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Leah GIL > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What are the differences in their muscularis mucosa

A
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2
Q

How is keratin replaced in keratinised stratified squamous mucosal epithelium of rumen, reticulum & omasum?

A

Keratin broken down by microbial population
They contain enzymes (keritinases) that degrade keratin

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3
Q

Why is a keratinised epithelium needed in ruminant forestomachs

A
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4
Q

What are these and describe them

A

Vary in shape & size depending on age, diet & location
High concentrations of VFA’s and fibre promote growth

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5
Q

Which digestive products are absorbed in rumen papillae

A
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6
Q

label the rumen papillae

A
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7
Q

How do ruminal papillae change with diet

A
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8
Q

Label the rumen

A
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9
Q

What is this & describe it

A

Reticulum

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10
Q

Why do solid objects end up in the reticulum

A
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11
Q

What is hardware disease and which structures are involved

A
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12
Q

Label the reticulum

A
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13
Q

What do we think the omasum does

A

water absorption
mechanical breakdown of ingested material
absorption of small nutrients

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14
Q

Label the omasum

A
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15
Q

Which groups of ruminants dont have an omasum

A

camelidae

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16
Q

Label the omasum

A
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17
Q

Apart from water, what else does saliva contain

A

Proteins
amylase
sodium ions
chloride ions
potassium ions
bicarbonate

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18
Q

Which of these statements about rumen is correct:
a. food storage to allow large meals to be eaten
b. allows fermentation to occur
c. allows water absorption
d. allows mixing of gastric enzymes

A

B

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18
Q

Briefly describe how small intestinal epithelium is regenerated under normal conditions

A
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19
Q

which nerve(s) supply most of the parasympathetic supply to the gastrointestinal tract?
a. lumbar splanchnics
b. dorsal vagus
c. dorsal and ventral vagus
d. perineal
e. pelvic ganglia

A

C

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19
Q

When assessing health of teeth from a radiograph, which of these signs indicate healthy teeth:
a. even radiolucent band between alveolar bone and tooth
b. radiolucent halo at apex of root
c. narrow pulp cavity
d. sclerosis of alveolar bone
e. radiolucent region around all roots of a tooth

A

A

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20
Q

Which are radiographic signs of dental disease:
a. even radiolucent band between alveolar bone and tooth
b. radiolucent halo at apex of root
c. narrow pulp cavity
d. sclerosis of alveolar bone
e. radiolucent region around all roots of a tooth

A

B, D, E

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21
Q

When performing a double-contrast gastrogram, why is the animals position important?

A
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22
Q

Why does a right-sided aortic anomaly cause megaoesophagus

A
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23
Q

What is choke in horses?

A
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24
Q

Label the liver

A
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25
Q

Label the organs and blood supply

A
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26
Q

Describe the liver blood supply

A
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27
Q

Describe regeneration of liver

A
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28
Q

What is hepatic parenchyma

A
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29
Q

What is hepatic stroma

A

Structural tissue of liver

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30
Q

Label the liver histology

A
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31
Q

Label the pig hepatic lobule

A

Pigs have more connective tissue in liver than other species

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32
Q

What is a liver lobule

A

Hepatocytes are organised in radial cords forming a 6 sided prism with portal triads at each corner and a single central vein

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33
Q

Label the liver lobule

A
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34
Q

Describe the histological organisation of the a liver lobule

A
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35
Q

How does blood flow in a liver lobule

A

centripetally to central vein

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36
Q

Label the portal tract

A
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37
Q

What is the limiting plate of a liver lobule

A
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38
Q

Label the liver lobule

A

Sinusoids: Region where blood is flowing where there is either absent, or very few endothelial cells

