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Metabolism and Excretion > General Revision > Flashcards

General Revision Flashcards

1
Q

When is the liver a haematopoietic tissue?

A

During foetal life

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2
Q

Outline the metabolic roles of the liver

A

The portal venous blood runs through the liver - allows for synthesis of:

  • fatty acid –> triglyceride –> VLDL
  • proteins, steroids
  • glycogenolysis and gluconeogenesis –> carboydrate synthesis
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3
Q

What does the liver secrete?

A

Bile, bilirubin

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4
Q

What happens to the end-products of protein catabolism/ammonia in the liver?

A

Converted into ammonia for excretion

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5
Q

What is synthesised in the liver?

A

Globulins, albumins, prothrombin, clotting factors, bile acids, anti-clotting factors, acute phase proteins, sugars, lipids, urea, ketone bodies

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6
Q

What is stored in the liver?

A

Glycogen, fat, some protein, some vitamins (A, B12), Cu, Fe

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7
Q

Where and what is found in the hilus?

A

The Hilus is found on the visceral surface of the liver

It contains the hepatic artery, nerves, lymphatic vessels. portal vein and common bile duct

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8
Q

On what border does the oesophagus and vena cave pass the liver?

A

The dorsal border.

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9
Q

What attaches the liver to the diaphragm?

A

R&L coronary process

R&L triangular

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10
Q

is the falciform ligament attached to anything other than the liver?

A

No - has a free edge at the ventral wall of the abdomen

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11
Q

What does the umbilical ligament transform into?

A

The round ligament, postnatally

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12
Q

Outline the bile duct system from canaliculi to the duodenum

A

Microscopic canaliculi –> hepatic ducts –> through porta of liver –> common hepatic ducts –> cystic duct –> Gall Bladder
with contraction of Gall Bladder:
Cystic duct –> common bile duct –> major duodenal papilla (most species in conjunction with pancreatic duct)

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13
Q

What causes the Gall Bladder to release its contents?

A

CCK (fat in duodenum)

vagal stimulation

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14
Q

Where does the hepatic artery stem from - what does it provide the liver with?

A

From the celiac artery.

Supplies the liver with blood (1/5) and oxygen (3/5)

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15
Q

How is the liver haemopoietic in utero?

A

Cells from yolk sac (endoderm derived) migrate into the liver = blood islands

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16
Q

Outline the development of the liver in utero

A

Diverticulum from primitive gut (endoderm) –> through (mesoderm) septum transversum –> endodermal buds for bile duct, gall bladder

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17
Q

Does a dogs bile duct open alone on the major duodenal papilla?

A

No opens with pancreatic duct

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18
Q

What kind of angle does the horse kidney form? Where is it found, how many lobes and what does the falciform ligament do? Does the bile duct open alone or in conjunction?

A

Oblique angle
higherst pt. right kidney, two thirds in right plane
Four lobes prom (l,r, q, c)
Falciform ligament: divides quadrate lobe from left
Bile duct with pancreatic duct

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19
Q

What kind of angle does the horse kidney form? Where is it found, how many lobes and what does the falciform ligament do? Does the bile duct open alone or in conjunction?

A

Oblique angle
higherst pt. right kidney, two thirds in right plane
Four lobes prom (l,r, q, c)
Falciform ligament: divides quadrate lobe from left
Bile duct with pancreatic duct

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20
Q

Describe the cow liver, how is it different to smaller ruminants?

A
  • almost all to right, rotated 90 degrees (=right lobe dorsal)
  • gallbladder extends past lat. margin of right lobe
  • bile duct alone on duodenal papilla

Sheep/Goat: similar but bile duct with pancreatic duct

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21
Q

What does the pig lack in terms of processes? How is it identified?

A

No papillary process
Prominent liver lobules (interlobular fibrous tissue)
Alone on duodenal papilla

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22
Q

What two animals bile ducts open alone on duodenal papilla?

A

Cow and Pig (and birds)

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23
Q

Why does the birds liver embrace the heart?

How many bile ducts does it have

A

No diaphragm
Two bile ducts, one on each lobe
Enter alone, close to pancreatic ducts

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24
Q

Do sinusoids have a basement membrane?

A

No they are only lined by fenestrated epithelium - they are blind ending capillaries

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25
Q

What is the sphincter of Oddi and where is it found?

A

At the end of the common bile duct, controls emptying

opens with gall bladder emptying - CCK, vagal stimlation

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26
Q

What makes up bile?

A 
Bicarb
bile salts
cholesterol
lecithin
bilirubin
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27
Q

Describe the production of bile pigments

hbbagus

A

Breakdown of harm –> biliverdin –> bilirubin(unc) bound to albumin –> hepatocytes: conj. with glucuronic acid –> bile
Duodenum w bacteria –> urobilinogen –> stercobilin –> faeces

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28
Q

What is taken up by the portal system?

A

Bile salts, vitamins, drugs

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29
Q

Describe the differences between periportal and periacinar hepatocytes in terms of function and organelles/enzymes

A

Periportal: zone 1: youngest, high mitotic rate, synthesis (protein, glycogen storage/release), high RER
Periacinar: zone 3: oldest, subject to least oxygen, high SER and cytochrome p450 – oxidising function/biotransformation

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30
Q

What cells are found in the sinusoidal lumen - what is their role?

A

Kupffer cells

phagocytosis/filtering especially in carnivores

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31
Q

What is found in the perisinusoidal space?

A 
Hepatic lymph
Pit cells (NK)
Stellate cells: fat storing but with hepatic injury --> collagen deposition and myofibroblast role = fibroplasia/capillarisation
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32
Q

What happens to skeletal muscle glycogen if broken down?

A

Glucose used by skeletal muscle - not put into circulation

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33
Q

Where is pantothenic acid used? Why is it important to have this in the diet?

A

Needed for coA = enzyme carrier (i.e. acetyl)

Need acutely CoA to be carried into the mitochondria for oxidative decarboxylation for energy

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34
Q

What other dietary needs are there for formation of NADH and FADH2?

A

niosine

riboflavin

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35
Q

Describe the pathway that releases energy from fat

A

stored fat –> liver: fatty acids and glycerol

  • fatty acids –> blood stream –> tissues: beta oxidation –> acetyl CoA to TCA
  • glycerol –> glycolysis in liver/kidney
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36
Q

What happens to the amino groups in protein catabolism?

A

De/transanimation - form urea and are then excreted in urine

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37
Q

What amino acids are ketogenic

A

leucine, lysine

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38
Q

What amino acids are both keto and glucogenic?

A

isoleucine, tryptophan, phenylalanine, tyrosine

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39
Q

What are the seven intermediates amino acids can go to when catabolised?

A

pyruvate, acetyl-coA, acetoacetyl-coA, a-ketogluterate, succinyl coA, fumarate, oxaloacetate

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40
Q

How do amino acids get to the liver for gluconeogenesis?

A

In muscle: protein –> amino acid –> TCA –> oxaloacetate –> pyruvate
pyruvate –> alanine = bloodstream to liver
alanine –> pyruvate –> gluconeogenesis: oxaloacetate –> glucose

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41
Q

Why are ruminants dependent on gluconeogenesis?

A

Unable to absorb glucose from diet thus need to make it

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42
Q

What are the five substrates for gluconeogenesis?

A
  • glycerol (from lipolysis)
  • lactate/pyruvate (incomplete oxidative metab)
  • amino acids
  • propionic acid (ruminants fermentation product)
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43
Q

What happens in starvation?

A

Glucagon is high:
Fatty Acids pour out of tissues –> liver overwhelmed cannot make enough fatty acids, low on oxaloacetate –> ketone bodies made - can be used for energy but not by ruminant brain

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44
Q

How do ruminants digest CHO, what are the three end products?

A

CHO –> simple sugars by extracell. microbial enzyme
simple sugars taken up by microbes –> pyruvate –> VFA’s
1) propionic acid
2) butyric acid
3) acetate

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45
Q

What is special about propionic acid?

A

Can be absorbed across rumen epithelium and is gluconeogenic
In liver: propionate –> propionyl CoA –> (with biotin and Mg2+) methylmalonyl CoA –> (with B12) succinate/succinyl CoA:
TCA: –> oxaloacetate –> glucose

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46
Q

What four things are necessary for propionic acid to be gluconeogenic and what is this pathway called?

A

Mg2+, CoA, biotin, VitB12

Methylmalonate Pathway

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47
Q

What happens to butyric acid?

A

absorbed in rumen and omasum
–> ketone body for energy
then metabolised in liver (acetyl CoA)

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48
Q

What happens to acetate?

A

Only VFA present in blood
converted by TCA to acetyl coA
- if low in energy = used for energy production
- if high in energy = de novo fatty acids

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49
Q

What is ketosis?

A

When ruminant is in a state of low energy and brain is using ketone bodies instead of glucose.

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50
Q

How do we detect ketosis and what would distinguish primary from secondary ketosis?

A

Animal is depressed, dehydrated, inappetent. Often after parturition = low energy state.
Assess: ketostix, biochem: high butyrate, acidic blood, CK high (muscle breakdown)

Secondary ketosis - also have temp increase, hear and respiration rate up

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51
Q

How is ketosis treated?

