoglycaemia

Back 680

- haemangiosarcoma
- leiomyoma/sarcoma
- renal carcinoma
- melanoma

Front 681

what hormones cause a delayed increase in blood glucose?

Back 681

cortisol,growth hormone

Front 682

what hormones cause an immediate increase in blood glucose?

Back 682

glucagon, catecholamines

Front 683

why with type II diabetes mellitus, do we commonly get impaired insulin release aswell?

Back 683

insulin is secreted with amyloid and amyloid deposits in beta cells causing dysfunctional beta cells + beta cell exhaustion
- several mechanisms

Front 684

what are the causes of diabetes mellitus in dogs?

Back 684

- autoimmune destruction (main cause)
- idiopathic
- obesity
- pancreatitis
- congenital
-metoestrus

Front 685

differentiate between complicated and uncomplicated diabetes mellitus

Back 685

1) uncomplicated= happy and hungry
- polyphagia (glucose not going to cells)
PU/PD (glucose causes osmotic drag = diuretic, ketones have same effect)
- weight loss
2. complicated- sick and sad
- vomiting
- depression (brain needs glucose)
- dehydration (PU/PD)
- pancreatitis or diabetic ketoacidosis

Front 686

describe the haemogram of a diabetic patient

Back 686

-normal or stress leukogram with uncomplicated DM
- stress leukogram with diabetic ketoacidosis
- may have inflammatory leukogram if pancreatitis involved
- PCV may be increased due to dehydration or DIC (pancreatitis)

Front 687

describe the biochemistry features for a diabetic patient

Back 687

> glucose
- hyperglycaemia >14mmol/L cars and dogs, can be >50mmol/l
- ddx stress hyperglycaemia cats
>electrolytes
- normal in uncomplicated DM
- marked abnormalities in complicated DM
> sodium decreased due to osmotic drag, GIT loss- vomiting or may be false hyponatraemia due to fluid shifts of water from ICF to ECF due to hypertonicity (glucose)
> potassium
- insulin needed for potassium to move into cells so may be increased or normal but will be a total body deficit b/c lost in urine
> phosphate
- tends to mimic K+ movement
- often low in DM and with insulin therapy can be critically low and hypophosphataemia can precipiate a haemolytic crisis
> ketonaemic/ketoacidosis
- ketones are unmeasured acidic organic anions - reduced HCO3 leading to metabolic acidosis
- B-OH-butyrate can be measured in blood
>liver enzymes
- AST, ALT and ALP commonly increased in DM due to hepatic lipidosis that accompanies peripheral mobilisation of fats
> renal analytes
- urea and creatinine usu normal but

Front 688

what should always be done before starting insulin therapy in complicated diabetes mellitus?

Back 688

administer IV fluids with K+ at least 2 hrs prior b.c insulin can decreased blood K+ and cause potentially fatal hypokalaemia

Front 689

renal disease secondary to diabetes is rare in animals compared to humans.
True or false?

Back 689

true

Front 690

describe urinalysis results of diabetic patient

Back 690

- azotaemia (pre-renal or renal if complicate)
- glucosuria
- UTI common (check sediment)
- proteinuria common due to UTI or glomerular damage (check sediment)
- ketonuria= ketonaemia

Front 691

what are the specific diagnostic tests that can be used to diagnose diabetes mellitus?

Back 691

1. plasma insulin
- unnecessary in diagnosis of DM in dogs and cats
2. glycosylated Hb
- produced from an irreversible non-enzymatic, insulin-independent binding of glucose to haemoglobin in RBCs
-the extent of glucose binding directly reflects the blood glucose concentration (of last 1-2months)
- affected by factors that affect RBC turnover (i.e. hyperTh)- limited clinical use
3. fructosamine
- serum proteins that have undergones non-enzymatic, insulin independent glycosylation in a manner similar to glycosylated Hb
- largely measures glycosylated albumin
- reflects glycaemic status of last 1-2 wks
- affected by anything that alters albumin or protein metabolism i.e. hyperTh

Front 692

what are the clinical uses of fructosamine test?

Back 692

- to distinguish stress hyperglycaemia from diabetes
- to monitor diabetes control

Front 693

describe the effects of glucocorticoids

Back 693

1. effects on carbohydrate metabolism
- hepatic gluconeogenesis
- mobilisation of amino acids from extrahepatic tissues mainly muscle
- decreased glucose utilisation by cells
2. increased protein breakdown
- need amino acids for gluconeogenesis
3. effects on fat metabolism
- mobilisation from adipose tissue
- despite fat metabolism glucocorticoids can also cause obesity--> increased appetite, central redistribution of fat
4. stress and anti-inflammatory
- benefit in stress presumably mobilisation of stores for energy and perhaps synthesis of compounds for repair
- inhibits phospholipase A2
5. effect on blood cells and immunity
- demargination of neutrophils- increase circulating pool and monocytes in dogs
- decreases eosinophils (eosinopaenia) by bone marrow sequestration and lymphocytes (lymphopaenia) via lympholysis
- significant atrophy in all lymphoid tissues which in turn decreases both T-cells and antibody production (B-cells)
- mild increase in RBCs in dogs by bone marrow stimulation

Front 694

ACTH has a major effect on mineralocorticoid and androgen synthesis.
True or false?