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39
Q

What are the 4 liver cell types

A
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40
Q

Label the liver cell types

A
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41
Q

Label the liver cell types

A
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42
Q

Fill in the liver cell types table

A
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43
Q

Label the liver under TEM

A
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44
Q

Label the liver

A
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45
Q

What is the role of HSC/Ito cells in liver

A
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46
Q

What liver cell in this

A
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47
Q

Fill in the hepatocyte organelles functions

A
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48
Q

Label the hepatocyte organelles

A
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49
Q

What are bile canaliculi

A
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50
Q

Label the liver

A
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51
Q

What is the function of the gall bladder

A

storage, concentration and release of bile

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52
Q

What are the functions of bile

A

fat digestion
hepatic excretion

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53
Q

Label the gall bladder

A
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54
Q

Label the gallbladder

A
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55
Q

Label the blood and bile flow diagram

A
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56
Q

What is a hepatic acinus

A
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56
Q

What is a portal lobule

A
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56
Q

label the hepatic parenchyma

A
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57
Q

What are the zones of hepatic acinus

A

Zone 1 closest to portal tract and receives most oxygenated blood and zone 3 the least

Zone 3 has higher biotransformation/detoxification activity

In toxic diseases, zone 1 suffers first (perilobular necrosis)

In hypotensive/congestive diseases zone 3 suffers first (centrilobular necrosis)

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58
Q

Which is the liver

A

B

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59
Q

Describe detoxification of foreign chemicals in liver

A

Xenobiotics
Phase I - cytochrome P450 modifies the chemical to allow phase II
Phase II - glucuronidation

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60
Q

Describe haem breakdown

A

Occurs in macrophages (mainly in spleen but also liver & bone marrow)
Iron toxic so important to remove

Damanged RBCs phagocytised by macrophages

Haemoglobin broken down into Fe2+, bilirubin (from haem) and amino acids

Amino acids enter blood stream

Bilirubin travels to liver to be excreted in bile

Fe2+ travels to bone marrow for erythropoeisis and to the liver to be stored as ferritin

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61
Q

Fill in the urea metabolism diagram

A

In ruminants urea is food source for microbial proteins

In mammals amino part of amino acid turns into NH4+

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62
Q

Fill in the energy metabolism table

1. amino acid 2. glucose 3. triglyceride 4. VFA

A
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63
Q

Where are liver enzymes in healthy and diseased livers

A

When liver is healthy, enzymes stay intracellular (wont be able to measure them)

If found in blood test there is liver damage

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64
Q

What are the liver enzymes involved in energy metabolism?

A

Aspartate aminotransferase (AST)
Alanine aminotransferase (ALT)

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65
Q

What is the function of aspartate aminotransferase (AST) in energy metabolism in the liver?

A

Glycolysis (Role in the malate-asparate shuttle)

AST catalyses the conversion between aspartate and oxaloacetate

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66
Q

What is the role of alanine aminotransferase (ALT) in energy metaolism in the liver?

A

Gluconeogenesis

Amino acid catabolism

Alanine reacts with alpha-ketoglutarate to form glutamate and pyruvate (catalyzed by ALT)
Pyruvate can be used to produce glucose or enter the Kreb’s cycle

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67
Q

What are some plasma proteins

A

Serum Albumin - highly abundant
- carrier protein
- maintains osmotic pressure
- Important so plasma is at same osmotic pressure as cells to prevent water transfer

VLDL

HDL

Fibrinogen & Prothrombin – coagulation cascade

Transferrin – iron transport

Complement proteins

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68
Q

Describe lipoproteins

A

Lipoproteins move insoluble fat around e.g., triglycerides, cholesterol esters
Describe according to density e.g, VLDL, HDL
Linked to proteins (apolipoproteins)

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69
Q

What are apolipoproteins

A

Each lipoprotein has own set of apolipoproteins
- e.g. Major protein in chylomicrons is apolipoprotein B, specifically apoB-48
- Give it its characteristics

Apolipoprotein functions:
- Activate enzymes
- Bind receptors
- Stabilise lipoprotein

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70
Q

Describe bile salts

A

Bile acids are cholesterol derivatives

Main bile acid is cholic acid

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71
Q

What are micelles

A

Bile salts in aqueous solution tend to form aggregates or micelles

These are amphiphilic i.e. inside +ve & outside –ve

Therefore internalised lipid core, water soluble exterior

The –ve external charge prevents them from coalescing.