A
  • increase glucose supply (iv) but short lived, hyperglycaemia stimulates milk production (worsens)
  • replenish TCA intermediates to increase oxaloacetate (give PROPYLENE GLYCOL)
  • increase propionic acid in diet
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52
Q

How and what from are ketone bodies formed

A

From acetate
has precursors from: aa, tryglycerides, acetate, butyrate

Normally enter TCA but if low oxaloacetate form ketone bodies

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53
Q

How are glucocorticoids involved in ketosis?

A

reduce ketone production, increase acetyl coA use for glucose production

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54
Q

What happens if the ruminant has a cobalt deficiency?

A

Cobalt is needed to make Vit b12
B12 needed for methylmalonate pathway, if unable to make glucose from propionate = ill thrift, ketosis
(Give cobalt injection, soil supplement or cobalt pellets)

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55
Q

What is pregnancy toxaemia?

A

When the animal is in a state of negative energy - increases fat catabolism - too much for liver to metabolise –> ketosis

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56
Q

Why does the liver have such a high regenerative capacity? Which cells in the parenchyma have the highest capacity to do so?

A

Long lifespan of cells that are stable

Periportal hepatocytes - youngest

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57
Q

What is needed for regeneration of liver parenchyma?

A 
Need scaffold (without = scarring, loss of function in that area)
Need adequate blood supply and drainage
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58
Q

Where do new hepatocytes come from?

A

Viable hepatocytes on edge of injury by mitosis
Oval cells/ductal precursors: epithelial stem cells –> cholangiolar epithelial cells or hepatocytes
Periductular liver progenitor cells - from circulating bone marrow stem cells

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59
Q

Why do drugs often exist as a weak acid or base?

A

Need to be soluble in lipid to diffuse across cell membrane - need to be non-ionised easily. pH dependent

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60
Q

What things determine the ability of absorption of a drug/

A 
pH
gut enzyme digestion
food binding
gastric emptying/trasnit time
absorptive capacity of gastric mucosa
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61
Q

What happens in phase 1 metabolism?

A
  • chemical functional group added

oxydation by p450 then conjugation with reduced glutathione

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62
Q

What happens in phase 2 metabolism?

A
  • add water soluble molecule - acetylation, sulphation, glucuronidation, methylation
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63
Q

What there things determine clearance?

A

glomerular filtration
tubular secretion (drugs can compete for these processes, probenacid banned in sport as will compete with other substances)
tubular reabsorption

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64
Q

What is clearance?

A

Volume of blood from which drug is removed in given period of time (ml/min)

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65
Q

When and how is steady state reached?

A

With constant regular dosing (4-5 t1/2) –> absorption = elimination

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66
Q

Why is the peak in an oral dose not as high as in iv dose?

A

As absorption has to occur and concurrent clearance is already occurring
First pass effect

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67
Q

What is the difference between first and zero order kinetics?

A

First order: rate is prop to conc in plasma with constant half life
Zero order: rate unprop to conc, variable t1/2

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68
Q

What is liver disease? When does this lead to liver failure?

A

A process that results in hepatocyte injury or cholestasis or both.
Only failure if >70% of parenchyma lost

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69
Q

What are some processes that can lead to liver injury?

A
  • hypoxia: anaemia, cardiovascular disease
  • metabolic: diabetes, cushings, hyperthyroidism
  • toxicoses: paracetamol
  • inflam: infection, non-infectious
  • trauma
  • congenital
  • bile duct blockage
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70
Q

How can liver disease be detected?

A

increased activity of ALT, AST, GLDH, SDH, ALP, GGT

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71
Q

What enzymes increase with hepatocyte injury? What does their activity depend on?

A

ALT, AST, GLDH, SDH

- depend on number injured, severity of injury and their serum t1/2

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72
Q

ALT - from where, what species, what does it indicate? What is it measured with?

A
  • use in dogs and cats (cat t1/2 = 3hrs = v recent)
  • cytosolic enzyme - released with hepatocellular injury
  • also found in myocytes - measure with CK
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73
Q

AST - from where, what species, what does it indicate? What is it measured with?

A
  • most species but not as tissue specific
  • cytosolic and mitochondrial
  • also in myocytes and RBC - measure with CK and PCV
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74
Q

GLDH - from where, what species, what does it indicate? What is it measured with?

A
  • most species, especially large as more specific than AST
  • mitochondrial = greater damage needed
  • acute damage, t1/2 <24hr
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75
Q

SDH - from where, what species, what does it indicate? What is it measured with?

A
  • horses and ruminants

- low stability

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76
Q

What two enzymes are measured with CK?

A

ALT and AST

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77
Q

What enzymes increase with cholestasis?

A

ALP and GGT

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78
Q

ALP - what is special about it, what does it indicate, what species is it useful for?

A

Has three isoforms
L-ALP = cholestasis, membrane bound in hepatocytes and biliary epithelium
B-ALP = bone, up in growing animals, tumour, fracture, resorption
C-ALP = corticosteroid, can be stress or hyperadrenocorticism - dogs specific

v. useful in cats: specific to cholestasis, any increase = significant
dogs: ALP precedes hyperbilirubinaemia but C-ALP decreases specificity

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79
Q

GGT - what is special about it, what does it indicate, what species is it useful for?

A

Liver - main source but also in Pancreas, kidney, intestine, epididymis, colostrum (identify successful transfer)
Sensitive indicator of cholestasis and/or biliary hyperplasia. All animals especially ruminant and horse
can precede ALP rise in cats

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80
Q

What do elevated enzyme levels indicate? What don’t they indicate?

A

The magnitude of activity relates to the severity of the damage
Don’t know if reversible, or if local/diffuse

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81
Q

What pigment does bilirubin turn into to cause yellow discolouration of urine?

A

urobilin

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82
Q

Why might there be evidence of hyperbilirubineamia with anorexia/starvation

A

High fatty acid mobilisation

interfere with receptor for unconjugated bilirubin uptake into hepatocytes = high Bu in bloodstream

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83
Q

What type of bilirubin do you expect in horses with hyperbilirubineamia?

A

Bu regardless of pre, hepat, posthepat. causes

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84
Q

What does poikilocytosis mean?

A

Abnormal morphology of cell

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85
Q

How can extra- and intravascular haemolysis be distinguished by looking at RBC?

A

extravascular - immune mediated haemolysis: spherocytes (balled up)
intravascular: ghost cells - only see outline

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86
Q

Why do you see bilirubinuria before bilirubineamia in dogs?

A

They have a low renal threshold for bilirubin, excreted easily

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87
Q

What can bile acids measurements be used for? When would they not be used?

A

They are produced in the liver and are recycled efficiently. Any increases is of concern.
increases if:
- reduced functional mass = impaired excretion from portal blood
- PSS
- cholestasis = retention and reflux

Don’t measure if know cholestatic = will be up

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88
Q

When would a dynamic BA assay be performed? When only one?

A

dynamic - in animals with Gall bladder to see BA levels before eating and then after contraction of gall bladder (challenging reabsorption)
only one - horses and camelids - don’t have gall bladder

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89
Q

Why is the measurement of ammonia problematic in assessing hepatic function?

A

Ammonia usually converted into urea in hepatocytes so if it doesn’t occur = function decrease, PSS, high urease bact, urease toxicosis but ammonia very unstable, has to be measure very fast after plasma extraction

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90
Q

In a serum bicohemistry test what three things indicate hepatic dysfunction?

A 
low albumin (but long t1/2 can take time to show up)
low urea 
decreased glucose (low glycogen and gluconeogenesis)
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91
Q

Why do we screen animals regarding their coagulation status before we perform a biopsy?

A

Liver involved in synthesis of coag. proteins. With hepatic dysfunction could be very low (synthesis down, DIC, reduced absorption of vit K in cholestasis) and thus very susceptible to haemorrhage

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92
Q

Why would hypostenuria be indicator towards liver dysfunction?

A

low urea = low concentration gradient in medulla of kidneys –> PU/PD and ammonium bruit chrystals

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93
Q

On an x-ray how do you distinguish between liver and diaphragm? The gall bladder and hepatic vessels?

A

You can’t - homogenous opacity in health. Apart from the ventral surface of the liver: falciform fat - darker opacity than liver

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94
Q

How can we get an approximate estimate on liver size?

A

by correlation to gastric axis - should be parallel with ribs - more horizontal with increased liver size, vertical with decrease

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95
Q

What is the echogenicity of normal liver parenchyma on ultrasound?

A

uniform and hypoechoic (low brightness)

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96
Q

How is the liver distinguished from vessels, kidney and diaphragm? What about the gall bladder

A

Portal vein - hyperechoic (reflects more)
isoechoic/hyperechoic to right renal cortex
Diaphragm: hyperechoic cranial to liver
Gall bladder: to right of midline, filled with black/anachoic material.

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97
Q

How thick is the normal gall bladder?

A

~2-3mm

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98
Q

What is the difference between portal and hepatobiliary scintigraphy?

A

Portal: to evaluate and quantify PSS. Give radiopharmaceutical into colon or spleen
Hepatobiliary: to quantify liver function and potency of bile duct. Radiopharmaceutical is extracted rapidly by first pass

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99
Q

What is technetium?

