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Leah GIL > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Describe the neuronal control of the GIT

A

Parasympathetic from vagus:
- cholinergic and excitatory

Sympathetic fibres are post-ganglionic to:
- BVs
- smooth muscle
- glands
- inhibit acetyl choline release from plexuses

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2
Q

Describe the GIT hormonal control

A
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3
Q

What are gastric secretion made of

A

acid
bicarbonate (base to neutralise acid)
mucus (protects lining os stomach)

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4
Q

How can gastric secretions be modified & give examples

A

neutralisation
- e.g. magnesium hydroxide & trisilicate

mucosal protection
- e.g. sucralfate (coats lining of stomach)

absorbents
- e.g. activated charcoal (binds bacteria & toxins)

histamine antagonist
- e.g. cimetidine

proton pump inhibitors
- e.g. omeprazole

Misoprostol (protects lining & prevents ulcers)

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5
Q

Why might we want to neutralise gastric secretions

A

ruminal acidosis
gastritis
oesophagitis

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6
Q

What is the effect of histamine antagonists on gastric secretion

A

Inhibits gastrin, histamine and acetylcholine stimulated secretion

Pepsin secretion falls (less volume of fluid)

Get a rebound increase on withdrawal

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7
Q

What is the effect of proton pump inhibitors on gastric secretion

A

highly effective

irreversible binding to ATPase

basal & stimulated release is inhibited

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8
Q

What is the effect of Misoprostol on gastric secretion

A

stable analogue of PGE1

inhibits acid secretion

increases mucosal blood flow

increases uterine contraction

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9
Q

What are the 2 centres that control emetics

A

chemo receptor trigger zone
- chemical stimuli
- BBB permeable
- also involved in motion sickness
- impulses pass to vomiting centre

vomiting centre in brainstem:
- coordinates & integrates vomiting

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10
Q

Describe the pathophysiology of vomiting

A

Impulse to vomiting centre via central, peripheral pathways or vestibular apparatus

substance P (neurotransmitter) binds to NK-1 receptors at cell membrane

signal travels via vagus nerve to abdominal muscles + diaphragm => vomiting

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11
Q

How can vomiting be induced (emetic examples)

A

apomorphine (dopamine agonist)
- IV or mucosa
- rapid effect

alpha2 agonists
- e.g. xylazine

syrup of Ipecac
- direct irritant
- cardiotoxicity in high doses

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12
Q

What are some anti-emetics

A

Dopamine antagonists

Cerenia (maropitant)

Anti-histamines

Anticholinergics

Cannabinoids

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13
Q

Describe the action of metaclopramide and domperidone (dopamine antogonists) as anti-emetics

A

Short action so need to infuse IV

Metaclopramide - centrally acting (CRTZ)

Domperidone - peripherally acting

Increase gastric emptying and increased motility

Do not use if vomiting due to obstruction (sends obstruction further down GIT)

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14
Q

What are some dopamine antagonists (anti-emetics)

A

phenothiazine derivatives

metaclopramide and domperidone

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15
Q

Describe the action of Cerenia as an anti-emetic

A

NK1 antagonist
competes with substance P

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16
Q

How is diarrhoea managed

A

maintenance of fluid balance:
- IV fluid therapy (Hartmann’s solution)
- oral fluids
- anti-infectives e.g., zinc = immune stimulant

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17
Q

why may you want to modify intestinal motility in cases of diarrhoea

A

reduce pain

increase transit time and reabsorption window

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18
Q

What are the 2 main classes of antimotility (spasmolytics) drugs

A

opiates
- increase contractions but decrease propulsion –> increased large intestinal tone –> constipation
- e.g. morphine, loperamide

muscarinic antagonists
- inhibit acetylcholine stimulatory effects from vagus nerve
- e.g. hyoscine (buscopan)

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19
Q

What drugs improve gut motility

A

laxatives
- saline & hyperosmotic agents
- irritants to stimulate movement
- bulk producing agents

prokinetics

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20
Q

How does bulk (a laxative) improve gut motility

A

e.g. agar bran

polysaccharide polymers that are not easily digested

form hydrates bulk in gut

hold water

promote peristalsis

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21
Q

How do osmotic laxatives aid intestinal motility?