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72
Q

Describe the action of bile

A

Emulsification: Bile acts like a detergent to break down fats into smaller droplets, increasing their surface area for better digestion.

Mechanism: Bile has hydrophobic sides that bind to fats and hydrophilic sides that mix with water, helping to mix fats into the watery digestive juices.

Nutrient Absorption: By emulsifying fats, bile aids in the absorption of fat-soluble vitamins (A, D, E, K).

Enzymatic Action:
Phospholipids: Broken down by pancreatic phospholipase A2.
Cholesterol: Broken down by cholesterol esterase.

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73
Q

Describe the synthesis of cholesterol in the liver

A
  1. Acetyl-CoA + actetoacetyl-CoA
  2. Carbon chain lengthens
  3. Decarboxylation => cholesterol
  4. Cholesterol can then be converted to bile salts in the liver or moved to endocrine glands to become steroid hormones
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74
Q

Describe the route of bile acids

A

Absorbed in ileum

  1. travel to liver via hepatic portal vein
  2. conjugate with cholesterol
  3. travel to gall bladder then into the duodenum where they cause fat absorption
  4. travel down to ileum and reabsorbed
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75
Q

How is fat absorbed in the small intestine

A
  1. Bile salts and pancreatic lipase break large fat droplets down
  2. Micelles formed as bile salts form aggregates, conjugated with phospholipids and cholesterol
  3. Micelles release into epithelial cells/enterocytes
  4. Free fatty acids and monoglycerides within mycelle diffuse into enterocyte
  5. Triglycerides resynthesised and chylomicrons formed in enterocyte (chylomicrons are exocytosed into lymph vessel)
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76
Q

Describe the urea cycle in the liver

A
  1. Ammonium reacts with CO2 => carbamoyl phosphate in the mitochondria
  2. Carbomoyl phosphate reacts with ornithine to produce citrulline
  3. Citrulline reacts with aspartate in the cytoplasm => arginine
  4. Arginine reacts with water to form urea and ornithine
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77
Q

describe the immunoregulation function of the liver

A

Kupffer cells (sit in sinusoids between liver cells)

Complement synthesis & metabolism

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78
Q

What does the liver store

A

Glycogen

Water-soluble vitamins

Fat-soluble vitamins

Iron
- Gives it dark color
- Too much iron being stored can cause damage

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79
Q

Define toxicology

A

study of harmful properties, actions & effects of chemicals on biological systems

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80
Q

Define toxin

A

antigenic poison/venom of plant or animal origin

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81
Q

Define toxicant

A

any toxic substance

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82
Q

Define poison

A

substance capable of causing illness or death of living organism

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83
Q

Define venom

A
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84
Q

Define xenobiotic

A

a chemical substance within an organism that is not naturally expected or foreign

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85
Q

Define toxicosis

A

any disease or condition caused by poisoning

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86
Q

Define no observable effect level (N.O.E.L)

A
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87
Q

Define developmental toxicology

A
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88
Q

Describe ways in which toxicants may produce toxicosis

A
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89
Q

When does a chemical become toxic

A
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90
Q

How can we measure how dangerous a toxin is

A
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91
Q

List the key information in the investigation of a suspected case of intoxication

A
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92
Q

How can toxicants be absorbed

A
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93
Q

How can toxicants be distributed

A
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94
Q

Where do toxicants go (storage)

A
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95
Q

How are toxicants eliminated

A
96
Q

What is lethal synthesis and give an example of it

A
97
Q

Describe the main metabolic pathways for elimination of fat soluble toxicants

A
98
Q

What factors effect toxicity?

