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Physiology II > Online Quiz 1 > Flashcards

Online Quiz 1 Flashcards

1
Q

How are proteins temporarily stored?

A
  • labile protein pool (intracellular amino acid pool)
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2
Q

When are amino acids metabolized?

A
  • after deamination to keto-analogs
  • > removal of amino group
  • HIGHLY reversible
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3
Q

Protein Synthesis

A
  • functional proteins are formed out of the labile protein pool
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4
Q

Pathway of Keto-analogs

A
  • follow carbohydrate metabolism
  • enter the Krebs cycle
  • for energy gain, gluconeogenesis, shunted via Citrate for Lipogenesis, and form Ketone Bodies via excess Acetyl CoA
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5
Q

Problem with the deamination of amino acids

A
  • deamination of amino acids involves removing an amino group, thus forming ammonia (NH3) which is potentially toxic and needs to be removed
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6
Q

How can Ammonia (NH3) be removed?

A
  1. Transamination = reuse of NH3

2. Urea formation = excretion of NH3

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7
Q

What is the process of transamination of NH3?

A
  • amino groups are transferred to a-ketoglutarate forming Pyruvate/Glutamate
  • > this forms Alanine = transport form of NH3
  • Alanine/Glutamate transfers the NH3 to other compounds for amino acid synthesis involving various Amino transferases (ALT and AST)
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8
Q

What are the Amino Transferases, what process are they involved in, where are they found?

A
  • found in muscle tissue and liver
  • involved in transamination of NH3
  • increase in enzyme plasma levels is important for clinical diagnosis
  • > indicates excess leakage of enzymes, necrotic cells, etc
    1. Alanine Amino-Transferase (ALT)
    2. Aspartate Amino-Transferase (AST)
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9
Q

What is the process of Urea formation?

A
  • if amino groups are not utilized for transamination, the liver will convert the potentially toxic ammonia (NH3) to urea
  • the kidney will then excrete the urea
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10
Q

Hepatic Encephalopathy Cause and Clinical Signs

A
  • Ammonia (NH3) is potentially toxic, if the liver does not convert it to urea for kidney excretion it will accumulate
  • accumulation of NH3 due to liver failure causes an interference with GABA, or glutamate neurotransmitters (affects CNS)
  • > causes neurotoxicity, depression, neurological deficits (“head pressing”), coma and death
  • -> all signs indicative of forebrain damage!!
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11
Q

What organ is damaged if you see an increase of Ammonia (NH3) in the plasma?

A
  • the Liver
  • > because the liver is supposed to convert NH3 to urea for kidney excretion, so if it is an NH3 accumulation the liver is not converting it
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12
Q

What organ is damaged if you see an increase in urea, but the NH3 levels are normal?

A
  • the Kidney
  • > the function of the kidney is to excrete the urea after the liver has converted the NH3 to urea
  • > but if the kidney can not not excrete it, then there will be an accumulation of urea
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13
Q

How do ruminants metabolize carbohydrates?

A
  • essentially all carbohydrates are fermented into Volatile Fatty Acids (VFAs)
    1. Acetate
    2. Butyrate
    3. Propionate
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14
Q

What is a problem for ruminant metabolism of carbohydrates?

A
  • Ruminants are potentially “hypoglycemic”
  • very little glucose reaches the intestines for absorption
  • BUT demands for glucose are the same, or higher during lactation
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15
Q

What do ruminants depend on to maintain adequate glucose levels?

A
  • Gluconeogenesis
  • > it is permanently ON and provides 90-100% of the blood glucose
  • -> 40-80 mg/dl vs 80-120 mg/dl in monogastrics = slightly lower in ruminants
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16
Q

What are the main glucose precursors for ruminants?

A
  1. Propionate (70%) = most important VFA for gluconeogenesis
  2. Amino acids (20%)
  3. Lactate, Pyruvate, Glycerol
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17
Q

Pathway of Propionate (C3) in Ruminants

A
  • extracted by the liver
  • glucose precursor used for gluconeogenesis
  • enters the Krebs cycle as succinate, undergoes carboxylation which requires Vitamin B12 which has Cobalt
  • > common deficiency in Florida, Australia and New Zealand
  • -> no gluconeogenesis can occur if no cobalt
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18
Q

Pathway of Acetate (C2) in Ruminants

A
  • absorbed by all tissues, except the liver
  • for ATP and Lipogenesis
  • Enter the Krebs cycle as Acetyl CoA for energy gain
  • > major energy supplier
  • Enters Lipogenesis as Acetyl CoA in mammary glands and fat
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19
Q

Pathway of Butyrate (C4) in Ruminants

A
  • partly converted in the rumen epithelium and after liver uptake to Ketone Bodies (B-hydroxybutyrate, acetoacetate, acetone)
  • for ATP and Lipogenesis
  • Ketone Bodies are utilized in peripheral tissues for energy gain after entering the Krebs Cycle as Acetyl CoA
  • Ketone Bodies contribute to lipogenesis via Acetyl CoA in fat tissue and mammary glands
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20
Q

What can cause metabolic disorders?

