Bryan - Clin Path - Test 2 Lectures 4-5 - Winter 2Nd Year

Front 1

What is the difference between serum and plasma?

Back 1

Clotting factors! Serum doesn't have any!

Front 2

What proteins are measured typically?

Back 2

Total protein
Albumin
Fibrinogen
Globulins

Front 3

Which is smaller - albumin or globulins?

Back 3

Albumin!

Front 4

What are some types of hyperproteinemia?

Back 4

Hyperalbuminemia & hemoconcentration
Hyperglobulinemia
Hyperfibrinogenemia

Front 5

T or F:
The only cause of hyperalbuminemia is hemoconcentration

Back 5

True! The only way to get hyperalbuminemia is through dehydration

Front 6

What are causes of increased globulin synthesis?

Back 6

Inflammation
Neoplasia (B-lymphocytes)

Front 7

What is a major cause of increased fibrinogen in large animals?

Back 7

Inflammation

Front 8

What types of neoplasia are usually associated with monoclonal gammopathy?

Back 8

Lymphoma, plasma cell tumor, lymphocytic leukemia

Front 9

What are some non-neoplastic causes of monoclonal gammopathy?

Back 9

Erlichiosis
Leishmaniasis
Chronic pyoderma

Front 10

What are the two patterns of gammopathy?

Back 10

Monoclonal and polyclonal gammopathy

Front 11

What are the two general causes of hypoproteinemia?

Back 11

Loss
Failure of synthesis

Front 12

How can proteins be lost? Which proteins will be lost in each case?

Back 12

Renal (loss via glomeruli) - albumin
GI loss - panhypoproteinemia

Front 13

What are some causes of hypoalbuminemia due to failure of synthesis?

Back 13

Liver failure
Prolonged malabsorption/maldigestion

Front 14

What are some causes of hypoglobulinemia due to synthesis failure?

Back 14

Failure of passive transfer (neonate);
Immune deficiency

Front 15

What are some tests for failure of passive transfer? Which animals is each test used for?

Back 15

Refractometer (calves)
NaSO3 (calves and crias)
ZnSO4 (calves and foals)
Glutaraldehyde coagulation (foals)
ELISA (foals)

Front 16

What is the difference between hyperlipemia and hyperlipidemia?

Back 16

Both indicate increased concentrations of lipids in the blood; hyperlipemia indicates that it is grossly visible

Front 17

When should hyperlipidemia peak post prandial? When should it be cleared?

Back 17

Peak 2-6h;
Clears by 8-16h

Front 18

What are some general causes of hypercholesterolemia?

Back 18

Endocrinopathies;
Protein losing glomerulopathy;
Cholestasis;
Acute pancreatitis

Front 19

How does protein losing glomerulopathy cause hypercholesteremia?

Back 19

Albumin loss leads to reduced oncotic pressure; liver then overproduces cholesterol to compensate

Front 20

What are some general causes of hypocholesteremia?

Back 20

Hepatopathy (decreased production)
Protein losing enteropathy
Hypoadrenocorticism
Severe malnutrition

Front 21

T or F:
Causes of hypertriglyceridemia are similar to causes of hypercholesteremia.

Back 21

Tru dat

Front 22

What are the regulators of glucose? Which one lowers blood glucose levels?

Back 22

Insulin (lowers blood glucose);
Glucagon;
Glucocorticoids;
Catecholamines:
Growth hormone

Front 23

What is the most common cause of hypoglycemia in bloodwork?

Back 23

Poor sample handling (not separating blood from serum)

Front 24

What are the major causes of hypoglycemia?

Back 24

Increased usage;
Decreased production

Front 25

What are the glucose evaluation methods?

Back 25

POrtable glucometers
Urine glucose
Serum insulin assay
Fructosamine
Glycated Hgb

Front 26

How can stress-induced hyperglycemia be ruled-out?

Back 26

Urinalysis;
Fructosamine assay

Front 27

Other than a serum insulin assay, what else is necessary to diagnose neoplastic hyperinsulinism?

Back 27

Blood glucose level (to calculate insulin:glucose)

Front 28

What are some causes of hyperketonemia?

Back 28

D. mellitus
Bovine ketosis
Pregnancy toxemia
Hepatic lipidosis
Starvation
Anorexia
Atkin's diet

Front 29

T or F:
PO2 can only be interpreted on arterial blood.

Back 29

True!

