removals 2

FAT ABSORPTION TEST (Plasma Turbidity Test)

-        LIPID present in plasma: Not enough to cause turbidity

-        Post-prandial hyperlipemia occurs 1-3 hours after a high fat meal

-        Fasting hyperlipemia: caused by mobilization of body fat rather than absorption

-        Fat being absorbed: +plasma turbidity

-        Lack of fat absorption: -plasma turbidity

§  SERUM LIPASE DETERMINATION

-        Estimation is based sa ability ng enzyme to hydrolyze a standard suspension of lipase oil

-        LIPASE: oil is hydrolyzed to glucose and fatty acid

-        ZYMOGEN (inactive form ng lipase): produced and stored in the acinar cells ng pancreas

§  SPECTROPHOTOMETRIC DETERMINATION

-        ↑ in serum lipase: caused by enzyme leakage sa pancreatic cells

-        Can also be caused by altered permeability due to inflammation

-        DEFECTED sha if naexcrete sha ng kidney

-        Considered specific indiciator of pancreatic function: kasi pancreas ang principal source ng enzyme na to, around 2/3 ng enzyme naoocupy nya while the rest ay sa gastric mucosa

-        CORTICOSTEROIDS= ↑ serum lipase activity

§  SERUM AMYLASE DETERMINATION

-        Determines the rate ng production ng starch (SACCHAROGENIC) or rate ng disappearance ng starch (AMYLOCLASTIC)

-        SACCHAROGENIC: measures sugar by the action of amylase of starch

-        GLUCOAMYLASE: lactase or intestinal amylase ng dogs

-        AMYLOCLASTIC: measures disappearance ng starch using turbidimetric/ colorimetric assay; requires CALCIUM kaya wag gagamit ng any chelating tubes

-        Less sensitive indicator

GLUCOSE DETERMINATION: measures level ng glucose

§  GLUCOSE ASSAY: glucose breakdown at rate of 1-% per hr at room temperature; SODIUM FLUORIDE and preservative

§  GLUCAGON RESPONSE TEST: provokes insulin release via hyperglycemic effect of glucagon; .3mg/kg IV; exaggerated response with functional cell tumor

§  GLUCOSE TOLERANCE TEST: ↑ blood glucose concentration post-prandial (1hr)

§  OGTT (Oral Glucose Tolerance Test): evaluates intestinal absorption; indicated in animals with PERSISTENT HYPERGLYCEMIA and GLUCOSURIA; only used in HORSES

DIABETES INSIPIDUS: KKK

-        Ketonuria

-        Ketoacidocis

-        Ketonemia

DIABETES MELLITUS: HGK

-        Hyperglycemia

-        Glucosuria

-        Ketonuria

-        Has two types:

o   Type 1 insulin dependent D.M

-very low insulin level and no response kahit IV

o   Type 2 non insulin dependent

-normal insulin pero walang response

HYPERGLYCEMIA:

-        Post prandial

-        Diabetis mellitus

-        Hyperadrenocorticism

-        Administration of therapeutic agents

o   GCC

o   ACTH – increase GCC

o   Epinephrine

o   IV with glucose

HYPOGLYCEMIA

-        Hyperinsulinism

-        Hypoadrenocorticism

-        Intestinal malabsorption

-        Canine renal glycosuria

PARATHYROID GLANDS

-        Regulates calcium and phosphorus homeostasis

Factors influencing serum calcium and phosphate levels:

§  Parathormone: controlled by ionized calcium; produced by parathyroid glands in response to hypocalcemia

o   Bone: produce bone reabsorption to increase calcium

o   Kidney: increase absorption in calcium

o   Intestine: increase absorption in calcium

§  Phosphorus: 80-85% found in skeleton; the rest ay sa ATP 2,3 DPG; deficiency = impaired chemostaxis and WBC phagocytosis

Calcium functions:

-        2ndary messenger in regulation of cell function (mitsosis)

-        Teams up with TROPONIN for muscle contraction

-        Essential in BLOOD COAGULATION

CALCITONINC/ THYROCALCITONIN

-        Produced by thyroid parafollicular cells in response to hypercalcemia

-        Acts by inhibitory effects on parathormone stimulated bone resorption

-        No effect on calcium reabsorption

METABOLICALLY ACTIVE VIT D

-        Formed in the kidney under parathormone regulation

-        Promotes calcium reabsorption

-        Active form: 25 hydroxycholecalciferol converted to 125 dihydroxycholecalciferol by 1 alpha hydroxylase sa PCT

MEANS OF EVALUATING Ca and P by PARATHYROID FUNCTION

-        Measured by COLORIMETRY using urine and serum

-        SAP is higher in young animals

ABNORMALITIES

§  HYPERCALCEMIA

§  HYPOCALCEMIA

-Vit D deficiency

-parturient paresis

-eclampsia

§  HYPERPHOSPHATEMIA

-reduced GFR

-mostly sa young animal

§  HYPOPHOSPHATEMIA

-parturient paresis

-hypercalcitonism

-hyperparathyroidism

LIVER/ HEPATIC FUNCTION TEST

-        LIVER: production of plasma proteins

-        Detoxifies blood na galling sa GI tract.