A
  1. Endocrine disorders (hormone imbalance)
  2. Nutritional deficiencies
  3. Genetic defects in enzymes or transport proteins
    - Lipidosis = fat storage causes NS issues
    - Glycogen storage diseases = polysaccharide storage myopathy (PSSM) in horses
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21
Q

Causes of Polysaccharide storage myopathy (PSSM) in Horses

A
  1. Glycogen can not be broken down because of a debranching enzyme deficiency
  2. Free glucose can not be released because of hepatic-glucose-6-phosphatase deficiency
    - hypoglycemia
  3. An abnormal glycogen type is formed and stored due to a glycogen-synthase mutation
    - Glycogen can not be mobilized
    - PSSM type 1
    - hypoglycemia
22
Q

Clinical signs of Polysaccharide storage myopathy (PSSM) in Horses

A
  1. Energy deficiency in muscles
  2. Muscle necrosis (rhabdomyolysis = muscle lysis/tearing) during forced exercise
  3. Hypoglycemia
  4. Hepatomegaly (liver swelling) and cardiomegaly
23
Q

Major Phases that fuel whole body metabolism homeostasis

A
  1. Absorptive Phases
    - excess energy goes into storage
  2. Post-Absorptive Phases
    - low energy continues mobilization
  3. Fasting/Starvation
    - fasting for survival and continued mobilization
24
Q

Absorptive Metabolism Phase Effects

A
  • post-prandial (eating) phase
  • hyperglycemia stimulates insulin release and inhibits glucagon release
  • > INSULIN HIGH AND GLUCAGON LOW (opponents)
  • glucose is oxidized in all tissues for energy
  • excess nutrients are stored as glycogen (glycogenesis) in a temporary protein pool and fat
25
Q

Absorptive Metabolism Phase active pathways in Liver/Muscle/Fat

A
  • excess energy goes into storage
  • time of active digestion and absorption of fuels
  • blood glucose, amino acids and chylomicrons increase
    1. Liver
  • glycogenesis
  • amino acid uptake, temporary storage and plasma protein synthesis
  • lipogenesis -> releases VLDLS
    2. Muscle
  • glycogenesis
  • amino acid uptake, temporary storage and plasma protein synthesis
    3. Fat
  • insulin stimulates endothelial LPL in fat cells
  • > fatty acids and glycerols are extracted from chylomicrons and VLDLs for fat storage
  • Lipogenesis
26
Q

What is different about the absorptive phase in a carnivorous diet?

A
  • amino acids and chylomicrons are absorbed, but very little glucose
  • Hypoglycemia (due to insulin release) stimulates glucagon release
  • > insulin and glucagon increase and work as partners
27
Q

Post-Absorptive Metabolism Phase active pathways in Liver/Muscle/Fat

A
  • digestion and absorption of fuels is completed
  • low energy causes mobilization
  • blood glucose, amino acids and chylomicrons decrease
  • Glucose is only available for glucose-dependent tissues due to the lack of insulin
  • glucose independent tissues use lipids for energy gain with the help of cortisol and epinephrine
    1. Liver
  • glycogenolysis
  • gluconeogenesis
  • FFA uptake from NEFAs for energy gain and some release of Ketone Bodies and VLDLs
    2. Muscle (responds to cortisol and epinephrine only - no glucose release)
  • Glycogenolysis for energy gain
  • FFA uptake from NEFAs, VLDLs and Ketone Bodies for energy gain
    3. Fat
  • Lipolysis via hormone-sensitive Lipase (HSL) with the release of fatty acids as NEFAs and glycerol
  • > lack of insulin causes HSL activation
28
Q

Post-Absorptive Metabolism Phase Effects

A
  • hypoglycemia stimulates Glucagon, Cortisol and epinephrine release
  • > INSULIN LOW AND GLUCAGON, CORTISOL AND EPINEPHRINE HIGH
  • glucose is reserved for glucose-dependent tissues
  • stored nutrients are mobilized and most tissues utilize FFAs
  • metabolic changes induce hunger, the animal eats their next meal and the absorptive phase starts up again
29
Q

Fasting/Starving Metabolism Phase

A
  • state of negative energy balance lasting more than a few days/weeks
  • post-absorptive phase continues
  • glycogen stores are quickly depleted
  • maintenance of basic glucose levels remain a top priority with dependency on gluconeogenesis from amino acids (proteolysis) and glycerol (lipolysis)
  • lipolysis provides fuel for all glucose-independent tissues
  • long standing dominance of GLUCAGON, CORTISOL AND EPINEPHRINE, WHILE INSULIN IS LOW
30
Q

Fasting/Starving Metabolism Phase active pathways in Liver/Muscle/Fat

A
  1. Liver
    - takes up more NEFAs (“fat sponge”) than it needs for energy
    - many are repacked and exported as VLDLS
    - > hyperlipidemia
    - liver cells run out of lipotropic factors and produce VLDLs (triglyceride/FFA accumulate in the liver causing cellular damage)
    - > Hepatic lipidosis
    - more ketone bodies are produced and released than can be utilized
    - > ketoacidosis
  2. Muscles
    - proteolysis increases and provides amino acids for gluconeogenesis
    - > organ and muscle wasting
  3. Fat
    - lipolysis increases and provides NEFAs for energy and glycerol for gluconeogenesis
    - release of NEFAs exceeds the body’s demand for energy, but continues because the hypoglycemia forces a hormonal situation which increases HSL action
31
Q