A
  • dose of toxin
  • environmental factors (e.g. temperature, humidity)
  • duration & frequency of exposure
  • inability to vomit
  • age & health of patient
  • seasonal or climatic changes
  • route of exposure
  • isomer of toxin
99
Q

Compare acute to chronic toxicosis

A
100
Q

What is chronicity factor

A

Duration of exposure can affect toxicity

CF is ratio of acute to chronic LD50 dose
- e.g. a compound may have low acute toxicity but if it accumulates in tissue it can lead to chronic toxicity = cumulative poisons
- CF of >2 suggests drug is relatively cumulative

Chronicity factor gives indication of cumulative danger (but could be affected by body developing tolerance)

101
Q

What is tolerance and how does it develop?

A
102
Q

What is resistance and how does it develop

A
103
Q

Outline therapeutic options for management of toxicosis

A
104
Q

Fill in the urea cycle

A
105
Q

What is NH4+ used for in mammals

A

feeds the Krebs cycle

106
Q

What is nitrogen converted to in fish, mammals, birds and reptiles

A

mammals: urea
Fish: NH4+ (because they are in water)
Birds and reptiles: uric acid

107
Q

Fill in the table

A
108
Q

What pathways can lead to an excess of nitrogenous compounds in animals body

A
109
Q

What is deamination

A

NH4+ removed from amino acid

110
Q

How is excess ammonia removed in the absence of amino acids?

A

formation of glutamate and glutamine from a-ketoglutarate

111
Q

Describe the amino acid catabolism

A
112
Q

What happens if ammonia builds up

A

hyperammonemia
damages brain cells => abnormal behaviour, dizziness, coma and death

113
Q

What conditions cause hyperammonemia

A

Liver dysfunction
Abnormality in hepatic portal flow
abnormality in urea cycle enzymes
starvation (body breads down skeletal muscle for energy -> more amino acid catabolism)

114
Q

What is the fate of a-keto acids (product of deamination)?

A

recycled into the TCA/Kreb’s/Citric acid cycle or used in lipid metabolism
Ketogenic amino acids - will feed lipid metabolism
Glucogenic amino acids will feeds gluconeogenesis

115
Q

What is first pass metabolism of a drug

A

Liver metabolism once drug is ingested
Liver protects body from drugs
Metabolism prior to drug entering systemic circulation

116
Q

How are polar drugs excreted

A

Polar drugs are more likely to be excreted

117
Q

How are non polar drugs excreted

A

If drug is not water soluble it must be metabolised by CYP450 to be excreted in urine

118
Q

Describe phases of drug transformation (polar drugs)

A

Phases occur in liver

Phase 1. catabolic
- oxidation
- reduction
- hydrolysis

If phase 1 not sufficient then to phase 2

Phase 2. anabolic
- synthetic conjugation (makes it more water soluble so it can be excreted in urine)

119
Q

What is the location of CYP450 enzymes

A

in endoplasmic reticulum of cells

120
Q

What is pharmacokinetics

A

How the drug enters, is transported and eliminated

121
Q

What is pharmacodynamics

A

effect drug has on body

122
Q

What is the role of CYP450

A

metabolise lipophilic/non-polar drugs into hydrophilic/polar compounds to allow excretion

123
Q

How can multiple drugs affect activity of each other

A

The product of one drug reacting with a CYP450 may decrease or increase the expression of another CYP450
So the activty of the drug the affected CYP450 acts on could increase or decrease

Interactions are less likely if drugs can be metabolised by more than 1 CYP450 enzyme

124
Q

Two positive contrast radiographs from the same patient are provided.
A catheter (marked by the arrow) has been placed in one of the tributaries of the hepatic portal vein and in each case a positive contrast medium has been injected into the vein to demonstrate the flow of blood from the intestinal tract to the liver. These are known as portal venograms.

Questions:
Which image shows a normal hepatic portal vascular pattern? Given the images are from the same patient, what has changed?

In one of the images blood from the GIT is by-passing the liver, into which vessel is blood from the GIT emptying? Which embryological structures could be involved?