A

Poorly absorbed solutes

Lactulose - broken down to lactic acid => lower pH => traps ammonia and water in gut => softens faeces => eases motility

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22
Q

What drugs are used in idiopathic inflammatory bowel disease?

A

anti-inflammatory
- steroids such as prednisolone
- sulphasalazine (pro-drug = broken down into active substance in liver)

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23
Q

What are antifoaming agents used for and give an example

A
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24
Q

Define catabolism and anabolism

A
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25
Q

What are metabolic pathways

A
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26
Q

Describe the intrinsic regulation of metabolism

A

Reactions which self-regulate to respond to changes in the levels of substrate or products

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27
Q

Describe extrinsic control of metabolism

A

a cell changing its metabolism in response to signals from other cells

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28
Q

Fill in the rest of the negative feedback loop for thermoregulation

A
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29
Q

Describe the basic reactions that produce energy

A

Energy comes from breakdown of glucose, fatty acids and amino acids into acetyl CoA

Acetyl CoA enters the Krebs cycle to produce energy in 2 ways:
- as ATP (substrate-level phosphorylation)
- through NADH/FADH2 which is processed through oxidative phosphorylation to produce more ATP

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30
Q

Describe the ATP-ADP cycle

A

as body functions use up energy, ATP is converted to ADP and an inorganic phosphate

ADP and inorganic phosphate are used to create ATP for energy

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31
Q

Describe the Krebs cycle

A

Acetyl CoA (precursor to cycle) is produced from AAs, fatty acids and glucose

Series of reactions that oxidise Acetyl CoA to CO2

Electrons lost from these reactions are used in oxidative phosphorylation to produce ATP

Some steps release energy that is directly captured as ATP (substrate level-phosphorylation)

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32
Q

Describe oxidative phosphorylation

A

Electrons from the Krebs cycle are transferred into the electron transport chain in mitochondrion
via an electron carrier

As electrons pass down the electron transport chain it releases energy which is used to pump protons out of the mitochondrion forming an electrochemical gradient

when protons flow back down their gradient they pass through ATP synthase (enzyme) => ATP synthesis

Electrons eventually join O2 to form water

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33
Q

what is resting metabolic rate (RMR)/ basal metabolic rate (BMR)?

A

energy required to maintain life

expressed in kcal/day

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34
Q

what effects the resting metabolic rate

A

body size
age
sex
species
body temperature
hyperthyroidism (increase)
hypothyroidism (decrease)
pregnancy & lactation
growth
genetic factors

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35
Q

Describe glucose during the fasting state

A

~2-4 hrs after a meal blood glucose levels return to basal levels and continue to decrease until the next meal

Insulin levels decline and glucagon levels rise which triggers release of fuels from the body stored

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36
Q

How is blood glucose maintained

A

during fasting liver produces glucose by glycogenolysis (release of glucose from glycogen) and gluconeogenesis (synthesis of glucose from noncarbohydrate compounds (mainly amino acids but also lactate & glycerol))

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37
Q

when is an animal in a starved state

A

when an animal has fasted for 3 or more days

prolonged period of low glucose cause animal to die due to lack of appropriate energy sources to maintain vital cells

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38
Q

What is the impact of increased blood glucose levels

A

increase in blood glucose (after digestion of carbohydrates) is detected by pancreatic islet cells

beta islet cells respond by releasing insulin into bloodstream

insulin signals tissues to store glucose as glycogen or fats

glucagon does the opposite and mobilises stores of glucose when levels are low

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39
Q

What are the 2 fates of glucose in the liver

A

absorbed by hepatocytes
or
continues through liver & enters general circulation

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40
Q

What happens to glucose if it enters hepatocytes

A

glucose can have multiple fates in hepatocytes:

  1. oxidised & used as energy source for hepatocyte
  2. under influence of insulin, it can be converted to glycogen & stored in liver
    - however liver has limited space to store glycogen
  3. can be converted to TAG (triacylglycerol) ready for export out of liver
    - storage of TAG in liver can lead to accumulation of fat in liver which prevents normal liver function & causes disease
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41
Q

Describe the exportation of TAG out of liver

A
42
Q

What is the importance of glucose in the brain

A

Brain and neural tissues can only use glucose as substrate for energy

They oxidise glucose via cellular respiration to generate ATP

Glucose is major precursor of neurotransmitters

Clinical signs of low blood glucose are usually neurological

43
Q

What is the lactate equation

A

Lactate builds up in anaerobic respiration

Lactate + NAD+ <=> pyruvate + NADH + H+

44
Q

What is the cori cycle

A

cycling of lactate & glucose between peripheral tissues & liver

45
Q

Describe the cori cycle

A

Lactate released from cells undergoing anaerobic glycolysis (usually muscle cells when O2 conc is low) taken up by liver and oxidised back to pyruvate

Pyruvate use to synthesise glucose (gluconeogenesis) which is returned to blood

46
Q

Define gluconeogenesis

A
47
Q

Describe anaerobic glycolysis in RBC

A

Glucose is only fuel for RBCs as they lack mitochondria

Glucose used to generate ATP in cytosol via anaerobic glycolysis

Pyruvate formed is converted to lactate and released into blood

48
Q

Describe the fate of glucose in muscles

A

exercising skeletal muscles can use glucose from blood or their own glycogen stores

glucose converted to lactate via glycolysis or oxidised completely to CO2 & H2O

49
Q

Describe the fate of glucose in adipose tissues

A

Adipocytes oxidise glucose for energy

Adipose cells also metabolise glucose to Acetyl CoA which can be turned into fat and stored

50
Q

Fill in the table

A
51
Q

Where does the body get energy from in starved state

A

Body limits amount of AAs used for gluconeogenesis in order to preserve muscle mass

Relies on ketones as source of energy

As there is limited glucose, the brain must rely on using intermediate energy source ketone bodies

=> elevated levels of ketone body in blood = ketosis

52
Q

What is glucose sparing

A

during starvation the brain uses ketone bodies as energy, therefore it needs less glucose

Glucose is still required for use by RBCs

Less glucose is used by the body to keep some ‘spare’

Liver needs to produce less glucose per hour during prolonged fasting than short periods

53
Q

How is protein spare during starvation

A

decreased rate of gluconeogenesis

Reserves proteins for essential functions such as biosynthetic function and new protein synthesis

54
Q

Describe the role of adipose tissue in starvation

A

adipose tissue continues to break down its triacylglycerol stores providing fatty acids & glycerol to blood for energy

in liver fatty acids are converted to ketone bodies which are oxidised for energy

55
Q

How does ketonemia occur

A

The rate of ketone body production exceeds rate at which they can be used

56
Q

Why is ketosis common in dairy cows

A

peak lactation has a high energy demand and cow is incapable of eating enough to support this

Body starts mobilising fats to provides energy => ketone production

Mobilisation of fats results in weight loss

57
Q

How does the body adapt to a starved state

A

The breakdown of protein (for AA for gluconeogenesis) becomes tissue or protein specific to guard against vital proteins/cells becoming depleted

This occurs due to elevated levels of cortisol resulting in body adapting to state of starvation

58
Q

Why do animals die of starvation

A

Proteins become so depleted that heart, kidney etc stop functioning

Animal can develop infection and not have adequate reserves to mount immune response

Deprived of vitamin and mineral precursors of coenzymes and other compounds necessary for tissue function

Lack of ATP and decreased electrolyte intake, electrolyte composition of cells or blood becomes incompatible with life