A

Scintigraphy used to evaluate Kupffer cell function. It is a sulfur colloid that is taken up by Kupffer cells, its distribution is restricted to sites of functional hepatic mass

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100
Q

Why should patients be fasted prior to FNA or biopsy?

A

Reduces stomach size - makes it easier to take liver sample

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101
Q

What info does FNA give? What doesn’t it give?

A

Neoplasia or vacuolar hepatopathies (lipid, steroid) can be identified
Does not give architectural representation of parenchyma

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102
Q

When can hepatogenous photosensitisation occur?

A

With cholestasis

Photodynamic agent backspins into blood - activated with UV light at skin - oxidative injury

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103
Q

What lesions are found in the brain with hepatic encephalopathy?

A

Ammonia accumulates in astrocytes causing cytotoxic oedema = swelling if astrocyte nuclei, extensive spongy vacuolation, oedema of myelin –> altered gene expression and neurotransmission

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104
Q

Why might one see Hypoalbuminaemia?

A

In chronic hepatic failure - 70-80% functional mass lost as liver only source of albumin
In protein loosing nephropathy and enteropathy – lose protein including albumin
Chronic protein malnutrition

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105
Q

is ascites due to hypoalbuminaemia?

A

No - can contribute but often chronic liver disease won’t cause drop in albumin to <10-15g/L. Ascites due to different causes (increase in pressure)

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106
Q

What is ascites and from what does it develop?

A

Ascites is non inflam oedema fluid from:

  • pre-hepatic: portal hypertension –> transudate
  • hepatic: increased hydrostatic pressure in perisinusoidal space –> hepatic lymph production = modified transudate
  • post-hepatic: resistance of blood flow out of sinusoids = increased pressure in perisinusoidal space –> lymph production increases = modified transudate
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107
Q

Why does the bodies physiological response to ascites worsen it?

A

Body responds to fluid drop in vasculature by retaining water and salt (ADH and …) this means higher hydrostatic pressure -> more ascites

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108
Q

What is bilirubinuric nephrosis?

A

Also known as hepatorenal syndrome

  • acute renal failure due to decreased renal perfusion (=degeneration/necrosis) stems from decreased blood volume (bilirubin diuretic effect or ascites)
  • kidneys are swollen, wet, yellow-orange
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109
Q

What clinical signs would make one suspicious of liver failure?

A
  • drug intolerance
  • foetor hepaticus (musky odour, mecaptans retained)
  • stteroid hormone malfunction (normally conjugated/excreted)
  • hepatocutaneous syndrome (keratinisation, crusting)
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110
Q

What does hyperammonaemia stem from and what can it lead to with supersaturation of urine?

A

From PSS or hepatic failure

Can cause formation of ammonium biurate crystals

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111
Q

What might cause displacement of the liver?

A
  • hepatomegaly or space occupying mass in the thorax –> caudal displacement
  • diaphragmatic hernia –> cranial displacement (strangulation by ring = conjestion and oedema, venous infarction)
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112
Q

What might cause diffuse atrophy of the liver?

A
  • decrease in nutritional supply,
  • congenital/acquired PSS,
  • impaired mitotic dividion (chronic pyrrolizidine alkaloids)
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113
Q

Diffuse atrophy how would you describe the liver and parenchyma

A

liver decreases in size, capsule can become loose and wrinkled. Harder due to contraction of connective tissue.
hepatocytes crowd, sinusoids more prominent and portal areas and central veins are closer

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114
Q

What causes localised atrophy?

A

local compression/pressure – decreased blood flow

local obstruction – decreased bile drainage (liver fluke, mycotoxin - sporidesmin)

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115
Q

Where is glycogen storage especially prominent in hepatocytes? What stimulates this?

A

In zone 2 hepatocytes

glycogen synthase stimulates storage (stimulated by glucocorticoids)

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116
Q

Does glycogen accumulation cause hepatic dysfunction?

A

No not usually and if stimulus stopped - reversible

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117
Q

What is the fate of fatty acids in hepatocytes?

A

While some fatty acids can be used by the mitochondria (oxidation), or to make ketone bodies, most are esterfied into tryglicerides then packed with apoprotein and then made into a VLDL for excretion into the blood to supply other tissues.

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118
Q

What is a cause of lipidosis in hepatocytes?

A
  • Starvation and fatty acid overload of the liver,
  • reduced ATP (apoprotein packaging and VLDL synthesis is very energy expensive),
  • decreased protein,
  • decreased phospholipids
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119
Q

Is lipidosis reversible?

A

Yes if it is not associated with remodelling of tissue architecture

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120
Q

What conditions cause lipidosis?

A
  • high energy diets
  • fasting obese animals
  • pregnancy toxaemia
  • ketosis
  • deficiencey on cobalt/vitB12
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121
Q

What is tension lipidosis and how might it occur?

A

sharply demarcated zone - thought that tension on capsule (fibrous adhesion) = impaired blood flow = sublethal hypoxic injury

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122
Q

How can amyloidosis lead to atrophy?

A

Deposited into perisinusoidal space –> decreases oxygen and nutrients to hepatocytes = atrophy

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123
Q

Where is Iron commonly found in the liver? What is it derived from?

A

Mainly in Kupffer cells. Mainly from RBC Hg

  • if diffuse haemosiderosis: extravascular haemolytic anaemia, Cu deficiency or anaemia
  • if local haemosiderosis: areas of haemorrghage, congestion (zone 3)
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124
Q

What is the difference between ceroid and lipofuscin pigment accumulation?

A

Ceroid - can accumulate intra and extracellular and can cause cellular dysfunction
lipofuscin - intracellularly, zone 3, indigestible residues often incidental

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125
Q

What is telangiectasis?

A

Enlarged sinusoids after embolism with no scarring

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126
Q

What is the outcome of massive necrosis?

A

No cells survive in entire acinus = no scaffold –> broad bands of scar tissue with nodular hyperplasia

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127
Q

In the mosaic of necrotic liver - what makes up the red and yellow areas of the tissue?

A

Red: necrotic and haemorrhage
Yellow: degnerate, surviving

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128
Q

What are anastomoses and when do they occur?

A

Abnormal connections in heavily scarred liver, will impair perfusion causing further injury –> cirrhosis

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129
Q

What are four things characteristic of a cirrhotic liver?

A
  • entire liver is affected
  • bridging or diffuse fibrosis is present
  • regenerative hyperplasia/nodules macro - in dogs)
  • permanent distortion of architecture and new anastomoses
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130
Q

What are some of the consequences to portal hypertension?

A

Congestion of viscera normally drained by portal vein
ascites
acquired PSS

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131
Q

What causes focal hepatitis? And what are these foci?

A

Foci - abscesses
Caused by:
- direct implantation or extension from lesion in adjacent tissue
- ascending infection up bile duct from duodenum
- haemotogenous infection (portal, umbilical, hepatic)

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132
Q

What can luminal acidosis lead to in the liver?

A

Portal embolism of bacteria - especially fusobacterium necrophorum = sharply demarcated zone of coagulative necrosis –> survive can form abscess

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133
Q

What does clostridium novyi cause?

A

Spore that persists in macrophage of liver
migration of liver fluke/decrease in oxygen to liver –> spore germination –> proliferation/exotoxin release –> necrosis of original lesion –> toxin in circulation –> vascular injury = systemic oedema, sudden death
–> Blacks disease

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134
Q

What does Chlostridium haemolyticum cause?

A

causes hepatic necrosis and intravascular homeless = anaemia, jaundice, haemoglobinaem/uria

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135
Q

What can non toxic/hypoxic agent can cause zonal hepatitis?

A

uncommon - canine adenovirus 1 and equine serum sickness

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136
Q

What causes chronic hepatitis? What does it progress too?

A
  • breed related, drug, immune (MHC2 aberrant expression), infectious???

progresses to cirrhosis, dog is ill for long period, increased ALT, eventually biochemical evidence for failure/dysfunction

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137
Q

What is Chronic Copper Storage Disease? What is the problem?

A

Cu is normally stored in hepatocytes - if excessive accumulation - breed related.
Valency of Cu acts as ROS = damage to membranes

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138
Q

What breeds are affected by Chronic Copper Diseases?

A

Dobermans, Cocker spaniels: zone 1, secondary to cholestasis
Dalmatians, Labs: in periacinar hepatocytes

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139
Q

What does cholangitis mean?

A

inflam of bile ducts

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140
Q

How would you describe inflammation of bile ducts spreading into hepatic parenchyma?

A

Cholangiohepatitis

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141
Q

How is an inflamed gall bladder described?

A

Cholecystitis

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142
Q

What is chronic fasciolisis?

A

Caused by liver flukes in lumen of bile ducts (often more severe in left)

  • suck blood, secrete irritating secretions and mechanical irritation
  • obstruct ducts, bile stasis
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143
Q

How does fasciolisis differ between sheep and cattle?

A

Sheep: not as responsive to it: mild dilation and inflammation of thin bile ducts, little reactive fibrosis
Cattle: bile duct fibrosis, more severe erosion and ulceration, irregular duct stenosis

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144
Q

From where does bacterial cholangitis and cholangiohepatitis come from?