Why do patients with this abnormality exhibit neurological signs?

Why would a patient with a urea cycle enzyme deficiency show similar signs?

A
125
Q

Why is paracetamol dangerous in cats

A

Because, compared to other species, they have limited capacity for glucoronidation of paracetamol metabolites (to make “safe” metabolites for excretion) and so “unsafe” metabolites accumulate which cause tissue damage through reactive oxidation including oxidation of haemoglobin and red cell damage. Glutathione, which is protective against oxidation, is quickly consumed leaving cells and tissue unprotected.

126
Q

Most of the metabolic enzymes used by the liver remain contained within the cells of the liver and we don’t learn anything about the livers activity by trying to measure those metabolic enzymes in the circulation.
However, there are some enzymes that will leak out of liver cells into the circulation if the liver cells are compromised or damaged. We measure these in the circulation, not because they are particularly interesting enzymes for liver function but because they are markers of cell damage.

Fill in the table

A
127
Q

Give examples of primary liver disease

A

Hepatitis
Parasitism (fluke)
Biliary obstruction (e.g. gall stone)

128
Q

Give examples of secondary liver diseases

A

Energy metabolisation disorders
- diabetes mellitus
- fatty liver

Systemic inflammation/sepsis
- e.g. pyometra

Pathology of GI tract or pancreas

129
Q

Why do we measure bile acids before and after a meal to assess liver function in dogs and cats but not in horses?

A

By providing a meal, we should stimulate a gall bladder contraction causing bile to enter the GI tract and bile acids to be resorbed back into the circulation from the gut. How well the liver recaptures these bile acids from the blood flowing through it gives an idea of how well it is functioning. We expect the liver to have recaptured this pulse of bile acids within 2 hours of the gall bladder contraction. In horses, without a gall bladder, we can’t stimulate this “challenge pulse” of bile acids into the enterohepatic circulation and just have to rely on the baseline concentration as measure of function.

130
Q
A

Patient 1 is more likely to have the bile duct obstruction and the impact on the biliary lining is reflected in the relatively higher activity of AlkPhos (a biliary enzyme). Patient 2, more suggestive of toxic insult directly to the hepatocytes (the increase in ALT is relatively greater (15x URL) than the increase in ALKP (<5xURL))

131
Q

The liver synthesises all of the coagulation factors except Factor VIII. Among these are vitamin K-dependent factors – which clotting factors are vitamin K-dependent?

A

2, 7, 9, 10

132
Q

In a patient with a coagulopathy resulting from hepatic failure, which of the following tests of the coagulation mechanism would be likely to be abnormal?
* Platelet count
* Von Willebrand Factor
* Whole blood clotting time
* Activated partial thromboplastin time
* One stage prothrombin time
* Fibrin degradation products
* Fibrinogen

A
133
Q

Why do some animals with liver disease have yellow mucous membranes and sclera

A
134
Q

Why do some animals with advanced liver disease have ascites? What is a transudate?

A
135
Q

How does avian metabolism & GI tract compare to mammals

A

high metabolism due to energy demands of flight

Short GI tract with low volume to keep weight low

136
Q

Label the bird

A
137
Q

Compare GI tract of seed/green leaf eating birds to carnivorous birds

A
138
Q

Label the bird GI tract

A
139
Q

Describe the structure of the beak

A
140
Q

Label the bird skull

A
141
Q

What muscles open and close the beak

A
142
Q

Name the birds and their beak adaptations

A
143
Q

Describe the avian oropharynx

A

oropharynx instead of soft palate, oral cavity & pharynx

Choana = connection between oropharynx & nasal cavity

infundibular cleft (caudal to choana) = common opening for pharyngotympanic tubules