Back 694

false, has little effect on synthesis of these. major effect on cortisol

Front 695

dogs and cats have diurnal variation of cortisol levels.
True or false?

Back 695

false

Front 696

describe diurnal variation in glucocorticoid release

Back 696

- occurs in humans and horses (not in dogs or cats)
- high levels of circulating cortisol at sunrise and low levels in the evening

Front 697

most cases of hyperadrenocorticism in dogs are
a) primary endocrinopathies
b) tertiary endocrinopathies
c) secondary endocrinopathies

Back 697

c) secondary endocrinopathies
- 80-85% pituitary adenoma ( usu microadenoma, 10% macro)

Front 698

in horses hyperadrenocorticism is due to

Back 698

- hyperplasia or adenoma of pars intermedia (pars intermedia adenoma)

Front 699

compare what happens to the adrenal glands in pituitary dependent hyperadrenocorticism and adrenocortical neoplasia (hyperA)

Back 699

- in pituitary dependent hyperA there is increased ACTH so there is increased cortisol production that does not cause negative feedback so ACTH (and therefore cortisol) remains high causing bilateral adrenal hyperplasia
- in adrenocortical neoplasia the tumour continuously secretes cortisol regardless of inhibition of ACTH (negative feedback) there is atrophy of the opposite adrenal (disuse)= unilateral atrophy

Front 700

list the clinical signs of Cushing's syndrome in dogs

Back 700

- polyphagia
- PU/PD
- pot belly, obesity
- exercise intolerance,muscle weakness
- bilaterally symmetrical alopecia
- leukoderma or hyperpigmentation, pyoderma (non-pruritic)
- dull dry hair coat
- panting
- testicular atrophy, feminisation
- pseudomyotinia, non-inflammatory degenerative myopathy
- UTIs

Front 701

explain the metabolic symptoms of hyperadrenocorticism in dogs

Back 701

1. polyphagia
- glucose not getting to the cells (insulin antagonist)
2. PU/PD
- interferes with AVP , may be psychogenic
3. pot belly
- central redistribution of the fat
- muscle wasting due to protein catabolism
- liver enlargement due to lipidosis and glycogenesis
- overdistended urinary bladder may contribute (effects on AVP?)
4. exercise intolerance/muscle weakness
- muscle wasting often obvious large breed dogs esp temporal and lumbar muscles , due to protein catabolism

Front 702

explain the possible causes of panting associated with hyperadrenocorticism in dogs

Back 702

- may be due to increased fat deposition over thorax and in abdomen, muscle wasting and weakness involved in muscles of respiration but also considered a peculiar canine feature from direct effects of glucocorticoids

Front 703

what are the neurological signs of pituitary macroadenomas? (rare)

Back 703

- altered mentation, disorientation, ataxia, pacing and less commonly seizures, coma, blindness

Front 704

what are the clinical signs of pars intermedia adenoma in horses

Back 704

signalment; older horses
- hirsutism- most common CS, thick, long hair coat and abnormal hair shedding, often retention of long hair in jugular groove, on legs and ventral abdomen
- PU/PD (up to 76%)
- laminitis (vasopressive effects of cortisol)
- muscle wasting
- weight loss
- pot belly
- bulging supra-orbital fat pads
- lethargy, narcolepsy
- recurrent infection

Front 705

what are the clinical signs of hyperadrenocorticism in cats?

Back 705

signalment: middle age- older cats, 85% concurrent diabetes
- PU/PD and polyphagia in cats with and w/o DM
- hepatomegaly
- pendulous abdomen
- obesity, weight gain
- muscle wasting
- alopecia (bilaterally symmetrical less common in cats than in dogs)
- unkempt hair coat/curling of pinnae in iatrogenic cases
- thin fragile skin- will tear (>50%)
- bruising

Front 706

what are the haematology findings in hyperadrenocorticism cats and dogs?