A
  • can be blood borne into liver and then descend into gall bladder (bile ducts)
  • commonly up from duodenum by common hepatic bile duct
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145
Q

What animals are especially prone to cholangitis/cholangiohepatitis?

A

Ruminants who have a constant low level circulation of bacteria in health
With bile stasis these can cause bacterial infection

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146
Q

What type of infection is cholangitis/cholangiohepatitis?

A

Inflam of bile ducts spreading into hepatic parenchyma.
Mainly suppurative = neutrophil rich
Acute stage: swelling, soft liver with pus in the lumen of intra and extra hepatic bile ducts
Subacute/chronic: fibrosis = narrowing, cholestasis, atrophy with biliary and nodular hyperplasia

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147
Q

How does cholangitis differ from lymphocytic cholangitis?

A

lymphocytic cholangitis is chronic inflammation with lymphocytes around bile ducts. Incompletely understood why, may be immune mediated.
Similar in that fibrosis develops –> biliary hyperplasia and cholestasis, jaundice and high protein ascites

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148
Q

What toxin causes fascial eczema? What other lesions does the toxin cause?

A

Sporidesmin - mycotoxin from fungus growing on pasture litter
It is a direct irritant to the bile duct epithelium = cholangitis –> necrosis –> obstructive cholestasis –> jaundice and photsensitisation

Also excreted into urine = mucosal oedema and haemorrhage in urinary bladder

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149
Q

How does Caltrop cause jaundice and photosensitisation?

A

Has steroidal sapogenins that are metabolised in the rumen and liver
–> salts with calcium ions = fine crystals = obstruction to bile outflow = cholestasis and photosensitisation in herbivores

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150
Q

Why do choleliths develop? Are they a problem to the animal?

A

Develop secondary to cholecystitis and supersaturation of bile. Not a problem usually as rarely cause obstruction.

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151
Q

What is a gall bladder mucoele? What are the consequences?

A

Excess mucin found in the gall bladder causing distension

–> collapse of thin walled veins = ischaemic necrosis and rupture = anorexia, lethargy, vomiting

152
Q

What causes accumulation of mucin in gall bladder?

A

Unknown related to

  • increased conc of bile salts
  • increased viscosity
  • bile stasis
  • -> mucous production stimulated
153
Q

Why is rupture of the biliary tree/gall bladder more significant than the reticulum?

A

The omentum cannot seal the rupture = leakage into peritoneum –> peritonitis
Septic peritonitis:
- underlying cause was bacterial
- from bile salts irritating mucosa of intestinal wall = leakage

154
Q

What features of the exudate point towards bile peritonitis?

A
  • staining: orange, yellow, green

- pigments in macrophages and mesothelial cells

155
Q

What is meant by secondary poisoning? Give examples

A

Through ingestion of animal/product that has eaten toxin

  • honey: from bees using Patterson’s curse pollen –> pyrrolozidine alkaloids
  • indiospicine poisoning in dogs: neurotoxin (horse - primary) and then hepatotoxin (dog = secondary after ingesting horse carcus)
156
Q

Describe some factors that influence the outcome of hepatotoxin exposure

A
  • sex: males have higher SER and MFO activity
  • adults > neonates
  • previous exposure can up regulate MFO
  • well nourished animals - short fast: glycogen mobilisation = mobilisation of stored MFO
  • low anti-ox/concurrent lipidosis

Protection:
- prolonged starvation - catabolism of proteins and enzymes (incl. MFO)

157
Q

What clinical signs and post mortem lesions are evident with acute hepatotoxicity?

A

Sudden death, not enough time for jaundice, photosensitisation
Post mortem: deep red and swollen liver, oedema in gall bladder, hilus
Zonal pattern, multifocal haemorrhages (DIC)

158
Q

What happens to liver parenchyma with a severe acute hepatotoxin

A

massive necrosis

159
Q

How does chronic hepatotoxicity develop and show

A

Long term low level exposure of toxins
–> jaundice, hepatic encephalopathy, photosensitiation, ascites
Post mortem: multiple lesions with sign of repair and regeneration. Evidence of cholestasis, biliary and nodular hyperplasia.

160
Q

What are some more defining lesions with diagnostic value in chronic hepatotoxicity?

A

karyomegaly: aflatoxins or pyrrolizidine alkaloids inhibiting mitotic division

161
Q

What is Amatoxin?

A
  • Amatoxins: mushrooms, inhibit RNA polym. = no protein synth = cell death
    Acute liver failure
  • blue green algae: in stagnant nitrogen and phosphate rich water: neurotoxins and hepatotoxins –> dissociate hepatocytes (cytoskeleton) = pooling of blood = shock
162
Q

Where do blue green algae proliferate and what do they cause?

A

in stagnant nitrogen and phosphate rich water: neurotoxins and hepatotoxins –> dissociate hepatocytes (cytoskeleton) = pooling of blood = shock in stagnant nitrogen and phosphate rich water: neurotoxins and hepatotoxins –> dissociate hepatocytes (cytoskeleton) = pooling of blood = shock

163
Q

What is the normal metabolism of paracetamol?

A

Normally paracetamol conjugated in phase 2 metab (sulphate/glucuronate) = excreted
Small portion by phase 1 –> reactive n-acetyl benzyoquinonime –> conj. with glutathione = excretion

164
Q

What problem to cats have with paracetamol?

A

Cats have a low conc. of sulphate and glucuronate = more phase 1 metabolism
not enough glutathione to conjugate with reactive intermediate = acute periacinar/massive necrosis

165
Q

What does paracetamol cause to RBC?

A

With glutathione depletion, RBC very prone to toxic injury = intravascular haemolytic anaemia and Heinz bodies with methaemaglobinaemia

166
Q

What is the problem with excess iron in hepatocytes? What causes excess irons in hepatocytes?

A
  • deficiency in selenium/vit e
  • acute skeletal myonecrosis
  • -> more Fe in hepatocytes = ROS due to valency = peroxidation
167
Q

What is the difference in reaction to cyads in sheep and cattle?

A

cyads have glycosides –> metabolite ob gut bacteria = toxic
Sheep: acute periacinar necrosis
Cattle: chronic hepatotoxin with alkylating effect

168
Q

What do pyrroline alkaloids do? In what plants are they found?

A

Chronic hepatotoxin
Found in Echium, Heloptropium etc
The MFO is periacinar cells activate alkylating agent (DHP) = binds covalently to protein and nucleic acid = inhibits mitosis

169
Q

Why is it unusual for pyrrolizidine alkaloids to cause acute hepatotoxicity? What animals are most prone to hepatotocity?

A
  • very unpalatable thus not large quantity ingested

- pigs

170
Q

Can one detoxify DHP/alkylating agent?

A

Yes by conjugation with glutathione

171
Q

What are the lesions of the liver like?

A

nodular regenerative hyperplasia with hepatocellular megalocytosis and karyomegaly
some hepatic fibrosis –> hypertension and ascites
jaundice, photosensitisation and hepatic encephalopathy also seen

172
Q

What do aflatoxins cause? Where are they from?

A

Aspergillum species found on moist feed

MFO’s activate alkylating agent similar to pyrrolizidine alkaloids

173
Q

Where may one see acute hepatotocity with aflatoxins?

A

In garbage feeding dogs –> sudden death,

174
Q

What do phomopsins cause and where are they from?

A

From green moist lupins
phomopsin A interferes with hepatocell cytoplasm formation and spindle microtubules in metaphase
–> atrophy and diffuse fibrosis with regenerative nodular hyperplasia

175
Q

What does lantana do? What is clinically evident?

A

Causes intense jaundice and photosensitisation

Paralyses gall bladder = cholestasis
(disruption of canaliculi support)
Also causes ruminal stasis and nephrosis = PU, dehydration, constipation and anorexia

176
Q

What is chronic Cu poisoning? What does accumulation arrive from?

A

The liver normally regulates intake/excretion of Cu
With cholestasis, increased accumulation of Cu = valency acting as ROS = peroxidation of membrane phospholipids
Cu poisoning with:
- excess intake (contam. pasture)
- increased availability of dietary Cu (decrease in sulphate, Zn or molybdenum)
- concurrent disease

177
Q

What normally happens to hepatocytes with too much Cu?

A

Normally apoptose and surrounding cells will take up Cu. Mitosis = apoptosis.
if apoptosis > mitosis = too much Cu = intravascular haemolysis and hypoxic damage to hepatocytes = more Cu

178
Q

What animals and breeds are especially prone to chronic copper poisoning?

A

Sheep especially british breeds as their liver has a strong affinity to Cu

179
Q

What are idiopathic nodular hyper plastic lesions of hepatocytes? Are they neoplastic?

A

Incidental lesions in old dogs liver
- modified lobules with central vein and portal areas.
- non encapsulated
non neoplastic and different to regenerative hyperplasia (loss of architecture and fibrosis)

180
Q

What are polyps called within the biliary tree? What are they caused from?

A

cystic mucosal hyperplasia –> polyps
sessile - hyperplastic and distended mucus secreting glands
mostly idiopathic but can be due to chronic inflam.

181
Q

Are neoplasms of the liver mostly primary or secondary?