Hyoid apparatus supports keratinised tongue

No teeth

Tubular salivary glands release mucin +- amylase

144
Q

How do birds swallow while eating

A
145
Q

How do birds swallow while drinking

A
146
Q

Describe the avian oesophagus

A
147
Q

Describe the avian crop

A
148
Q

What is sour crop

A
149
Q

Describe the mechanisms of the crop

A
150
Q

Label the avian GI tract

A
151
Q

Describe the avian proventriculus and gizzard

A
152
Q

Label the avian GI tract

A
153
Q

Describe egestion in birds

A
154
Q

Compare the function of gizzard thin and thick muscles

A
155
Q

What is grit

A
156
Q

Describe the avian liver & pancreas

A
157
Q

Describe the avian small intestine

A
158
Q

Describe avian small intestine physiology

A
159
Q

Describe avian caeca

A
160
Q

Describe the avian large intestine

A
161
Q

Describe the avian cloaca

A
162
Q

Describe the 3 compartments of the cloaca

A
163
Q

Describe avian excretion

A
164
Q

Define laparotomy

A

surgical procedure that involves making incision through abdominal wall

165
Q

Define laparoscopy

A

minimally invasive technique that uses laparoscope to view inisde abdominal cavity

166
Q

Define coeliotomy

A

surgical incision through abdominal wall

167
Q

define paralumbar fossa

A

hollow area located on side of lumbar vertebrae in animals (esp. cattle).
Site is commonly used to access abdominal cavity

168
Q

Define linea alba

A

fibrous band of tissue in midline of abdomen that serves as attachment site for abdominal muscles

169
Q

Define pre-pubic tendon

A

fibrous band of connective tissue in pelvic region that provides support to abdominal wall

170
Q

Define parietal, visceral and mesenteric peritoneum

A
171
Q

Where do crura arise from

A

lumbar vertebrae

172
Q

Where are costal and sternal attachments

A
173
Q

What are the 3 openings of the diaphragm

A

aortic hiatus
oesophageal hiatus
inferior vena cava

174
Q

What is the innervation of the diaphragm

A

phrenic nerves

175
Q

What are the muscular boundaries of the abdominal cavity

A
176
Q

Label the limits of the abdominal cavity

A
177
Q

Describe the directions in which the muscles of the abdominal wall run?

Why are they in a crossed pattern?

A

contributes to strength and stability of abdominal wall

178
Q

Describe the location of the paralumbar fossa

A
179
Q

Describe the peritoneum

A

peritoneum is serous membrane which lines abdominal cavity

3 sections
- parietal
- visceral
- mesenteric

Sac between each section is called peritoneal cavity (contains peritoneal fluid)

Peritoneum can excrete and resorb fluid and resorb gas

Diseases include peritonitis, neoplasia, haemorrhage

180
Q

Label the layers of the lateral abdomen

A
181
Q

What are the arrows pointing at

A
182
Q

Describe the Ligamentum teres

A

Extra ligament in horses holding hip joint together

comes from head of femur

attaches to acetabulum of hip bone

Prevents excessive adduction and extension

183
Q

What is the arrow pointing at

A
184
Q

Why are abdominal surgeries done on the left side in ruminants

A

everything can be reached easily from the left

185
Q

describe the inguinal canal

A
186
Q

Do females have inguinal canals

A

yes but its smaller and less well defined

it doesnt transmit a spermatic cord but does allow for passage of round ligament of uterus

187
Q

Describe the innervation of the abdominal wall

A
188
Q

What is a paravertebral nerve block

A
189
Q

Describe the vasculature of the abdominal wall

A
190
Q
A
191
Q

Fill in the intestinal anatomy table

A
192
Q

What are the layers of the small intestine

A
  1. lumen
  2. mucosa
    a. single epithelial layer
    b. lamina propria
  3. submucosa
  4. tunica muscularis
  5. serosa
193
Q