Back 706

- stress leukogram- mild neutrophilia, lymphopaenia, eosinopaenia and monocytosis in dogs
- may have mild polycythaemia due possibly to ventilator problems and in females increased androgens
- mild increased nucleated RBCs

Front 707

describe the biochemistry findings of a dog with hyperadrenocorticism

Back 707

> hyperglycaemia
- 50-60%
- glucosuria if >renal threshold
> urea may be decreased
- due to continual loss- PU/PD
>hepatic enzymes
- ALT often mildly increased in dogs and cats- liver damage - swollen hepatocytes + glycogen accumulation
ALP- (CS isomer)- most common biochemical abnormality in dogs (only)- 90-95%
GGT- often mild to med increased in dogs
>cholesterol, TAG and lipaemia
-increased in 80-90% dogs
-lipaemia can also cause haemolysis and interfere with RBC indices, TP protein, albumin, bilirubn, ALP, calcium, phosphorus, amylase, lipase and Na+
> electrolytes
- often normal
- sometimes decreased K+ etc due to osmotic diuresis

Front 708

describe the urinalysis findings associated with hyperadrenocorticism

Back 708

- urine typically hyposthenuric or isosthenuric (<1.013)
- usu able to concentrate urine if water deprived but only minimally (effect of cortisol on ADH)
- 40-50% of dogs have UTI may have bacteruria w/o pyuria (corticosteroids immunosuppressive)
- frequently proteinuria even in absence of UTI
- glucosuria common in cats concomitant DM and in horses

Front 709

list the specific endocrine function tests for diagnosing hyperadrenocorticism in dogs

Back 709

1. basak blood cortisol
- little to know diagnostic value, non-specific
2. UCCrR
- low specificity, high sensitivity
- normal result unusual for hyperA- expect high
3. ACTH stimulation test
- gold standard to diagnose iatrogenic hyperadrenocorticism
- also used for diagnosing hypoA
- only test to assess adequacy of milostane and trilostane
4. low dose dexmethasone test
- very useful to diagnose spontaneous hyperadrenocorticism
- suppression of cortisol <30nmol at 4hrs but not at 8hrs diagnostic of PDH
- no suppression at either time = AT
- no use for therapeutic monitoring
5. high dose dexmethasone test
- used to differentiate between PDH and AT
- a proportion of PDH cases will suppress cortisol in response to higher dose of dexmethasone
- ATs secrete cortisol independent of ACTH therefore no dose dexmethasone no matter how high will in theory suppress cortisol in this case
6. plasma endogenous ACTH concentration
- used to differentiate AT and PDH
- relatively expensive + stringent

Front 710

what test would you use to diagnose iatrogenic hyperthyroidism?

Back 710

ACTH stimulation test

Front 711

what test(s) would you use to diagnose spontaneous hyperadrenocorticism (PDH or AT)?

Back 711

- low dose dexmethasone test
- UCCrR

Front 712

what tests would you use to distinguish between PDH and AT hyperadrenocorticism?

Back 712

- high dose dexmethasone test
- plasma ACTH

Front 713

what are the specific endocrine tests for diagnosing hyperadrenocorticism in cats?

Back 713

> blood cortisol
- limited diagnostic value esp in cats- stress hyperglycaemia
> UCCrR
- sensitive but not specific
> ACTH stimulation test
- due to convenience preferred test for cats
>LDDT - 15-20% normal cats fail to supress in response to 0.01mg/kg IV (low specificity i.e. stress) so failure of suppression must be followed by HDDT
> HDDT
- used for diagnosis rather than differentiation in cats
> adrenal ultrasonography or endogenous ACTH assay preferred for differentiation

Front 714

describe the specific endocrine tests used to diagnose hyperadrenocorticism in horses

Back 714

- basal cortisol no value
- UCCr little value
- Dexmethasone suppression test with cortisol measurements 15-19hrs after is recommended test
- ACTH stimulation test unreliable in horses
- combined DST and ACTH not recommended in horses or dogs

Front 715

describe primary hypoadrenocorticism

Back 715

- well recognised in dogs, rare in cats
90% of cases (primary endocrinopathy) and 90% of those are typical Addison's disease; immune mediated or idiopathic (usu) destruction of adrenal cortex. 10% atypical. Usually results in deficiency of both mineralocorticoids and glucocorticoids
- may be iatrogenic due to milostane or trilotane therapy

Front 716

describe secondary hypoadrenocorticism

Back 716

- rare in dogs, not reported in cats
pituitary ACTH deficiency- may be due to pituitary neoplasia= decreased glucocorticoid secretion and no affect on mineralocorticoids
- dogs on CS therapy can have hypoadrenocortical crisis

Front 717

what is the signalment for hypoadrenocorticism?

Back 717

- dogs
- F>M
- ave age 4y (0.3-14)
- pure breeds> mixed

Front 718

describe the haematological features of hypoadrenocorticism

Back 718

- mild to severe anaemia- may be mild due to suppression of bone marrow due to decreased glucocorticoid or can be severe in case of GIT haemorrhage
- anaemia may be masked by dehydration or shock causing haemoconcentration
- lymphocytosis and eosinophilia (should have stress leukogram but dont b/c dont have cortisol)
- lack of stress leukogram in a collapsed may be only indication (also bradycardia due to hyperkalaemia when dog is in shock- should be tachycardic)