A

Mostly secondary - metastasising malignant tumour - due to position - a lot of blood flows through and is filtered

182
Q

What are the four main secondary tumours seen in the liver?

A

1) carcinoma (epithelial origin - especially endo/exocrine pancreas). Firm scirrhous
2) sarcoma (mesenchymal origin), nodular, cream/white, smooth
3) haemangiosarcoma (vascular epithelium from liver, spleen). Dark red, blood filled
4) Haematopoietic malignancies - lymphoma, metastasising mast cell tumour - often diffuse

183
Q

What is a hepatocellular adenoma?

A

Benign often solitary mass, sharply demarcated but not encapsulated
Hepatocytes but lacking architecture of lobules

184
Q

What is a hepatocellular carcinoma?

A

Malignant solitary mass - can have multiple smaller metastases
Typically invades veins or lymphatic vessels = haematogenous/lymphogenous metast.
–> lungs or lymph nodes

185
Q

What is the urinary system composed of?

A

kidneys
ureters
urinary bladder
urethra

186
Q

What are the muscular tubes found in the urinary system?

A

Paired ureters

Single urethra

187
Q

What is the function of the urinary system>

A
  • to make and secrete urine (filtration, reabsorption and secretion)
  • regulate BP
  • regulate body fluid: composition and volume
188
Q

What components of the urinary system are shared with the reproductive system?

A

In a female: vestibule = tube with urethral and vaginal opening –> to exterior
In male: entire urethra is shared

189
Q

What is a renal lobe?

A

The basic unit of a kidney

  • cortex = cap and medulla = pyramid
  • papilla = apex of medulla –> pelvis or calyx
190
Q

What is the difference between a calyx and a pelvis

A

Pelvis - fused cortex, expanded end of ureter

Calyx - branch of ureter in unfused cortex

191
Q

Where is blood filtered? And where is the filtrate concentrated broadly?

A

Blood comes in through renal artery into cortex = filtered in corpuscle
Filtrate drains into medulla for concentration = loop of Henle

192
Q

What are the differences between unilobar, multilobar, and multi lobar fused cortex, mulitlobar fused cortex and medulla?

A

Unilobar: i.e. rodents
- renal medulla and cortex are fused, single papilla, single pelvis
Multilobar i.e. ox
- lobes distinct medulla and cortex individual, major and minor calyces –>ureter
Mulitlobar fused cortex: pig
- exterior looks like unilobar but can see distinct medullary pyramids
- major and minor calyces and pelvis
Mulitolobar fused cortex and medulla: dog, sheep, goat, horse
- crest type, have pelvis
- blood vessels, undulation at corticomedullary junction and lateral ridges = lobations

193
Q

What are pseudo papillae and in which kidneys do they form?

A

Pseudo papillae look like papillae but don’t open into ureter. Formed in multi lobar fused cortex and medulla kidneys.
Occurs by fusion of medullary pyramids = crest/ridge formation

194
Q

Are the kidneys in roughly the same position on either side of the body?

A

No the right kidney is more cranial than the left as it is tightly anchored to abdominal roof

195
Q

Why are kidneys covered in peritoneal fat?

A
  • protection and stabilisation
196
Q

What does the Hilum open into and what is this usually filled with?

A

Hilum –> sinus –> pelvis

Sinus usually filled with fat

197
Q

What enters/exits through the hilum?

A

The renal artery and vein
The ureter
Autonomic nerves

198
Q

Where is the renal crest?

A

At the junction of renal medulla and the pelvis in a fused medulla/renal papillae kidney

199
Q

What three colours can you distinguish roughly in the internal organisation of a kidney?

A
  • cortex: red pale brown

- medulla: outer zone: purple inner: pale

200
Q

What is the corticomedullary junction?

A

boundary between cortex and medulla

201
Q

How is there evidence of lobulation in a fused cortex kidney?

A

interlobar and renal columns/medullary rays between lobes

202
Q

Describe the ateries of the kidneys starting at the hilus

A

renal artery –> interlobular arteries –> arcuate arteries –> interlobular arteries –> functional end arteries

203
Q

What are the veins found in the kidneys

A
  • satellite
  • capsular/stellate
  • renal vein
204
Q

What is a lobule defines as in the cortex?

A

Interlobular arteries form boundaries

205
Q

What are the two types of nephrons found in the kidney?

A
  • superficial cortical: in renal cortex, with short loop of Henle
  • juxtamedullary: at corticomedullary junction with long loops
206
Q

What part of the descending Lopp of Henle is in the medulla?

A

Only the descending thin

207
Q

What is the medullary ray formed of?

A

Collecting duct travelling towards medulla

208
Q

What is the vasa recta?

A

The blood supply down into medulla
Maintains concentration gradient of interstitial but supplies oxygen and nutrients
descending = arteriolar

209
Q

What is the difference between a true and a false descending vasa recta?

A

True: from interlobular arteries
False: from efferent arteries

210
Q

What controls filtration in the glomerulus?

A
  • pressure of afferent arterioles can be controlled by contraction
  • basement membrane
  • pododcytes
  • filtration slits
  • fenestrated capillaries
211
Q

What are the four layer through which a molecule has to pass in order to be filtered in the glomerulus?

A

Glycocalyx on endothelial cell - covers luminal surface
Fenestrated epithelium
Basement membrane
Epithelial podocytes = filtration slits

212
Q

What types of cells line the proximal convoluted tubule?

A 
Simple cuboidal
large cells boundaries difficult to distinguish, interdigitate
have brush border
basal striations
eosinophilic
213
Q

What type of cells line the descending loop of henle? What might be found here in a dog?

A

Simple cuboidal, similar to proximal convoluted

Dog: may contain lipid = pale medullary rays

214
Q

What type of cells line the thin loop of Henle?

A

Simple squamous
round nuclei
few microvilli
few basal striations

215
Q

What cells line the Distal convoluted tubule>

A 
simple cuboidal
smaller cells than proximal, larger lumen
no brushborder
some basal striations
tight junctions
216
Q

What cells line the straight collecting duct?

A 
Two types of cells
- principal
- intercalated
Lined by simple cuboidal 
- distinct boundaries between cells
- complex tight junctions
- thin apical cell coat bulge into lumen
217
Q

What three things is the juxtamedullary apparatus composed of? At what pole are they found?

A
  • macula densa
  • juxtamedullary cells
  • mesangial cells

At the vascular pole

218
Q

What does the juxtamedullary apparatus control

A

Blood Pressure through

  • GFR
  • Na/H20 regulation
219
Q

Where is the macula dense? What is it composed of and what is its role?

A

In distal convoluted tubule

  • tightly packed columnar epithelial cells
  • in contact with vascular pole of corpuscle and mesangial cells
  • no basement membrane
  • detects salt concentration in the tubules –> if high –> trigger contraction of afferent arteriole = decrease in GFR
220
Q

What are juxtaglomerular cells? Where are they found and what is their role?

A

Modified smooth muscle cells in afferent arteriole
Gap junctions with mesangial cells
Innervated by sympathetic nerves
- baroreceptors sensing blood volume
Contain renin granules - released by stimulation (mesangial, sympathethic B adrenergic) - RAS active release to increase water reabsorption

221
Q

What are mesangial cells? What do they sense and do?

A

Ellipsoid cells between arterioles and macula densa in core of glomerulus

  • Gap junctions between themselves and with juxtaglomerular cells
  • chemorecepetors via macula densa
  • phagocytose
  • supportice
  • contractile –> GFR influence
  • generation of vasoactive agents
222
Q

Where does the right kidney leave an impression on in dog, sheep, goats?

A

On the liver, caudate lobe

223
Q

How does the shape of a cats kidney vary to that of a dog

A

Rounder

224
Q

What is special about the horses kidney?

A

Two different shapes
- heart shaped (right)
- bean shaped (left)
They have a small renal crest and pelvis but long terminal recesses

225
Q

What kind of liver does the pig have?

A

Multi lobar with cortical fusion
has major and minor calyces
Does NOT contact the liver
distinct medullary pyramids and papillae

226
Q

What type of kidney does the ox have? Is a pelvis present?

A

It is multi lobar with no fusion - lobation externally distinct
major and minor calyces
no pelvis

227
Q

What is the tube like structure/s called that allow urine to be excreted? Outline the wall structure

A 
Ureter --> urethra
epithelium = transitional
lamina propria/submucosa
tunica muscularis
adventitia/serosa
228
Q

What is significant about the layers in the tunica muscularis?

A

3 distinct layers instead of 2

  • inner longitudinal
  • middle circular
  • outer longitudinal
229
Q

Why is the epithelium transitional

A
  • has to be impermeable to urine

- has to maintain integrity with tension

230
Q

What part of the urinary tract is not line by transitional epithelium?

A

terminal urethra

231
Q

What is special about the renal pelvis in a horse?

A

Has mucus glands in submucosa (also in proximal ureter)

232
Q

How does the ureter run?

A

Over abdominal roof, passes into bladder obliquely

233
Q

What is the mucosal flap valve and where is it found?

A

Found in the bladder - prevents reflux of urine into ureters

234
Q

What kind of appearance does the lumen of ureters have? Why?

A

Stellate

longitudinal folding of mucosa

235
Q

What are the three regions of the urinary bladder?