59
Q

What are the functions of proteins

A

transporters for hydrophobic compounds in blood

cell adhesion molecules

hormones

ion channels

enzymes

60
Q

Describe protein metabolism after eating

A

Ingested proteins digested to amino acids in stomach and SI

AAs transported to liver via hepatic portal vein

AAs used to synthesise new proteins (biosynthesis) or converted to energy sources (gluconeogenesis)

AAs also enter general circulation and go into tissues to be synthesised into new proteins

61
Q

What happens to amino acids in the liver

A

Synthesis of serum proteins &
biosynthesis of nitrogen-containing compounds that need AA precursors e.g., non-essential AAs, haeme, hormones, neurotransmitters, DNA

Oxidizes AAs to produce energy via Krebs cycle in the fed state

62
Q

How is the balance of amino acids in the blood maintained

A

Proteins undergo turnover, constantly being synthesised and degraded, especially in muscle tissue

AAs released by protein breakdown enter the same pool of free AAs in the blood from the diet

63
Q

Describe protein metabolism in fed state

A

AAs released from digestion of dietary proteins travel to liver for synthesis of proteins

Excess AAs converted to glucose or triacylglycerols

Triacylglycerols packaged and secreted in VLDL

Glucose stored as glycogen or released into blood if blood glucose levels are low

AAs that pass through the liver are converted to proteins in the cells of other tissues

64
Q

Describe protein metabolism during fasting

A

AAs released from muscle protein

Some enter blood

Some are partially oxidised and the nitrogen is stored as alanine and glutamine which enter the blood (gluconeogenic AAs)

AAs enter the liver, nitrogen is converted to urea (excreted in urine) and carbons converted to glucose and ketone bodies which are oxidised for energy

65
Q

What is beta-oxidation

A

catabolic process in which fatty acids are broken down to generate acetyl CoA which can enter the krebs cycle

66
Q

Where do chylomicrons go?

A

Chylomicrons are synthesised in epithelial cells, secreted into lymph, pass into blood & become mature chylomicrons

then taken to adipose cells

lipoprotein lipase (LP) digests triacylglycerols (TG) of fatty chylomicrons to fatty acids & glycerol

FA oxidised in muscle or stored in adipose cells

remnants of chylomicrons are taken up by liver and digested

67
Q

What is lipogenesis

A

metabolic formation of fatty acids from excess dietary carbs (glucose converted to Acetyl CoA => fat synthesis) or protein in the liver

Fatty acids combined with a glycerol molecule => TAGs

68
Q

How are TAGs exported from hepatocytes

A

packaged with cholesterol, phospholipids and proteins => VLDL

VLDLs secreted into blood

69
Q

Describe what happens to TAG in a fed state

A
  1. Lipoprotein lipase cleaves TAGs in both VLDL and chylomicrons
  2. forms fatty acids and glycerol
  3. Fatty acids enter adipose cells and are activated forming fatty acetyl CoA
  4. This reacts with glycerol-3-phosphate (formed from glucose) to form TAGs
  5. stored as large fat droplets in adipose tissue
70
Q

describe lipid metabolism in starved state

A
  1. During fasting - adipose TAGs are mobilised (lipolysis)
  2. This releases fatty acids and glycerol into blood
  3. Fatty acids transported in blood with albumin are oxidised for energy in cells
  4. Glycerol used to produce energy via gluconeogenesis in liver

Increased amount of fat mobilised during starvation as decreased AAs used

71
Q

How are ketone bodies produced

A

beta-oxidation of fatty acids produces Acetyl CoA during prolonged fasting

Acetyl CoA converted to ketone bodies in liver

ketone bodies oxidised to produce energy

72
Q

Describe fatty acid oxidation

A

Beta-oxidation:
- fatty acid => acetyl CoA + NADH + FADH

Oxidation of acetyl CoA:
- into Co2 in Krebs cycle
- produces NADH+ & FADH2 through oxidative phosphorylation

ATP generation:
- ATP generated from NADH and FADH via respiratory electron chain

73
Q

What are the 3 ways in which metabolic homeostasis is achieved

A
74
Q

What tissues are dependent on glycolysis for all/most of their energy needs?