Front 719

explain the clinical signs of hypoadrenocorticism

Back 719

1. non specific: lethargy, weakness, depression (low glucose-brain), vomiting, diarrhoea
- possibly dehydration and shock- increased loss of Na+ (and inadvertenly water)
- signs exacerbated in electrolyte disturbances (hyponatraemia and hyperkalaemia)--> shivering, shaking
- hypothermia (no energy for heat generation?)
- bradycardia caused by hyperkalaemia- if animal is in shock should be tachycardic so know something is wrong
- PU/PD due to excessive Na+ in urine with resultant medullary wash out

Front 720

describe the biochemistry findings associated with hypoadrenocorticism

Back 720

1. hyponatraemia
- deficiency of aldosterone = increased renal loss
- additional GIT loss if vomiting/diarrhoea
2. hypochloraemia
- follows sodium
3. hyperkalaemia
- decreased renal excretion associated with aldosterone deficiency
- also due to ICF- ECF fluid shifts
4. Na: K ratio
- normal is 27-40
&lt;25>&lt;15 = hypoA
5. hypercalcaemia
- about 30% dogs (aldosterone deficiency = decreased calcium excretion)
- may be related to glucocorticoid deficiency?
- more likely in hyperkalaemic patients
6. hypoglycaemia
- not consistent finding- about 20% dogs
- can be severe if not eating as well + cortisol important insulin antagonist
7. hyperphosphataemia
- decreased renal excretion
8. liver enzymes
- mild increase in AST, ALP
- non specific
9. hypoalbuminaemia

Front 721

describe urea and urinalysis changes associated with hypoadrenocorticism

Back 721

> pre-renal azotaemia
- dehydration, shock'
- urine concentrated but dogs with hypoA have decreased ability to concentrate urine due to medullary washout caused by continuous loss of Na+ and loss of normal medullary gradient- therefore technically a renal azotaemia but not due to primary renal disease
- hypoA often misdiagnosed as renal disease- look at BCS

Front 722

describe a way to grossly differentiate between renal disease and hypoadrenocorticism

Back 722

- hypoadren dogs will have normal body condition whereas dogs in renal failure have poor BCS

Front 723

describe the specific adrenocortical function tests used to diagnose hypoadrenocorticism

Back 723

1. blood cortisol
- basal cortisol concentrations of little diagnostic use however a collapsed dog with cortisol <10nmol (should have high cortisol, stress leukogram) is excellent indication to treat hypoA whilst waiting for further test resultts
2. ACTH stimulation test
- gold standard
- flatline result- positive result = <60nmol/L = hypoA
- depicts glucocorticoid deficiency only
3. endogenous ACTH
- generally not required to confirm diagnosis of hypoA

Front 724

what is the signalment for primary hyperaldosteronism (Conn's syndrome)

Back 724

cats, rarely dogs
middle- old aged

Front 725

describe Conn's syndrome in cats

Back 725

- middle-old age
- increased aldosterone secretion by abnormal zona glomerulosa
- in cats Na+ often not affected and main abnormalities= systemic hypertension and hypokalaemia--> muscle weakness and ventroflexion of the neck
- hypertension can cause retinal blindness
- diagnosed by adrenal mass on US (adenoma/adenocarcinoma)

Front 726

how is hyperaldosteronism treated?

Back 726

- preferrably surgical resection of adrenal tumour
- otherwise treatment with spironolactone an aldosterone antagonist (K+ sparing diuretic= reduced loss of K+) accompanied by anti-hypertensive drugs i.e ACE inhibitors and potassium supplementation can be suffice

Front 727

what can cause an enlarged thyroid gland/goitre ?

Back 727

1. iodine deficiency
2. ingestion of goitrogenic toxins which inhibit iodine trapping-->interfere with thyroxinogenesis
3. tumours
4. hyperactivity (hyperTh)
5. excessive or decreased dietary iodine
6. genetic enzyme deficiency- rare, merino sheep- failure of thyroglobulin synthesis

Front 728

what is thyroglobulin?

Back 728

an iodinated glycoprotein that serves to store thryoid hormone and it's precursors
T3 and T4 are stored bound to thyroglobulin

Front 729

in excess quantities thyroid hormones increase sensitivity of CVS and nervous system to catecholamines.
True or false?

Back 729

true

Front 730

goitre can only be caused by hypothyroidism.
True or false?

Back 730

False. Can be caused by hypo- and hyperthyroidism
but hypothyroidism goitre more common in animals (esp dogs)

Front 731

what are the two most common causes of hypothyroidism in dogs?

Back 731

primary endocrinopathy
- lymphocytic thyroiditis
- idiopathic atrophy

Front 732

congenital hypothyroidism in any species can present as dwarfism.
True or false?

Back 732

true. but dwarfism = proportional and hypoTh= disproportional

Front 733

list the clincal signs of hypothyroidism

Back 733

related to decreased metabolism
> lethargy
>weight gain
> weakness
>heat seeking
> endocrine alopecia (symmetrical), pyoderma, hyperpigmentation (rat tail-dogs)
> myxoderma - rare
> polydipsia is NOT a sign of hyperthyroidism

Front 734

polydipsia is not a sign of hypothyrodism.
True or false?