A

apex
body
neck –> urethra

236
Q

Where do ureters enter?

A

laterally and dorsally
under mucosa within ridges
converge near urethral crest, open just before ridges meet

237
Q

What is the trigone?

A

The ureteral opening on either side

Converging mucosal folds

238
Q

How is the bladder stabilised?

A

By three ligaments
2 lateral near neck
1 ventral median plane to floor

239
Q

What is the urethra?

A

Muscular tube carrying urine from bladder neck to floor of pelvis –> external urethral orifice

240
Q

What kind of epithelium is found at the terminal end of the urethra?

A

stratified squamous

241
Q

What is the suburethral diverticulum and in which species is it found?

A

In cows and sows

Urethra opens into roof of a small diverticulum at vestibule floor

242
Q

how does the urethral orifice differ between males and female?

A

Male - is at distal extremity of penis

Female - opens into vestibule (shared with vagina)

243
Q

How can the kidney control body fluid osmolarity and volume?

A

By changes in water and Na+

244
Q

What hormones are produced/activated by the kidneys?

A

Renin –> RAS = BP, salt and blood flow
Calcitriol (from vitD) –> intestinal Ca2+ absorption increases
EPO
PGE’s = blood vessel tone

245
Q

What effect can sympathetic nerves have on the kidney?

A
  • stimulate juxtamedullary cells to release Renin
  • regulate GFR by constriction of afferent and efferent arterioles
  • change sodium reabsorption at tubular cells
246
Q

What five hormones act on the kidney and in what way?

A

1) ADH (post. pit) –> collecting duct aquaporins
2) Aldosterone (adrenal cort) –> collecting duct, Na+ reabsorption
3) Atrial Natriuretic Peptide –> baroreceptors sense stretch, heart releases = increased h20 secretion (no ADH response)
4) Parathyroid Hormone –> parathyroid gland = phosphate excretions, calcium reabsorption and calicitriol production
5) Angiotension 2 –> from Ang.1 to prx. convoluted tubule = Na+ reabsorption

247
Q

What is flirtation at the glomerulus proportional to?

A

glomerular perfusion pressure
= systemic BP
= afferent and efferent arterial tone

248
Q

What is GFR defines as? What is it determined by?

A

vol. of fluid filtered/unit time
- filtration coefficient (hydrostatic permeability and SA of glomerulus)
- Net Filtration Pressure - sum of opposing hydrostatic and colloid pressures across capillary (Starlings forces)

249
Q

What do the negatively charged anions of glycocalyx and basement membrane cause?

A

A negatively charged membrane - restricts movement of some molecules

250
Q

What does Bulk flow cause?

A

High hydrostatic pressure - favour filtration

Oncotic pressure will oppose filtration

251
Q

What can reduce pressure within the glomerulus? What can increase it?

A

If afferent arterioles constrict = reduced

If efferent arterioles constrict = relaxed

252
Q

What other cell types are able to control GFR?

A

Mesangial cells - smooth muscle type with contractile ability (and renin secretion) - if contract = decrease GFR
Podocytes - slit size

253
Q

What is meant by auto regulation of GFR and renal blood flow? Why is this necessary?

A

Systemic BP can vary, but only small changes occur in GFR or blood flow - this is to ensure blood still gets filtered accordingly and urine is formed.

254
Q

How is auto regulation achieved? (2 mech)

A
  • myogenic: stretch = Ca2+ into smooth muscle = contraction –> afferent arteriole constriction
  • tubule-glomerular feedback = macula dense detect increase na+ conc = increase flow –>
    a) vasoconstrictive chemical release - adenosine
    b) activate smooth muscle cells in adjacent afferent arteriole
    c) Ca2+ release = vasconstriction
  • -> decrease GFR
255
Q

How and why is auto regulation overridden?

A
  • in order to maintain blood volume in disease (i.e. haemorrhage, amount filtered is reduced to maintain BV)
    Overridden by:
    symp nerves, vasodilators (PGE/PGI, NO), ang 2
256
Q

What happens if systemic BP is low?

A

Baroreceptors in carotid sinus and aortic arch sense low BP

Sympathethic stimulation –> NA –> a1 recep on afferent arteriole = constriction = decrease GFR, increase TPR

257
Q

What are three causes of renin released?

A

decreased pressure in afferent arterioles
decreased Na+ in distal convoluted tubule
symp stimulation of juxtaglomerula cells

258
Q

What does Renin then form

A

Allows formation of Ang2

259
Q

What action does Ang2 have in terms of renal blood flow and GFR?

A
  • To AT1 receptor = constriction of afferent and efferent arterioles –> decreases renal blood flow and GFR
  • To mesangial cells - contraction = decreased SA = decreased GFR
260
Q

Why are PGE and PGI needed with Ang2 and sympathetic stimulation to decrease GFR and renal blood flow

A

Potent vasodilators on afferent arteriole
balance constrictor effects
decrease likelihood of kidney damage

261
Q

What is endothelin? When is it released?

A

Peptide from vascular epithelium. Released by shear force, Ang2 and ADH –> cause vasoconstriction of smooth muscle, ETA receptor

262
Q

What is the action of NO, why is it released?

A

Vasodilator
NO –> smooth muscle cells –> guanylate cyclase to increase cGMP –> PKG = vasodilation as Ca2+ levels drop
Released with drop in BP, blood flow, ACh, histamine, stress, bradykinin, stretch

263
Q

Broadly speaking what are the 3 processes for urine formation?

A

1) glomerular filtration
2) reabsorption of water and solutes
3) secretion of selected solutes from peritubular capillaries into tubular fluid

264
Q

Is tubular reabsorption driven by bulk flow?

A

No the gradients are no large enough. It is by diffusion, active transport, endocytosis and osmosis - paracellular and transcellular routes

265
Q

Why is Na+ reabsorption active?

A

depends on conc gradient set up by basolateral Na+/K+ ATPase

266
Q

What happens to Cl-?

A

Reabsorbed with Na+, can be passive or active

267
Q

Outline what reabsorption occurs in the proximal tubule

A

65% reabsorption
Na cotrans with: glucose, aa, lactate, phosphate
Na antitrans with H+

H20 by osmosis follows Na

268
Q

What reabsorption occurs in the loop of Henle?

A

Depends on descending vs. ascending
- descending: no reabs of salt
- ascending: 25%
Na symp: Na+, K+, 2Cl- symport

269
Q

What kind of transport mechanism is there at the distal convoluted tubule?

A

Na, Cl symport

270
Q

Where are the principal cells found? What is their role?

A

Found in the collecting duct

  • ADH and Aldosterone act on
  • Atrial natriuretic peptide - decreases H20 reabsorption
  • ADH: Aquaporins
  • Aldosterone: Na+ channels, and Na+/K+ ATPase
271
Q

Outline the transporters found on the basolateral side of kidney peritubular cells

A

Na+/K+ ATPase
K+ channel
3HCO3-/Na+ symport

272
Q

What segments of the tubular apparatus are very permeable to water? Which segments require more control?

A

proximal tubule, descending loop of henle and distal tubule – very permeable
Collecting duct - depends on if ADH is present or not

273
Q

How are organic solutes absorbed?

A

Often by con transport with Na+

- proximal tubule

274
Q

What kind of metabolism occurs within the tubules?

A

synthesis of NH4+ and HCO3-

275
Q

How are proteins reabsorbed?

A

large: by endocytosis
small: catabolised by peptidase –> symport with H+

276
Q

What are the barriers of tubular secretion?

A

tight junctions

basolateral and luminal membranes

277
Q

What transporter allows for movement from blood into tubular cell for then secretion by diffusion of organic ions such as penicillin, barbituates, urate and oxalate?

A

Antiporter at basolateral surface with alpha-ketoglutarate

278
Q

What about the movement of organic cations - adrenaline, histamine, choline, dopamine, morphine?

A

facilitated diffusion into tubular cell by OC+ transporter
active secretion: ATP-carriers
OC+/H+ antiporters

279
Q

What can the urine concentration vary? Why?

A

50 - 5000mOsmol/L

in order to maintain normal water and sodium content: 290-300mOsmol/kg

280
Q

What is meant by the term obligatory water loss?

A

Mass of wastes - urea, creatinine - that have to be removed, and are dissolved in water
600mOsm/day –> into maximal urine conc of 1400mOSm/L
= 0.44L/day at least

281
Q

Give a step by step description of countercurrent multiplication within the kidney

A
  • tubular fluid flows through loop
  • ascending loop - pushes sodium out of tubules into interstitium
  • descending loop - allows water to move into interstitium to balance concentration
  • the longer the loop, the more concentrated interstitium can get
  • constant flow of tubular fluid - can concentrate more until reaches equilibrium
282
Q

How is the concentration maintained within the interstitium

A

Vasa recta - supplies blood without washing away gradient
hairpin turn, with very slow flowing blood - takes up water into circulation
enough time for solutes to diffuse back out into interstitial = countercurrent exchange

283
Q

What role does ADH play in concentrating urine?

A

High osmolarity at hypothal. or decreased BV at baroreceptors = release from posterior pituitary
–> prinicipal cells of collecting duct: G protein, cAMP = insert aquaporins, H20 will move out into interstitium by osmosis.

