Lecture 2: Plasma Proteins, Lipids, Carbohydrates Flashcards

1
Q

What is plasma protein composed of?

A

Albumin, globulins and fibrinogen

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2
Q

What does serum protein NOT contain

A

Fibrinogen

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3
Q

What is the function of plasma proteins?

A

They are nutritive | exert colloidal osmotic pressure | aid in the maintenance of acid-base balance | Individual proteins serve as enzymes, hormones, clotting factors, antibodies and transport substances | coagulation

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4
Q

Collodial Osmotic Pressure: describe it and the diseases that come with it as well as the procedure to obtain the fluid.

A

It is the pull to keep water inside the body | When fluid wants to leave the bloodstream into tissues (edema) & when fluid wants to leave the bloodstream into the abdomen (ascites) | take fluid out of the abdomen and measure the values of the cellularity & protein levels

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5
Q

What is the 1st major site and the second major site of the synthesis of plasma proteins

A

1st = liver | 2nd = immune system (because antibodies are proteins)

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6
Q

What does total protein equal (HINT: calculation)

A

Albumin + globulin

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7
Q

Where is albumin produced and what are they specifically called?

A

produced by the liver | specifically called hepatocytes

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8
Q

How much does albumin make up of total protein?

A

35-75%

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9
Q

What protein is accounted for 75% of the colloidal osmotic pressure activity in plasma

A

Albumin

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10
Q

What are the types of globulins?

A

Alpha, beta, gamma

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11
Q

Where are alpha and beta globulins synthesized

A

mostly by the liver (transport proteins)

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12
Q

Where are gamma globulins produced

A

produced by plasma cells as immunoglobulins

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13
Q

What can total protein concentration in the blood be affected by?

A

Synthesis in liver | Excretion (kidney)/breakdown | Dehydration/over-hydration|Shock | Distribution of protein in the body & nutritional status

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14
Q

What causes increased/decreased albumin concentration:

A

Increased: dehydrated animals | Decreased: chronic liver disease, starvation,

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15
Q

How do you calculate the A:G ratio

A

Serum albumin / serum globulin

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16
Q

What is failure of passive transfer

A

To test for colostral antibody levels in ruminants and foals

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17
Q

What are adequate and inadequate levels of IgG

A

<200mg/dL at 24-48hrs after birth confirms failure | >800mg/dL indicates adequate transfer

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18
Q

How is the failure of passive transfer tested?

A

Through the snap test, must be done 12hrs after birth as it allows for IgG from the colostrum to be absorbed

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19
Q

What is the most common immunoglobulin?

A

IgG

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20
Q

What makes acute phase proteins and how to they get into circulation?

A

Made by hepatocytes right after injury or inflammation

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21
Q

When do you see negative vs positive acute phase proteins

A

Negative: decrease in inflammation | Positive: increase inflammation (good indicator of inflammatory process)

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22
Q

What are examples of acute phase positive proteins

A

Fibrinogen | Serum amyloid A (SSA) | Haptoglobin | C-reactive protein | Complement |

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23
Q

What is 1 example of a negative acute-phase protein

A

Albumin

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24
Q

What are Acute phase proteins used for (monitoring purposes)

A

SSA specifically - good for monitoring the treatment and diagnosis of subclinical inflamm. conditions

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25
Q

What is a good indicator of inflammation in cattle and horses

A

Fibrinogen

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26
Q

What organ produces fibrinogen?

A

liver

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27
Q

How would you estimate the concentration of fibrinogen in a clinic?

A

clotting factor time - if plasma serum does not clot over a period of time there could be a fibrinogen problem

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28
Q

Where is C-reactive protein (CRP) made

A

Liver

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29
Q

Is CRP negative or positive acute phase?

A

Positive

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30
Q

When does CRP increase

A

with cardiac disease, sepsis and neoplasia

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31
Q

What species is CRP testing most helpful

A

rabbits and dogs

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32
Q

What are the 5 major types if lipid in plasma

A
  1. Cholesterol
  2. Cholesterol esters
  3. Triglycerides
  4. Phospholipids
    Non-esterified fatty acids (NEFAs) (long-chain fatty acids)
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33
Q

What 2 major lipids in plasma can be measured

A

Cholesterol & triglyceriedes

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34
Q

What are lipoproteins

A

They are lipid-peptide complexes in plasma consisting of the 5 major lipids in plasma in varying amounts

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35
Q

Where are Lipoproteins formed?

A

Formed in the liver and small intestine (secreted into plasma)

36
Q

How is the density proportioned of lipoproteins

A

protein : lipid

37
Q

What are the proportion of proteins from least dense to most dense

A
  1. Chylomicra (composed of triglycerides)
  2. Very low-density lipoproteins (VLDL)
  3. Intermediate-density lipoproteins (IDL)
  4. Low density (lipoproteins (LDL)
  5. High-density lipoproteins (HDL) most desne
38
Q

What part of the Chylomicra is hydrophobic and hydrophilic

A

tail is hydrophobic and the head is hydrophilic

39
Q

Why does lipemia have a milky appearance

A

due to the increase of chylomicra and VLDL

40
Q

Where are NEFAs (non-esterified fatty acids) produced

A

liver, adipose and mammary gland tissue

41
Q

What species are NEFAs commonly tested

A

ruminants

42
Q

What causes increased NEFAs

A
  • Hepatic lipidosis in cats
  • Equine Cushing’s disease
  • Bovine ketosis
43
Q

How to measure plasma lipids

A
  1. lipemia-refrigeration test (not quantitive)
  2. Serum cholesterol determination
  3. Serum triglycerideide determination
  4. Lipoprotein determination
  5. Non-esterified fatty acid determination
44
Q