A

brain
RBCs
lens of eye
kidney medulla
exercising skeletal muscle

75
Q

What are insulin counterregulatory hormones

A

hormones that appose actions of insulin by mobilising fuels

e.g. cortisol, epinephrine & glucagon

76
Q

How does the release of insulin counterregulatory hormones occur

A

hypoglycaemia is one of the stress signals that stimulates release of cortisol, epinephrine and norepinephrine

ACTH is released from pituitary => release of cortisol from adrenal cortex when hypothalamic regulatory centre detects low blood glucose

When hypothalamic regulatory centre detects low blood glucose => release of epinephrine from adrenal medulla and norepinephrine from nerve endings

77
Q

What is the impact of stress on metabolism

A

SNS => epinephrine and norepinephrine release:

  • promotes release of glucagon from pancreas
  • promotes glycolysis and gluconeogenesis in hepatocytes
  • binds to muscle cell receptors => glycolysis
  • activates hormone sensitive lipase => mobilises fatty acids for use as fuel
78
Q

What is clinical biochemistry

A

analysis of different body fluids for purpose of diagnosis or monitoring

can asses:
- substrates/products
- enzymes
- hormones

79
Q
A

glucose and ketone bodies

80
Q

to analyse metabolism

A
81
Q
A

triglycerides and cholesterol

82
Q

What are the 2 categories of liver enzymes

A

hepatocellular
- contained in hepatocyte
- leak out if there is liver damage
- e.g. AST & ALT

cholestatic
- found on membrane of cells that line bile ducts
- increased conc. in blood if there is issue with flow of bile through liver
- e.g. ALKP & GGT

83
Q

What is hepatic encephalopathy

A
84
Q

What is the calculation for resting energy requirement

A
85
Q

What is the maintenance energy requirement

A
86
Q

What is the effect of having a high energy intake on biochemistry

A

high glucose
high liver enzymes
high cholesterol
high urea
high insulin
high triglycerides

87
Q

what impact does anorexia have on biochemistry?

A

ketosis

dehydration

body mobilises fat stores => increased fatty acids

Less WBCs due to lack of proteins

Increase liver enzymes

88
Q

What is hepatic lipidosis

A

fat accumulates in hepatocytes due to hypoglycaemia as fat is mobilised from adipose tissue and builds up in liver

89
Q

How does fatty liver syndrome develop secondary to ketosis

A

Ketosis is caused by excessive mobilisation of fats for energy

The liver can become overwhelmed with large amounts of lipids leading to accumulation in hepatocytes

90
Q

How can LDA be related to ketosis

A

Gas builds up in abomasum due to abnormal contraction => floats in abdomen to LHS

Ketosis => inappetence => decreased rumen size => more room for abomasum to move

91
Q
A
92
Q
A
93
Q
A
94
Q

What is gross energy and why is it not a useful measure in animal nutrition?

A

Amount of energy in feed

Not the same as the energy they get out of it

95
Q

In what ways is energy lost from food

A

Faecal energy
Urine and gas energy
Heat
Maintenance

96
Q

What is metabolisable energy

A

measure of how much energy can be used by the animal from a feed

97
Q

What is hyperlipidaemia

A

presence of elevated lipid conc in the blood

98
Q

What is hyperlipaemia

A

metabolic disease of ponies, miniature horses and donkeys

Fatty infiltration of organs leading to subsequent organ failure

99
Q

What causes hyperlipaemia

A

negative energy balance

Decreased feed/energy intake

Insulin resistance

e.g., starvation, lactation, pregnancy, stress, obesity

100
Q

Describe metabolic pathways that lead to hyperlipidaemia

A

Low blood glucose => glucagon => lipases

convert triglycerides into glycerol and fatty acids in adipose tissue => FAs and glycerol enter blood

Excess dietary CHO => converted to glucose => converted to fatty acetyl CoA => converted to triglycerides => packaged as VLDLs => into blood

Leah GIL (12 decks)

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