Label the small intestine

A
194
Q

What are the adaptations of the SI to increase surface area for absorption

A

ridges/folds
villi
microvilli

195
Q

Label and describe their function

A
196
Q

Label and describe their function

A
197
Q

Label red and blue arrows

A
198
Q

Label

A
199
Q

What are Brunner’s glands

A
200
Q

What is the arrow pointing at

A

Ileum

Last bit of small intestine

201
Q

What are the 6 cell types of the small intestine

A
202
Q

Label

A
203
Q

where are cells of small intestine produced and how long does it take

A

stem cell zone at neck of crypts

Takes 3-4 days for cells to travel from crypts to tip of villus

204
Q

What are the functions of enterocytes

A
205
Q

Label the villus

A
206
Q

Describe entero-endocrine cells

A

produce hormones

207
Q

Label the small intestine

A
208
Q

Describe paneth cells

A
209
Q

What is this showing

A

Paneth cell granules

210
Q

Describe peyers patches

A
211
Q

Describe lymphoid follicles and lymph nodes

A
212
Q

Label the ileum

A
213
Q

Describe M cells

A
214
Q

Label the M cell

A
215
Q

Describe tuft cells

A

Sparse cells

sit between epithelial cells so still columnar

Have long fingers which project sideways into neighbouring epithelial cells

Produced by stem cells

Modulate immune system responses (esp. against protists and metazoa)

216
Q

Label

A
217
Q

How does venous blood from pancreas drain

A
218
Q

Describe cat and dog pancreatic lobes and ducts

A

Both have dorsal (left, accessory) and ventral (right, main) lobe

Dogs have dorsal and ventral ducts

Cats only have ventral duct because they fuse

219
Q

What are the secretions of the pancreas

A
220
Q

Label the pancreas

A
221
Q

Describe pancreatic stimulation

A
222
Q

Describe Islets of Langerhans

A
223
Q

Describe blood supply to GIT

A
224
Q

Describe Coeliac artery branches

A

only those in bold

225
Q

Label the arteries

A
226
Q

Describe enteric nervous system supply to GIT

A
227
Q

What do enterocyte enzymes break down and absorb

A
228
Q

What are the arrows pointing at

A

crypts

229
Q

In which parts of the GIT are villi found

A

duodenum, jejunum, ileum

230
Q

Where do you find goblet cells and what is their purpose

A

epithelium of small and large intestines

purpose is to lubricate & protect lining of GIT, trap foreign particles & pathogens & facilitate movement of materials

Inflammatory signals stimulate them to produce more mucus in case of inflammation

231
Q

What kind of feedback mechanisms operate to tell crypts to re-form villus if they had been destroyed

A
232
Q

What is the ingredient in rat poison that is poisonous

A
233
Q

How would you treat a patient that consumed rat poison

A
234
Q

What clinical signs would you expect in a sheep with rhododendron poisoning and how would you treat it

A

abdominal pain
bruxism (grinding teeth)
regurgitation
death
loss of appetite
lethargy
nausea
salivation
vomiting
bradycardia

235
Q

Why might a toxin affect 2 patients differently

A
236
Q

Assuming the effective doses of the substances below are the same, which is more dangerous ?

A. LD50 of 20mg/kg
B. LD50 of 50mg/kg

A

A

237
Q

What is photosensitisation

A

common in horses

caused by impaired liver function due to ingesting plants toxic to liver

chemicals from toxic plant are not excreted due to impaired liver function so they build up in blood

They are activated by sunlight and cause irritation

clinical signs: sore muzzle (cracking & crusty), yellow tinged mucous membranes, not eating

238
Q

What clinical signs would you see in a cat that consumed ethylene glycol (antifreeze)

A
239
Q

How would you treat a cat that consumed ethylene glycol (antifreeze)

A
240
Q

How would a buzzard ingest lead and what would the clinical signs be

A
241
Q

What organs are affected by lead toxicity and what tests would you do to confirm it

A
242
Q

What would be the likely causes of lead toxicity in a parrot? what clinical signs would you notice and how would you treat it?

A
243
Q

What would be likely causes of lead ingestion in a pet rabbit

A

toys
lead paint
cage
things around house if let out

Leah GIL (12 decks)

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