Back 734

true. and any disease causing PD is likely to affect TT4 and T3 assays i.e. hyperadrenocorticism

Front 735

what are the haematology changes associated with hypothyroidism?

Back 735

- mild non regenerative normocytic normochromic anaemia (due to decreased stimulation RBCs) <50%
- leptocytes and codocytes often seen due to cholesterol loading
- hypercholesterolaemia >75% (decreased thyroid hormone = decreased cholesterol metabolism)
- often marked >12mmol/L hypertriglyceridaemia and lipaemia
- normal cholesterol does not exclude hyperT

Front 736

what are the hallmarks of hypothyroidism?

Back 736

- hypercholesterolaemia
- mild anaemia
- overweight patient

warrant testing for hypoT

Front 737

what is euthyroid sick syndrome? and list some common causes

Back 737

occurs when T3 and T4 are below reference interval but thyroid gland is not dysfunctional. common causes include:
- suppression of hypothalamus and pituitary gland
- decreased synthesis of T4
- decreased concentrations of binding proteins i.e. albumin(?)
- drugs; corticosteroids (potential hyperadrenocorticism), sulphonamides, NSAIDs
- decreased de-iodination of T4 i.e. selenium deficiency= decreased glutathione peroxidase- an iodinising enzymes
- often seen in starvation, critical illness and patients in intensive care

Front 738

what is the most common test used for thyroid function testing?

Back 738

TT4
- often first test used
- cost effective and readily available

Front 739

a normal TT4 result rules out hypothyroidism, true or false?

Back 739

true

Front 740

give examples of when T4 may be decreased but animal is not hypothyroid

Back 740

1. breed- greyhounds (and probably other sighthounds) have lower T4 ref range
2. age- i.e. young labradors have lower T4
- decreased in dogs >6y
- higher in younger animals
3. Euthyroid sick syndrome- concurrent illness esp hyperadrenocorticism
4. daily fluctuations
5. body size- large dogs (>30kg) have lower T4 than smaller dogs (<10kg)

Front 741

if we get a TT4 test result back lower than reference range but absence of anaemia and hypercholesterolaemia +/- overweight what should we do?

Back 741

consider present clinical signs, haematology, any concurrent illness/medications i.e. hyperadrenocorticism or corticosteroids and do additional testing--> TSH test

Front 742

what is the most accurate test of thyroid function and is this test commonly used?

Back 742

- free T4
- more specific that TT4
- less affected by illness
- not commonly done b/c costly and not readily available
- more so done when have confusing TT4 results

Front 743

what is the gold standard test for differentiating hypothyroidism from euthyroid sick syndrome?

Back 743

TSH stimulation test
- ESS T4 should increase
- hypoTh- neglible increase <20mmol/L

Front 744

what is the gold standard test to diagnose primary hypothyroidism?

Back 744

TSH stimulation test

Front 745

hyperthyroidism (cats) is most commonly a
a) primary endocrinopathy
b) secondary endocrinopathy
c) tertiary endocrinopathy

Back 745

a) primary endocrinopathy
most commonly a functional adenoma or adenomatous hyperplasia of thyroid gland
- independent of TSH

Front 746

what are the clinical signs of hyperthyroidism in cats?

Back 746

- older cats
- weight loss
- poor unkempt hair coat
-polyphagia
- PU/PD (increased GFR- increased renal perfusion)
- vomiting (thyroitoxicosis)
- hyperactivity, aggression, hyperkinesis
- tachycardia, heart murmur
- may have goitre
- often have abnormalities involving several organ systems which may or may not be secondary to thyrotoxicosis

Front 747

describe the haematology changes associated with hyperthyroidism in cats

Back 747

- may say mild relative erythrocytosis (increased PCV) due to stimulation of RBC precursors and epo by thyroid hormone
- usu stress leukogram

Front 748

How can hyperthyrodism mask chronic renal failure?

Back 748

increases renal blood flow and GFR- exact cause of PU/PD unknown may be medullary wash out affect
- no azotaemia (increased GFR)

Front 749

how do we diagnose hyperthyroidism in cats?

Back 749

1. clinical signs
- goitre- palpate thyroid
- unkempt hair coat, tachycardia, weight loss etc
2. CBC and biochem
- stress leukogram
- may have mild relative erythrocytosis
- ALT and ALP often high
3. TT4
- will be high
- do multiple tests
- normal T4 does not rule out
4. T3 suppression test
- used to assist diagnosis if TT4 results are confusing

Front 750

describe the T3 suppression test

Back 750

- sometimes used to facilitate diagnosis of suspected hyperthyroidism in cats (when T4 results confusing)
- give T3 and evaluate responsiveness of TSH b/c T3 cannot be converted to T4
- so positive result = high T4 and TSH will be low because already suppressed by high T4
- in normal animal the high T3 should suppress TSH and subsequently suppress T4 so should have low TSH and T4
- suppression to >50% is consistent with normal thyroid function

Front 751

what are the causes of acromegaly (cats)?