284
Q

Describe the differences between the descending and ascending vasa recte

A 
Descending = continuous epithelium -- salt, urea, water in
Ascending = fenestrated - rapid diffusion out of salt, urea into interstitium
285
Q

Is the vasa recta permeable to plasma proteins?

A

No, means a high colloid pressure is maintained, pulling water in out of interstitial
= interstitium hypertonicity maintained

286
Q

How does medullary washout occur?

A

If blood flow through vasa recta increases = inappropriate solute exchange
–> decreased osmotic gradient in medulla = more difficult to concentrate

287
Q

What is meant by urea recycling?

A

Urea reabsorbed in proximal tubule but then no movement out until collecting duct
with ADH present in inner medullary collecting tubules = urea transporters to move urea into interstitium increases osmolarity to drive h20 reabsorption

288
Q

Where are baroreceptors found? And what do they sense?

A
  • carotid sinus, glomerular afferent arterioles, aortic arch, cardiopulmonary circulation
    sense vascular stretch due to increase in ECV
289
Q

What is the ECV proportional to?

A

The NaCl concentration

290
Q

What do the kidneys do when there is a low ECV?

A

Increase Na+ reabsorption to increase water reabsorption

291
Q

When is the ECV low but ECF high? Does kidney function help in these circumstances?

A

In cardiac failure with oedema

Increased water retention will not help as it increases intravascular pressure increasing oedema formation

292
Q

What does stimulation of baroreceptors cause?

A

Change in volume is sensed:

  • sympathetic nerves
  • ang 2
  • ADH
293
Q

Describe pathway from Liver to Ang 2

A

Liver releases Angiotensinogen

  • with increased tubular pressure in Kidney: RENIN from juxtaglomerular cells is released
  • Renin converts to Ang1
  • lungs release ACE
  • ACE convert to Ang 2
294
Q

What are the six main roles of Ang2?

A

1) constrict afferent and efferent arterioles and mesangial cell contraction = decrease GFR
2) Increases tubular salt reabsorption as activate Na+/H+ antiporter
3) Adrenal cortex to release Aldosterone to increase (2)
4) Arteriolar vasoconstrition by AT1/2 receptors = high BP
5) Pituitary gland to release ADH –> aquaporins
6) increases thirst

295
Q

What three sites does atrial natriuretic peptide act at?

A

1) inhibits release of Renin
2) inhibits release of Aldosterone
3) inhibits aquaporin insertion at collecting duct

296
Q

What is Aldosterone and what role does it play in concentrating urine?

A

Steroid hormone from adrenal cortex

  • increases Na+/K+ ATPase activity
  • increases number of Na+ channels at luminal membrane
297
Q

How are sympathetic nerves activated?

A

Low ECV in kidneys = alpha adrenergic receptors activated

298
Q

What are the 3 main roles of sympathetic nerves in terms of water conservation?

A
  • constrict aff arterioles = decreased GFR
  • renin secretion from juxtglom cells – Na+ reab up
  • increase HR = increase cardiac output to restore BP
299
Q

What three inputs into juxtaglom. cells regulate renin release?

A
  • sympathetic nerves, baroreceptors sense low BP (= low Na+&volume)
  • intrarenal baroreceptors - juxtaglom cells in afferent arterioles sim with low ECV
  • macula densa - senses low Na+ conc in tubules
300
Q

Where does atrial natriuretic peptide come from? Why?

A

From myocytes in heart in response to atrial stretch (high ECV)

301
Q

What are the five main roles of ANP?

A

1) dilate afferent arterioles, constrict efferent to increase GFR
2) inhibit Renin release
3) inhibit Na+ reabsorption in collecting duct
4) inhibit ADh action on collecting duct
5) inhibit Aldosterone release (directly and indirectly)

302
Q

Where is potassium mainly found? What does it determine?

A

Found mainly intracellularly
determines
- electrical potential of membrane

303
Q

When is one hypokalemic/hyperkalemic?

A

Hypo: <3.5mEq/L
Hyper: >5mEq/L

304
Q

What is the only way K+ can be secreted into urine? Why?

A

Only by secretion by principal cells in collecting duct, as all is reabsorbed

305
Q

How is K+ reabsorbed in the proximal tubule?

A

Diffusion by set-up of Na+/K+ ATPase????

306
Q

How is K+ reabsorbed in loop of henle

A
  • Na/K/Cl transporter apically with K/Cl co trans basolaterally
  • Na+/K+ ATPase and K+ ion channels (=pump-leak mechanism)
307
Q

What are the two cell types found in the collecting ducts? How do they differ in handling potassium?

A

Principal cell - secrete K+
Intercalated cells - reabsorb K+
– which one is more active depends on diet

308
Q

What drives K+ movement in principal cell?

A

Na+/K+ ATPase at basolateral membrane = K+ into cells (from interstit), diffuses through channels, into lumen of tubules

309
Q

What drives K+ movement in intercalated cells?

A

K+/H+ ATPase at tubular lumen - acitve uptake, K+ then diffuses into blood by K+ channel

310
Q

What are the five mechanisms for the kidney ro regulate K+ excretion?

A

1) altering K+ channels in luminal and basolateral membrane of collecting duct
2) Aldosterone - stimulate secretion of K+
3) increasing K+ conc inside cells to increase conc gradient
4) tubular flow rates
- increase gradient for K+
- increase Na+ delivery for reabsorption = Cl- left behind = electrochem gradient for K+
5) pH altering K+ channles and Na+/K+ ATPase, K+/H+ ATPase
i. e. in acidosis = decreased K+ secretion

311
Q

What are the four substances that are H+ forming in the kidney?

A

1) non-vol. acids: sulphur, phosphoric
2) sulphur containing aa: methionine, cysteine
3) cationic aa: arginine, lysine
4) hydrolysis of dietary H2PO4

312
Q

What two substances are alkali generating in the kidneys?

A

1) anionic amino acids: glutamate, aspartate

2) oxidation of anions: citrate, lactate

313
Q

How is the pH of 7.4 maintained even with varying H+ levels?

A
  • buffering: intra&extacell
  • alveolar ventilation to regulate CO2
  • Renal excretion of HCO3- to control levels in plasma
314
Q

What are buffers? What does the pK mean?

A

A weak acid/base, not fully dissociated

At a given H+ conc, defined amount of buffer exists as HA and defined amount as A-. pK = ration of HA to A-

315
Q

What is the major buffering system in the body? What is pH?

A

The bicarbonate offering system
H+ + HCO3- = CO2 + H20

pH = pK + log[HCO3-]/[CO2]

316
Q

What upper and lower pH limits prior to death?

A

<6.8

>8

317
Q

Where are buffers present?

A

extracellularly and intracellularly and bone

  • Extra: HCO3-
  • Intra: proteins, phosphate (H2PO4- = H+ + HPO4-), RBC Hb
  • Bone: buffer excess H+ in exchange for K+, Na+, dissolution of bone mineral (NaHCO3, KHCO3, CaCO3, CaHPO4)
  • urine: ammonia
318
Q

What sits in the medulla oblongata? What does it regulate with drop in [H+]?

A

The respiratory centre, with low H+ causes reflex hypoventilation, to increase CO2.

319
Q

Can respiratory system control the H+ balance alone?

A

No just pH, the H+ regulation is by the kidneys

320
Q

How does the kidney regulate pH?

A

Through excreting bicarb and secreting into tubular fluid by intercalated cells (type B)

321
Q

What occurs if low pH/high H+

A

kidney tubular, intercalating type A cells reabsorb HCO3- into plasma
Achieved by tubular H+ cycle/secretion

322
Q

What is meant by H+ cycle/secretion in tubular cell trying to reabsorb HCO3?

A

Inside cell: CA produces HCO3- (–> into blood, Na+/3HCO3- symport, HCO3-/Cl- antiport) and H+ (–> into tubular fluid by Na+/H+ ATPase, or H+Atpase)

In tubular fluid: excess HCO3- and H+ come to CA –> H20 + CO2 –> diffuse into cell —> into blood

323
Q

How is this HCO3- reabsorption different in the intercalated cells?

A

Excretory mech into tubular fluid for h+ (H+ATPase, K/H+ antiporter)
Basolaterally: only HCO3-/Cl-

324
Q

What happens if all available HCo3- is reabsorbed? What does this ensure?

A

secreted H+ will combine with other urinary buffers - ammonium and phosphate

  • ensures H+ conc gradietn maintained for excretion into tubular fluid
  • protection of depth cells as pH doesn’t drop
325
Q

What is the problem with phosphate buffers?

A

They don’t work below a pH of 5.7

326
Q

Where does the ammonium buffer come from?

A

Glutamine metabolism
Most NH4+ reacts in liver with HCO3 = urea
But some hepatic glutamine synth. to proximal tubule for ammontagenesis = NH4+ liberation into urine

327
Q

What is ammontagenesis?

A 
Glutamine in tubular fluid - reabsorbed wit Na contransport. Glutamine in blood reabsorbed with Na citrons. Broken down into Glutamate and releases NH4+. (Glutamate to alpha ketoglut. to glucose to blood)
NH4+ produced then broken into 
1) Nh3 (-->diff into tubule)
2) H+ (H+ATPase)
3) H+ (H+/Na+ antiporter)
In tubule form NH4+
328
Q

What is metabolic acidosis? What will be compensatory response?