Front 30

Which of the following values is/are calculated? Which is/are measured directly in the blood?
a) pH
b) PO2
c) HCO3-
d) PCO2

Back 30

HCO3 is measured indirectly (calculated); the remaining values are measured directly

Front 31

The actual bicarb value minus the normal bicarb value denotes the...

Back 31

...base excess

Front 32

A negative base excess denotes...

Back 32

...ACIDOSIS

Front 33

CO2 + H2O <-->H+ + HCO3 -

Which side is under lung control? Which side under kidney control?

Back 33

Lungs control CO2
Kidneys control H+ and HCO3-

Front 34

low pH and low [HCO3-]

Back 34

metabolic acidosis

Front 35

high pH and high [HCO3-]

Back 35

metabolic alkalosis

Front 36

low pH and high PCO2

Back 36

respiratory acidosis

Front 37

high pH and low PCO2

Back 37

respiratory alkalosis

Front 38

For every 1mEq/L change in HCO3-, there is a concurrent change in PCO2 on the order of...

Back 38

...0.7mm/Hg

Front 39

What are the two basic mechanisms explaining metabolic acidosis?

Back 39

Secretional (hyperchloremic);
Titrational metabolic acidosis

Front 40

How does secretional or hyperchloremic metabolic acidosis occur?

Back 40

INcreased loss of bicarb (stool/saliva/urine);
Kidneys then retain Cl- to make up for bicarb loss

Front 41

What are causes of titrational metabolic acidosis?

Back 41

Shock (lactic acid);
diabetes/starvation (keto acids);
Uremic acids;
Exogenous acids (EG, salicylates);
other exogenous acid

Front 42

How can secretional and titrational metabolic acidosis be differentiated?

Back 42

Anion Gap; increased AG = titational acidosis

Front 43

What is the basic formula for anion gap? What are normal values?

Back 43

(Na+K)-(Cl + HCO3);
15-25 for cats/dogs;
10-20 for large animals

Front 44

What is the upper normal limit for PCO2? What happens above this level?

Back 44

PCO2 can't be above 60mmHg without causing respiratory acidosis

Front 45

What are major causes of metabolic alkalosis?

Back 45

HCl loss or sequesteration (vomiting, DA, vagal indigestion);
Iatrogenic bicarb;
electrolyte imbalances

Front 46

What is the progression of paradoxical aciduria with metabolic alkalosis?

Back 46

Hypovolemia from vomiting causes kidneys to retain Na. Kidneys can't resorb Cl to maintain electroneutrality, so they EXCRETE H+!

Front 47

What are some major causes of respiratory alkalosis?

Back 47

Extrathoracic hyperventilation (fever, pain, excitement);
Intrathoracic hyperventilation (due to decreased PO2)

Front 48

What are the major electrolytes of laboratory interest?

Back 48

Na, K, Cl, and HCO3

Front 49

What is the major cation in plasma? How 'bout intracellular cation?

Back 49

Na (plasma)
K (intracellular)

Front 50

Which hormones regulate Na in the body?

Back 50

Aldosterone;
Atrial Naturetic Factor

Front 51

What are major causes of hypernatremia?

Back 51

Dehydration
Salt poisoning (+ no water)
Hyperadrenocorticism (slight low Na)
Primary adipsia (RARE)

Front 52

What are major causes of hyponatremia?

Back 52

Hypoadrenocortism;
Diarrhea;
Renal dz;
Sequestration (3rd space loss; DA)

Front 53

T or F:
Serum [K+] reflects body [K+].

Back 53

False!

Front 54

What can affect serum potassium concentration?

Back 54

Diet;
Renal excretion;
Compartment shifting

Front 55

What are major causes of hyperkalemia?

Back 55

Addison's dz (hypoadrenocortism);
Renal dz;
acidosis;
insulin deficiency;
other shit

Front 56

What hormone shifts K into cells?

Back 56

Insulin

Front 57

What are some causes of hypokalemia?

Back 57

GI loss;
Urinary loss;
hyperadrenocortism
Alkalosis
Insulin therapy

Front 58

How can the urinary system cause hypokalemia?

Back 58

Osmotic diuresis;
Non K-sparing diuretics;
cats w/chronic metabolic acidosis

Front 59

How is Cl usually lost? What metabolic condition is this usually associated with?

Back 59

with gastric or abomasal fluids (associated w/metabolic alkalosis)

Front 60

What metabolic condition causes hyperchloridemia?

Back 60

Secretional metabolic acidosis

Front 61

T or F:
Na concentration pretty much controls osmolality.

Back 61

Tru dat!