Hyperlipidemia cause and clinical signs

A
  • in horses mainly
  • fat releases excess NEFAs due to hypoglycemia (low insulin) accelerating HSL
  • the liver acts as a fat sponge and takes up more NEFAs than it needs for energy
  • > Many FFAs are repackaged and exported as VLDLs, but more VLDLs circulate than can be used in peripheral tissues
  • increases blood viscosity and decreases perfusion causing neurological signs
  • > depression, drowsiness, inappetence, ataxia, seizures and colic
32
Q

Hepatic Lipidosis cause and clinical signs

A
  • in cats, cows and horses
  • liver cells run out of lipotropic factors to produce VLDLs
  • > FFA/Triglycerides accumulate in the liver causing cellular damage
  • “Fatty Liver”
  • reduced detoxification (NH3) capacity causes neurological signs/hepatic encephalopathy
  • metabolic breakdown including worsening hypoglycemia, reduced plasma proteins, jaundice, anorexia and vomiting
33
Q

Metabolic Ketoacidosis causes and clinical signs

A
  • more ketone bodies are produced and released in the liver than can be utilized
  • long term cellular damage (Na/K pump affected causing cell swelling)
  • Hyperkalemia causing excitability of nerve and muscle tissues
  • osteomalacia with increased calcium levels
34
Q

Causes of Ketosis/Hepatic Lipidosis

A
  • the lack or unavailability of carbohydrates (hypoglycemia)
35
Q

When is Ketosis/Hepatic Lipidosis often seen

A
  1. During fasting, starving and anorexia (CATS)
  2. During times of excessively high glucose demands such as:
    - late pregnancy in ponies, small ruminants and guinea pigs
    - > pregnancy toxemia
    - peak lactation in dairy cows
  3. Hormonal imbalances
  4. Dietary imbalances such as high protein and low carbs (hypoglycemia)
36
Q

Consequences of Fasting/Starvation

A
  1. Muscle and Organ Wasting/Malfunctions
  2. Hepatic Lipidosis
  3. Metabolic Ketoacidosis
37
Q

Main liver functions

A
  1. Defense
  2. Blood reservoir
  3. Protein metabolism
    - urea formation
    - synthesis of plasma proteins
  4. Carbohydrate metabolism
    - glucose homeostasis
  5. Fat metabolism
  6. Detoxification and excretion of drugs, hormones, Bilirubin (important diagnostic tool), and urea
38
Q

What would you see in the plasma if the liver malfunctioned?

A
  1. Ammonia (NH3) increase
  2. Urea decrease
  3. Plasma protein (albumin) decrease
  4. Blood glucose levels decrease
    - hypoglycemia
39
Q

What is bilirubin and where does it originate from?

A
  • main bile pigment (orange/yellow in color)

- originates from heme breakdown

40
Q

Unconjugated Bilirubin formation

A
  • when bilirubin leaves RES cells and binds to Albumin it is in plasma form
  • > U-BILI, or indirect Bili
41
Q

Rate limiting step in horses for Bilirubin

A
  • Unconjugated Bilirubin formation

- > plasma form

42
Q

Conjugated Bilirubin Formation

A
  • when U-BILI is taken up by liver cells and conjugated with glucuronic acid it is C-BILI, or direct-Bili
43
Q

Rate limiting step of Bilirubin in all species, except horses

A
  • secretion of Conjugated Bilirubin into bile ducts
44
Q

What type of Bilirubin is present in the plasma?

A
  • Both U-BILI and C-BILI are normally present in the plasma at about 50:50
  • > BUT in horses it is predominantly U-BILI because of their rate limiting step
45
Q

Jaundice

A
  • the yellow pigmentation of the skin, mucosa, or body fluids caused by the deposition of bilirubin (increase of bilirubin in the blood)
46
Q

Pre-Hepatic Jaundice

A
  • occurs before the liver (unconjugated)
  • caused by excessive breakdown of hemoglobin
  • > signs of anemia
  • U-BILI is initially elevated
47
Q

Hepatic Jaundice

A
  • occurs in the liver
  • caused by damage to liver cells
  • > hepatic lipidosis
  • C-BILI is elevated in most cases due to regurgitation
48
Q

Post-Hepatic Jaundice

A
  • occurs after leaving the liver
  • caused by obstruction of bile ducts
  • > tumors, intrahepatic cholestasis
  • increased intrahepatic pressure can ultimately cause hepatocellular injury
  • C-BILI is VERY dominant
49
Q

A dog comes into the clinic with internal bleeding while presenting with Jaundice. What form is this likely to be?

A
  • Prehepatic Jaundice because of the excess blood destruction
50
Q

Cat comes into the clinic with hepatic lipidosis while presenting with jaundice. Which form of Bilirubin will be predominant?

A
  • Conjugated Bilirubin (C-BILI) will be increased

- > most likely hepatic jaundice because of damage to liver cells

Physiology II (3 decks)

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