Back 751

1. GH secreting pituitary tumour -usu diagnosed in insulin resistant diabetes
2. hypothalamic dysfunction- increased GHRH or decreased GHIH
3. progestrone excess in dogs mostly, uncommon

Front 752

what are the clinical signs of acromegaly (cats)?

Back 752

1. PU/PD
2. polyphagia
3. weight gain
4. lameness
5. CNS signs
6. increased size of paws
7. broad facial features
8. stridor--> high pitched wheezing sound resulting from turbulent air in upper airway- due to excess soft tissue around pharynx and larynx
9. prognathia inferior- undershot jaw
10. may develop renal disease, murmurs

Front 753

what stimulates secretion of AVP/ADH?

Back 753

increased plasma osmolality (solutes) 1-2%
other stimuli include volume depletion, hypotension and RAAS activation (hyperaldosteronism?)

Front 754

ionised calcium is the only physiological important calcium in circulation.
True or false?

Back 754

true

Front 755

does hyperphosphataemia influence total calcium levels?

Back 755

no, only decreases ionised calcium levels

Front 756

parathyroid hormone secretion is governed by both pituitary and hypothalamic control.
True or false?

Back 756

false. produced by PT gland, no pituitary or hypothalamic control

Front 757

what factors increase PTH secretion?

Back 757

1. decreased ionised calcium (true hypocalcaemia)
2. decreased vitamin D

Front 758

describe the actions of PTH

Back 758

1. bone effect- primary target
- ca mobilisation
- also phosphate and magnesium mobilisation--> PO4 immediately captures calcium= decreased ionised calcium (hypocalcaemia) this is why need kidney effect
2. kidney effect
- increased calcium reabsorption from DT and PO4 excretion
3. GIT
- mild indirect effect
- increases Ca uptake mainly via action of vitamin D

Front 759

increased pH/alkalosis will decrease Ca2+ in blood
true or false?

Back 759

true, alkalosis forces binding with albumin, acidosis releases Ca from albumin

Front 760

describe the types of hyperPTHism that can occur in animals

Back 760

1. primary hyperPTHism
- associated with adenoma of
parathyroid and hypersecretion PTH
- persistent hypercalcaemia and hypophosphataemia
- if severe hypercalcaemia persists due to metastatic calcification of soft tissues
2. renal secondary HyperPTHism
- decreased excretion of PO4 =hyperphosphataemia
+ decreased production of vitamin D= decreased Ca resorption from GIT and bone--> hypocalcaemia = increased PTH= Ca release from bone , GIT and renal resorption but PO4 immediately captures= continuous cycle--> loss of bone density (rubber jaw)= renal osteodystrophy
3. nutritional secondary hyperPTHism
- patients fed Ca deficient or excess phosphorus diet (all meat diet in carnivores)
- metabolic bone disease can develop
- most common horses
4. humoural hypercalcaemia of malignancy
= paraneoplastic syndrome
- secretion of PTHrp
- apocrine gland carcinoma and lymphoma most common
- patients have normal PTH
- diagnosis: normal to low PTH and hypercalcaemia (increased ionised calcium)

Front 761

what are the hallmarks of primary hyperparathyroidism?

Back 761

1. high Ca
2. low PO4
3. high PTH

Front 762

name 3 neoplasms that may produce PTH-related peptide

Back 762

1. apocrine gland carcinoma
2. lymphoma
3. pulmonary carcinoma

Front 763

how can a bicarbonate solution infusion cause hypocalcaemia?

Back 763

by inducing alkalosis--> causes Ca to bind albumin (decreases ionised calcium)

Front 764

what are the causes of hyperphosphataemia?

Back 764

1. decreased renal excretion
- decreased GFR (renal disease, pre-renal)
- bladder rupture or obstruction (post renal)- rare
- hypoPTHism
2. increased GIT uptake
- excessive dietary intake
- excessive vitamin D
- ischaemic lesions in GIT
3. shift from ICF to ECF
- tumour lysis
- severe mypathy i.e. rhabdomyolysis
4. spurious
- leakage with sample aging
- WBC, RBC leakage

Front 765

what are the causes of hypophosphataemia?

Back 765

1. increased renal excretion
- prolonged diuresis
- hyperPTHism
- PTHrp i.e. lymphoma, apocrine adenoma
- Fanconi syndrome- dogs (decreased reabsorption)
2. decreased GIT uptake
- anorexia
- vit D deficiency
- malabsorption
3. shift into ICF
- insulin
- glucose infusion (insulin)
- alkalosis esp respiratory
4. defective mobilisation from bone
- eclampsia in dogs
- milk fever in cows
- severe hypophosphataemia may result in haemolytic anaemia- occ seen in dairy cows and treated diabetic ketoacidosis- us due to altered red cell energy metabolism and membrane integrity

Front 766

when are sheep most susceptible to hypomagnasaemia?