What is the cream like layer on top of clear serum

A

chylomicrons

45
Q

What does turbidity indicate on a lipemia refrigeration test

A

Indicates VLDL and chylomicra

46
Q

What causes Hyperlipidemia (increased cholesterol) HINT primary & secondary causes

A

Primary causes: inherited disorders of lipoprotein metabolisim (ex. mini schnauzer)

Secondary
- Cholestasis (bile flow blocked)
- diabetes mellitus
- Hepatic lipidosis
- Hypothyroidism
- Cushing’s disease (dogs)
- Acute pancreatitis
- Corticosteroid therapy
- Glomerular disease (kidney)
- Negative energy balance in miniature horses, ponies and donkeys

47
Q

How long should you fast animal when wanting a serum triglyceride test

A

4-6 hrs : because post prandial increase in triglycerides occurs 4-6 hrs after eating

48
Q

What causes hypertriglyceridemia

A

increase in the concentration of chylomicrons and VLDL

49
Q

Why would you see hypertriglyceridemia in a sample

A
  • may occur after eating
  • a primary disease in certain breeds
  • secondary to renal, endocrine, pancreatic or hepatic disorders
50
Q

What is Hyperlipidemia

A

increase in plasma lipids

51
Q

What is postprandial hyperlipidemia?

A

transient rise in plasma lipids 4-6 hrs after a meal

52
Q

Fasting or persistent hyperlipidemia

A

occurs when there is excess lipids in blood even after the animal has been fasted for 12 hrs

53
Q

What are the 3 sources of blood glucose

A
  1. Dietary carbohydrate
  2. Glycogenolysis (to break down)
  3. Gluconeogenesis (to make)
    • stored glucose
    • gets broken down and spat out when levels are too low
54
Q

How many hrs does the liver store glycogen?

A

24

55
Q

Where are dietary carbohydrates digested?

A

the small intestine in monogastric

56
Q

What are monosaccharides

A

simple sugars: fructose, glucose, galactose

57
Q

What happens when there is excess glucose?

A

it will get stored as glycogen, amino acids or fats

58
Q

True or false: in ruminants or herbivores, glucose is their energy molecule

A

false

59
Q

What molecule do ruminants and herbivores use for their energy

A

Volatile fatty acids

60
Q

Where does the degradation of glycogen occur?

A

Liver ——> produces glucose ——-> released into blood

61
Q

What is the primary source of glucose during short period of fasting

A

Glycogen

62
Q

What does muscle glycogenolysis produce

A

lactate and pyruvate
- it is then transported to the liver to be converted to glucose

63
Q

What liver disease are cats prone to?

A

hepatic lipidosis

64
Q

What is glycogenolysis promoted by

A

Catecholamines & glucagon

65
Q

When are catecholamines released?

A

During fear, excitement and muscle exertion

66
Q

When is glucagon released

A

in response to hypoglycemia

67
Q

What cells make glucagon and what cells make insulin

A
  • Glucagon: Alpha cells
  • Insulin : Beta cells
68
Q

What is gluconeogenesis

A

The breakdown of glucose from proteins and lipids

69
Q

Gluconeogenesis promoted by:

A
  • Corticosteroids (antagonistic to insulin = decreased uptake and use of glucose by tissues)
  • Glucagon
  • Growth hormone
  • Certain drugs
70
Q

How does glucose in the bloodstream get into cells?

A

insulin
- it opens the protein doorway for glucose to enter the cell

71
Q

Where is insulin produced and by what cell

A

produced in the pancreas by Beta cells (islet cells)

72
Q

What are the target tissues of insulin?

A

Skeletal muscle, liver and adipose tissue

73
Q

When can you see hypoglycemia?

A
  • insulin overdose
  • insulinoma
  • starvation
  • excessive use of glucose
  • prolonged contact of serum w/ RBCs in vitro = pseudohypoglycemia
74
Q

What is the rate of glucose loss per hr in pseudohypoglycemia?

A

10%/hr

75
Q

When can hyperglycemia be seen?

A
  • decreased use of glucose by the tissues
    • Endogenous cortisol
    • Exogenous corticosteroid administration
    • Glucagon release
    • Uncontrolled diabetes mellitus
76
Q

what needs to be balanced in order to maintain blood glucose concentration

A
  • glucose absorption
  • Insulin production
  • Insulin antagonists (glucagon, corticosteroids, growth horomone)
77
Q

How do you convert American units to SI units for mg/dL

A
  • mmol/L —> mg/dL = / by 18
  • mg/dl —> mmol/L= x by 18
78
Q

What do you want to avoid when prepping a patient to take blood for a blood glucose concentration test

A
  • Avoid frightening the animal
    • stress patients will falsely elevate tests
  • Try fasting if there are no contraindications
79
Q

What color tube inhibits glycolysis

A

white top

80
Q

what inhibits glycolysis?

A

sodium flouride

81
Q

where are ketones produced and what do they provide

A
  • produced in liver
  • provide a good source of energy for many tissues
82
Q

What are examples of highly acidic ketones

A
  • acetoacetate
  • B-hydroxybutyrate
83
Q

What are the major causes of ketonemia and ketonuria

A
  • uncontrolled diabetes mellitus
  • bovine ketosis
  • pregnancy toxemia in sheep
    • happens during pregnancy
84
Q

Why do ketones get released

A

due to negative energy balance

85
Q

What ways you can measure ketones

A
  • dipstick - ketonuria
  • ketones in milk (MUN)
  • Ketone meter for blood
86
Q

When is lactate produced?

A

during excess anaerobic metabolism

87
Q

What is anaerobic metabolism

A

ATP production without using oxygen