A

High H+ or low HCO3- (source other than CO2)

  • lactic acid
  • ketone bodies (diab. mellitus, fasting)
  • loss of bicarb (diarrhoea, diuretics)
  • renal failure (retaining diet sulphuric acid)

Hyperventilation to increase plasma pH

329
Q

What is respiratory acidosis? What is the compensatory response?

A

low pH, high Co2 - from inadequate ventilation

  • tuberculosis/lung tissue damage
  • pulmonary oedema/impaired gas exchange
  • polio/paralysis of resp muscles
  • reduced chest motility

Kidneys excrete more H=/conserve HCO3-

330
Q

What is metabolic alkalosis? What is the compensatory response?

A

High pH, low CO2

  • increased artificial ventilation
  • hypoxia
  • hypervent. from pain or anxiety

kidneys reduce HCo3- reabsorption

331
Q

What is the role of diuretics? What is an example

A

To increase vol of urine excreted when disease state retaining NaCl and H20

– inhibit, Na+, Cl-, HCO3- reab

Piamox: CA inhib

332
Q

What is meant by Azotaemia?

A

elevation on non-protein nitrogen compounds (urea and creatinine) in the blood
often due to decreased GFR with >75% loss of nephron function

333
Q

What is creatinine and what is it from?

A

non-protein nitrogen

breakdown of creatinine phosphate in muscle

334
Q

What is cystocentesis?

A

Collection of urine from the bladder with needle and syringe

335
Q

What are the USG’s used to classify urine as hypo, iso, hyperstenuric to plasma?

A

hypo: <1.008
iso: 1.008 - 1.012
hyper: >1.012

336
Q

What is oliguria and pollakuria?

A

Oli - excret of abnormal small vol

polla - increased freq or urination

337
Q

When can SDMA be used and for what?

A

It will increase with >40% renal function loss
It is a compound (symmet dymeth.arg) released in proteolysis - excreted through kidneys = glom filtration rate can be measured
Unable to dif. renal from pre-renal azotaemia

338
Q

How is uraemia diagnosed?

A

With clinical signs (wt. loss, weakess, lethargy, depression, ulceration of mucosa, halitosis)
And azotaemia

339
Q

What is a urine creatinine ratio used for?

A

Used with unexplained protein loss in urine
Ration gives estimation of loss is glomerular or tubular
high UP:C = glomerular loss rather than tubular

Not used in UTI/cystitis. USG will be normal/high - protein from inflammation

340
Q

At what %loss of nephron function is PU evident? What does that mean? What does it cause?

A

66%
regulatory failure - cannot conc urine

Causes: metabolic acidosis and electrolyte abnormalities

341
Q

When is azotaemia present?

A

With >75% loss of function = nitrogen wastes accumulate

Excretory failure

342
Q

What is used as a marker for Biosynthetic Failure?

A

unable to synth. EPO –> non-regen anaemia

343
Q

How is urea handled in the kidneys? Why does urea increase?

A

Filtered and some reabsorbed
Urea increases with decreased GFR
Causes can be pre-renal, renal, post-renal

344
Q

What are causes for pre, renal, post renal increases of urea?

A
  • Pre: decreased renal perfusion with dehydration
    high protein diet
    GIT haemorrhage/protein loss
  • Renal: insufficiency, nephron function lost
  • Post-renal: urinary obstruction, uroabdomen
345
Q

In what species would you not measure urea?

A

Ruminants and horses:
not renal system that excretes urea
ruminants - rumen
horses - l. intest

Birds and reptiles - dont produce urea, only uric acid

346
Q

Why is creatinine a better indicator of GFR than urea?

A

No significant tubular reabsorption

conc not affected by diet

347
Q

What are causes of increased creatinine?

A 
decreased GFR (pre, renal, post)
training/rhabdomyolosis
large muscle mass

fake increase with reaction of dipstick with - bilirubin, lipid, glucose, cephalosporin, ketones

348
Q

When is creatinine low?

A

In severe muscle wastage

349
Q

In what species is creatinine not used?

A

In birds - not marker of renal function

350
Q

What are USG’s a measure of?

A

tubular function

  • ability to reabsorb/secrete H20
  • PU with >66% renal tubular funct
  • measures solutes in urine
  • need to know hydration status as can vary
351
Q

What is the reading of a USG dependent on, how is it read?

A

Read of a refractometer
Dependent on temp
Other substances can increase USG - not from tubular function: albumin and glucose

352
Q

What would you expect the USG’s to be like for a dehydrated healthy cat, dog, l.animal, bird?

A

cat >1.035
dog >1.030
l.animal > 1.025
bird >1.020

353
Q

What other things have to be considered in a USG reading?

A
  • hydration status
  • serum electrolytes
  • extern factors (hypercalcaemia, hyperadrenocort, liver disease)
  • drugs (diuretics, corticosteroids)
  • protein/glucosuria
354
Q

What three things if renal medullary hypertonic dependent on?

A
  • resorption of NaCl w/out H20 (ascend.)
  • resorpt of urea at collect duct (w ADH)
  • renal medul. blood flow (if high = washout –> hypercalcaemia, hyperthyroidism, PU)
355
Q

What does central diabetes insipidus cause?

A

Decreased/deficient ADH = decreased secretion

356
Q

What causes decreased ADH action from nephrogenic diabetes insipidus?

A

hypokalaemia, hypercalcaemia, corticosteroids, endotoxin, pyelonephritis

357
Q

What would you measure in a pre-renal azotaemia? What causes this?

A
  • elevated urea, creatinine
  • high USG = can still concentrate

dehydration = decreased renal perfusion, drive to reabsorb water = more solutes in urine
protein catabolism = high urea –> high USG without dehydration

358
Q

What would be measured in renal azotaemia?

A
  • elevated urea, creatinine
  • low USG for hydration status - can’t conc.
    = evidence of renal failure (>60-70% nephron funky loss)
359
Q

In renal azotaemia is it certain whether function loss is reversible, acute or chronic?

A

NO

360
Q

What can cause renal azotaemia?

A
  • parenchyma damage: toxic insult (ethylene glycol, grapes, lillile), sclerosing parenchymal damage
  • secondary factors from outside kidney affecting renal tubular function:
    primary diabetes insipidus, secondary/nephrogenic diabetes insipidus (hypercalcaemia, hyperadrenocorticism, pyometra)
    loss of medal. conc. gradient (electrolyte/urea depletion)
361
Q

What is the USG like in post-renal azotaemia? What is post-renal azotaemia?

A

Variable

Failure to excrete urine

362
Q

How does one diagnose post-renal azotaemia? What causes this?

A

History: strang/dysuria, physical exam, imaging, hyperkalaemia, decreased urine output, distended bladder, uroabdomen

From obstruction: urethral, ureteral - calculi, plug
Breach in post-renal urinary tract: bladder rupture, ureter, urethra torn

363
Q

When would you see hyperkalaemia?

A

In anuric, oliguric, obstructive disease

decreased GFR, decreased secretion, acidemia

364
Q

When would you see hypokalaemia?

A

in PU renal disease -
high fluid flow rate = decreased absorption
tubule dysfunction

365
Q

When would you see hyperphosphataemia?

A

With low GFR and in growing animals, from bone

366
Q

In what animals is hypophosphataemia associated with renal disease?

A

IN horses with chronic kidney disease

367
Q

In what species is hypocalcaemia a marker of chronic renal failure?

A

In dogs and cats, secondary to hyperphosphatemia and low vit D

368
Q

In dogs and cats what is the calcium level like in acute kidney injury?

A

Variable can be hyper/hypocalcaemia

369
Q

What do horses display with acute and chronic renal disease?

A

hypercalcaemia

- due to high calcium diet, the kidneys secrete excess

370
Q

When may you see hypermagnesiumaemia?

A

With decreased GFR

371
Q

What would sodium and chloride levels be like with renal insufficiency?

A

Vairable depends on water vs electrolyte loss and change can be marked by dehydration

372
Q

What does marked hyponatraemia and/or hypochloridemia point to?

A

Alert if with renal azotaemia

  • impaired tubular function - medullary washout
  • secondary renal azotaemia
  • severe GIT disease, hypoadrenocorticism
373
Q

What happens to acid base balance in renal insufficiency?

A

Metabolic acidosis

  • titrational = uraemic acid +/- lactic
  • secretory = bicarb loss
374
Q

What happens to the levels of amylase and lipase in the blood with renal insufficiency?

A

Increase due to decreased GFR

375
Q

What is the difference between acute and chronic renal insufficiency? Is the magnitude of azotaemia a marker?

A

Acute: abrupt decline (hrs - wks)
Chronic: progressive decline in renal function (wks - yrs)

Cannot use magnitude if azotaemia, no accepted system - need history, chin signs
PU = chronic
Ca2+/PO4-
anaemia

376
Q

What is secondary renal insufficiency?

A

When renal system cannot function secondary to another cause

377
Q

What are some causes of renal insufficiency

A

hypochlorid/hyponatraemia = washout and impaired

Metabolism and Excretion (1 decks)

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