Back 766

2-6weeks after lambing

Front 767

what are the functions of the skin?

Back 767

1. protective barrier- chemical, physical, thermal, solar
2. thermoregulation- hair, blood supply
3. storage- proteins, fat, electrolytes
4. secretion- sebaceous and sweat glands - important for hair coat and skin barrier function
5. sensory perception
- tactile mechanoreceptors in skin, whiskers
6. endocrine role
- vitamin D
7. behaviour
8. immunosurveillance
- Langherhans cells, WBCs

Front 768

what is the highest layer of the skin where we should still see mitotic figures?

Back 768

basal layer of epidermis/stratum basale- should not see mitotic figures any higher than here

Front 769

name two desmosome proteins that can be targets of disease or immune system and where they are found

Back 769

1) desmoglein 1 found commonly in stratum spinosum and more commonly oral cavity
2) desmoglein 3 found in stratum basale and more commonly hair coat

Front 770

what are the stages of hair follicle growth

Back 770

1. anagen- growth
2. cetagen- growth cessation- involution
3. telogen- resting/quiescent phase

Front 771

with primary skin lesions will the epidermis be intact or not?

Back 771

will be intact, as soon as lose epidermis get secondary skin infections

Front 772

describe the primary skin lesions

Back 772

1. macules or patches
- colour changes, loss or adding
2. papules and plaques
- skin thickening
- papules less than 1cm area skin thickening
3. pustule
- neutrophil accumulations, can be eosinophilic or lymphocytic
4. vesicles, bullae
5. wheals
6. nodules
- greater than 1cm area skin thickening
7. tumour or cyst

Front 773

what is the difference between papules and nodules?

Back 773

papules = area of skin thickening less than 1cm and nodules are areas of skin thickening greater than 1cm

Front 774

what are the skin lesions that can be primary or secondary?

Back 774

1. alopecia
- hyperpigmentation- secondary
- primary- endocrinopathies
2. scale
- keratosis
3. crust
= scale + exudate
4. follicular casts
5. comedo (black heads)
- can be primary-endocrinopathies or secondary to tumours
6. pigment changes
- leukoderma

Front 775

what are the secondary skin lesions (always secondary)?

Back 775

- due to chronicity or epidermal compromise- secondary complication
1. epidermal collarette
- exduate + keratin in a circular or flake type arrangement
2. scar
- min 14 days (up to a month)
- lots of collagen on biopsy
3. excoriation
4. erosion/ulcer
5. fissure
- thickened
6. lichenification
- thickened
7. callus
- thickened

Front 776

what is acanthosis?

Back 776

hyperplasia of the stratum spinosum
- non specific response to metabolic alteration in skin

Front 777

describe the two types of hyperkeratosis

Back 777

1. orthokeratotic keratosis
- increased in normal mature keratin squames due to increased production or abnormal retention
- may appear as thick tough layer i.e. callus or thin grey-white flakes (seborrhea sicca)
2. parakeratotic hyperkeratosis
- increase in partially keratinied cells which retain their nuclei- usu greasy texture (seborrhoea oleosa)
- appear as grey-brown scales or flakes +/- crusts
- zinc deficiency--> greasy pig disease

Front 778

describe sebaceous adenitis

Back 778

sebacaeous glands destroyed and hair follicles become brittle and dry-loss of nutritive effect from sebaceous glands- really a systemic epidermal lesion but presents patchy

Front 779

what are the causes of pustules?

Back 779

1. infectious
- most commonly Staph infections
- also Pasteurella, Strep,
- Candida, Microsporum
2. sterile
- pemphigous foliaceous, pemphigus group
- important to have in tact pustule for diagnosis

Front 780

what are the causes of vesicles and bullae?

Back 780

- these are primary lesions due to infective or immune (degenerative causes)
1. infectious
- viral stomatides-FMD, SV, SVE, vesicular stomatitides
- bovine herpesvirus-2,
- equine coital exanthema
2. sterile
- allergy: histamine, spongiois of epidermis
- autoimmune disease i.e SLE, bullous pemphigoid, dermatomyositis
-degenerative- defects in cellular adhesion molecules

Front 781

describe the gross appearance of spongiotic and exudative lesions in the skin

Back 781

primary: erythema, papules, plaques, vesicles--> exudation-->crusting
secondary: erosion, ulceration, excoriation

Front 782

name 3 viruses that induce epithelial tumours

Back 782

1. papilloma virus
2. pox viruses
3. polyoma viruses

Front 783

name the common primary and secondary epidermal neoplasias

Back 783

1. primary
a) benign: papilloma, epithelioma, keratoacanthoma, melanocytosis
b)malginant: SCC, basal cell carcinoma, malignant melanoma
2. secondary
- epitheliotrophic lymphoma--> leukocytes infiltrating epidermis--> papules, plaques, skin thickening etc--> difficult to recognise b.c doesnt present with typical signs of lymphoma i.e. swollen lymph nodes

