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Clinical Pathology > Lecture 2: Plasma Proteins, Lipids, Carbohydrates > Flashcards

Lecture 2: Plasma Proteins, Lipids, Carbohydrates Flashcards

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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
What is a good indicator of inflammation in cattle and horses
Fibrinogen
26
What organ produces fibrinogen?
liver
27
How would you estimate the concentration of fibrinogen in a clinic?
clotting factor time - if plasma serum does not clot over a period of time there could be a fibrinogen problem
28
Where is C-reactive protein (CRP) made
Liver
29
Is CRP negative or positive acute phase?
Positive
30
When does CRP increase
with cardiac disease, sepsis and neoplasia
31
What species is CRP testing most helpful
rabbits and dogs
32
What are the 5 major types if lipid in plasma
1. Cholesterol 2. Cholesterol esters 3. Triglycerides 4. Phospholipids Non-esterified fatty acids (NEFAs) (long-chain fatty acids)
33
What 2 major lipids in plasma can be measured
Cholesterol & triglyceriedes
34
What are lipoproteins
They are lipid-peptide complexes in plasma consisting of the 5 major lipids in plasma in varying amounts
35
Where are Lipoproteins formed?
Formed in the liver and small intestine (secreted into plasma)
36
How is the density proportioned of lipoproteins
protein : lipid
37
What are the proportion of proteins from least dense to most dense
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
What part of the Chylomicra is hydrophobic and hydrophilic
tail is hydrophobic and the head is hydrophilic
39
Why does lipemia have a milky appearance
due to the increase of chylomicra and VLDL
40
Where are NEFAs (non-esterified fatty acids) produced
liver, adipose and mammary gland tissue
41
What species are NEFAs commonly tested
ruminants
42
What causes increased NEFAs
- Hepatic lipidosis in cats - Equine Cushing's disease - Bovine ketosis
43
How to measure plasma lipids
1. lipemia-refrigeration test (not quantitive) 2. Serum cholesterol determination 3. Serum triglycerideide determination 4. Lipoprotein determination 5. Non-esterified fatty acid determination
44
What is the cream like layer on top of clear serum
chylomicrons
45
What does turbidity indicate on a lipemia refrigeration test
Indicates VLDL and chylomicra
46
What causes Hyperlipidemia (increased cholesterol) *HINT* primary & secondary causes
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
How long should you fast animal when wanting a serum triglyceride test
4-6 hrs : because post prandial increase in triglycerides occurs 4-6 hrs after eating
48
What causes hypertriglyceridemia
increase in the concentration of chylomicrons and VLDL
49
Why would you see hypertriglyceridemia in a sample
- may occur after eating - a primary disease in certain breeds - secondary to renal, endocrine, pancreatic or hepatic disorders
50
What is Hyperlipidemia
increase in plasma lipids
51
What is postprandial hyperlipidemia?
transient rise in plasma lipids 4-6 hrs after a meal
52
Fasting or persistent hyperlipidemia
occurs when there is excess lipids in blood even after the animal has been fasted for 12 hrs
53
What are the 3 sources of blood glucose
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
How many hrs does the liver store glycogen?
24
55
Where are dietary carbohydrates digested?
the small intestine in monogastric
56
What are monosaccharides
simple sugars: fructose, glucose, galactose
57
What happens when there is excess glucose?
it will get stored as glycogen, amino acids or fats
58
True or false: in ruminants or herbivores, glucose is their energy molecule
false
59
What molecule do ruminants and herbivores use for their energy
Volatile fatty acids
60
Where does the degradation of glycogen occur?
Liver ------> produces glucose -------> released into blood
61
What is the primary source of glucose during short period of fasting
Glycogen
62
What does muscle glycogenolysis produce
lactate and pyruvate - it is then transported to the liver to be converted to glucose
63
What liver disease are cats prone to?
hepatic lipidosis
64
What is glycogenolysis promoted by
Catecholamines & glucagon
65
When are catecholamines released?
During fear, excitement and muscle exertion
66
When is glucagon released
in response to hypoglycemia
67
What cells make glucagon and what cells make insulin
- Glucagon: Alpha cells - Insulin : Beta cells
68
What is gluconeogenesis
The breakdown of glucose from proteins and lipids
69
Gluconeogenesis promoted by:
- Corticosteroids (antagonistic to insulin = decreased uptake and use of glucose by tissues) - Glucagon - Growth hormone - Certain drugs
70
How does glucose in the bloodstream get into cells?
insulin - it opens the protein doorway for glucose to enter the cell
71
Where is insulin produced and by what cell
produced in the pancreas by Beta cells (islet cells)
72
What are the target tissues of insulin?
Skeletal muscle, liver and adipose tissue
73
When can you see hypoglycemia?
- insulin overdose - insulinoma - starvation - excessive use of glucose - prolonged contact of serum w/ RBCs in vitro = pseudohypoglycemia
74
What is the rate of glucose loss per hr in pseudohypoglycemia?
10%/hr
75
When can hyperglycemia be seen?
- decreased use of glucose by the tissues - Endogenous cortisol - Exogenous corticosteroid administration - Glucagon release - Uncontrolled diabetes mellitus
76
what needs to be balanced in order to maintain blood glucose concentration
- glucose absorption - Insulin production - Insulin antagonists (glucagon, corticosteroids, growth horomone)
77
How do you convert American units to SI units for mg/dL
- mmol/L ---> mg/dL = / by 18 - mg/dl ---> mmol/L= x by 18
78
What do you want to avoid when prepping a patient to take blood for a blood glucose concentration test
- Avoid frightening the animal - stress patients will falsely elevate tests - Try fasting if there are no contraindications
79
What color tube inhibits glycolysis
white top
80
what inhibits glycolysis?
sodium flouride
81
where are ketones produced and what do they provide
- produced in liver - provide a good source of energy for many tissues
82
What are examples of highly acidic ketones
- acetoacetate - B-hydroxybutyrate
83
What are the major causes of ketonemia and ketonuria
- uncontrolled diabetes mellitus - bovine ketosis - pregnancy toxemia in sheep - happens during pregnancy
84
Why do ketones get released
due to negative energy balance
85
What ways you can measure ketones
- dipstick - ketonuria - ketones in milk (MUN) - Ketone meter for blood
86
When is lactate produced?
during excess anaerobic metabolism
87
What is anaerobic metabolism
ATP production without using oxygen

Clinical Pathology (2 decks)

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