Front 784

describe the causes of alopecia in animals

Back 784

1. failure to grow
i) metabolic
- sex hormone imbalance
- hypoTh, hyperadreno
ii) unknown
- post clipping
iii) post inflammatory
- sebaceous adenitis, dermatomyositis

2. growth of weak fragile hair
- follicular dysplasia- sphynx cats, chinese crested hairless dogs
- colour mutant alopecia- blue and fawn dog breeds (colour dilutions)- dont get protective melanin effect in epidermis- hair follicles, hair shafts fracture easily, brittle, scaled coat
- generally demonstrate patchy, often symmetrical changes
> colour mutant alopecia
> cyclical flank alopecia
> canine follicular dysplasia
> acquired pattern alopecia

3. destruction to hair follicle
- folliculitis and furnculosis
i) infectious
- parasites: demodex
- bacteria- Staph, dermatophilus, Corynebacterum pseudotuberculosis (horses)
- fungi: trichophyton, Microsporum
ii) sterile
- auto-immune- pemphigous folicaceous, alopecia areata, sterile eosinophilic pustulosis and furunculosis
- hypersensitivity- mosquito bite
- comedomes (ac

Front 785

describe the pathogenesis of removal of hair/pruritis alopecia

Back 785

- combination of type I, III and IV hypersensitivities
- vasoactive amines, neuropeptides causing itchiness
- if infectious= release of more inflammatory mediators

Front 786

what is the common factor shared by tumours, nodules and papules?

Back 786

something has been added

Front 787

broadly describe what can cause tumours, pustules and nodules on the skin

Back 787

1. increase in cells
- inflammatory, neoplastic, endogenous- hyperplasia, blood
2. acellular deposit
- mineral, protein (collagen, amyloid), lipid, fluid
3. foreign organism
- parasite, sticks, grass seeds etc

Front 788

describe the signalment of histiocytomas

Back 788

common in young dogs <5yrs

Front 789

what are the 4 common categories of disease we see associated with the dermis and panniculus?

Back 789

1. papular and nodular disease
2. vascular diseases
3. interface diseases
4. connective tissue diseases

Front 790

describe the inflammatory causes of papules, nodules and tumours

Back 790

1. infectious
a) granulomas
- mycobacteria, nocardia
- cryptococcus
- parasites: habronema, draschia (eosinophilic granuloma horses), demodex
- algae and protozoa
b) abscess
- Pasteurella, staphs, streps, Arcanobacterium
- parasites- onchocerca, strongyloides

2. sterile
a) granulomas
- hypersensitivity- insect bites, medication
- foreign bodies
- idiopathic
b) draining sinus
- foreign body

Front 791

describe the neoplastic causes of papules, nodules and tumours in skin

Back 791

1. epithelial
- either arising from epidermis or adenexae (sweat glands, hair follicles)
- usu clustered
- more likely benign in dogs and cattle, more likely malignant in cats, pigs, sheep and goats
> SCC- cats, sheep, dogs
>anal sac adenocarcinoma- dogs

2. round cells
- mast cells, macrophages
- histiocytomas affect dogs <5y
- malignant lymphoma dogs>cats>other species

3. mesenchymal
- fibroblasts, erector pili, stem cells (can differentiate)
- more likely to be solitary masses
- lipoma- dogs
- fibrosarcoma- cats
-sarcoid- horses
- haemangioma- pigs
- melanoma- goats
4. multifocal
- round cell- most common
-metastatic spreading to skin uncommon

Front 792

list the aetiologies of vascular lesions of dermis and panniculus

Back 792

1. inflammatory
> infectious
>sterile
2. degenerative
> hereditary, familial
3. neoplastic

inflammatory most common

Front 793

list the specific aetiologies/aetiological agents of inflammatory vascular disease of dermis and panniculus

Back 793

1. bacteria- Erysipelothrix, Streptococcus, Salmonella
2. viruses- BVD, circovirus, MCF
3. parasites- dirofilaria, onchocerca
4. hypersensitivies
5. photosensitisation
6. toxins- ergot alkaloids, drugs
7. auto-immune- SLE,

Front 794

what is an immediate sign of an interface dermis disease?

Back 794

hypopigmentation- epidermal cells lose melanin

Front 795

describe the aetiopathogenesis of connective tissue diseases of the dermis and panniculus

Back 795

- diseases that target the stroma of dermis or hypodermis
1. dysplastic
- changes in connective tissue structure= altered physical properties such as elasticity and strength i.e. dermatosporaxis (cutaneous asthenia)- dermis prone to tearing
2. depositional
- mineral, protein, ground substance (hereditary, toxic or metabolic_ --> papules, plaques, nodules i.e. calcinosis cutis