-        Essential for UREA production

-        Can regenerate

3 MAIN TYPES OF HEPATOBILIARY DISEASE:

§  Hepatocellular Injury: ↑ALT, AST

§  Cholestasis: ↑bilirubin; bile blockage

§  Hepatic Insufficiency: Alter production of substance

PURPOSE OF HEPATIC FUNCTION TESTS:

-        To differentiate types of jaundice

o   Pre-hepatic: hemolytic jaundice ( increase urobilinogen; orange feces)

o   Hepatic: Obstructive jaundice (decrease urobilinogen; clay feces)

o   Post-hepatic: hepatocellular injury

-        to determine the presence or absence of liver disease

-        Determine disease process: static; progressing; regressing

LIVER FUNCTION TESTS

§  SERUM BILIRUBIN DETERMINATION

-Bilirubin: nakukuha is nabreakdown ang hemoglobin to HEME (Iron) and GLOBIN (protein > AA)

-Bacteria in intestine reduce bilirubin into UROBILINOGEN tas if naoxidize sha = UROBILIN (urine) STERCOBILIN (feces)

o   UNCONJUGATED BILIRUBIN: bilirubin carried by albumin

o   CONJUGATED: macoconjugate sya through LIGANDIN which will pass sa endoplasmic reticulum para malagyan nya yung bilirubin ng GLUCORONIC ACID

-Bilirubin is excreted via BILE CANACULI

2 tests:

o   ICTERUS INDEX

-crude test of bilirubin determination

-intesity of color compares sa standard K DICHROMATE

-Normal: 2-6

-Increase index: hemolysis, hepatocellular damage, biliary obstruction

-Decrease index: bone marrow depression

o   VAN DEN BERGH TEST

-Determines CONJUGATED bilirubin

-Uses DIAZOVENZOSULFOCHLORIDE to form RED-VIOLET PIGMENT

-if may obstructive jaundice=REACTS AGAD

-If testing for hemolytic disease=add alcohol sa test (indirect measurement) = <20% conjugated or if mas marami uncojugated

->40% conjugated bilirubin = CHOLESTASIS

§  Complete blockage of common bile duct

§  Primarily conjugated bilirubin

§  Makes hepatocytes less able to take up and conjugate

HEPATOCELLULAR INJURY

-        Bilirubin diffuses back sa Disseminated space into sinusoids = REGURGITAION

-        Causes conjugated hyperbilirubinemia

-        Causes MIXED CONJUGATED AND UNCONJUGATED

HYPERBILIRUBINEMIA

-        Increase in unconjugated or conjugated bilirubin

-        Seen as ICTERIC or JAUNDICE

URINE UROBILINOGEN

-        Ito tingnan if magddifferentiate ng obstructive and hemolytic jaundice

-        Increase: hemolytic

-        Decrease: obstructive

LEAKAGE ENZYMES

§  ALT (Serum Alanine Aminotransferase)

-Greatest amount in: PRIMATES, DOG, CAT

-specific for HEPATIC DISEASE in dogs and cats

-hemolysis and lipemia = false elevation

§  SDH (Sorbitol/Iditol Dehydrogenase)

-specific for HORSES

-liver specific

-disappears within 24hrs

-found in lower concentrations in kidneys, intestine, and skeletal muscle

-High concentrations in liver

§  AST (Serum Aspartate Aminotransferase)

-not specific for liver

-Increase = cell necrosis

-dependent sa inflammation

-used to detect liver and muscle damage

-Higher levels sa working horses

§  Glutamic Dehydrogenase

-enzyme of choice for CATTLE

-found in mitochondria ng hepatocytes

§  SAP ( Serum Alkaline Phosphatase)

-Most sensitive indicator for CHOLESTASIS

-higher in YOUNGER ANIMALS

-walang kwenta sa ruminants

§  Gamma Glutamyl Transferase

-More sensitive indicator of CHOLESTASIS

-Sa horse din

Detects CHOLESTASIS: serum bilirubin, SAP, GGT

Detects LEAKAGE: ALT, AST (small animals) SDH (large animals)

ADRENAL/ PITUITARY GLANDS

-        if a particular hormone is bound to another molecule = INACTIVE

-        Insufficiencies due to :

§  Hyposecretion of hormone

§  Increase degradation/ hormone exretion

§  Excess binding of hormone

§  Failure of target organ to respond

§  Secretion of inactive hormone

-        Excesses due to:

§  Increase hormone secretion

§  Decrease destruction

§  Decrease binding of hormone

§  Functional over response of organ

ANTERIOR PITUITARY

-        Produces hormones such as:

§  ACTH – makes cortisol

§  MSH – controls skin pigmentation

§  GH – growth hormone

§  LTH – produce milk in mammals

§  FSH – helps in egg and sperm development

§  TSH – stimulates thyroid gland to make thyroid hormones for metabolism

-        Hypofunction: pituitary dwarfism, panhypopituitarism

-        Hyperfunction: acromegaly; gigantism

POSTERIOR PITUITARY (sa hypothalamus)

-        Necessary for ADH release

-        ADH (anti-diuretic hormone): reduces water loss by increase kidney reabsorption of water

-        Hypofunction: Diabetes insipidus

o   Hypothalamus fails to synthesize ADH

o   Receptors cant detect increase in osmotic pressure

o   D.I fails to reabsorb water due to absence of ADH

ADRENAL CORTEX

-        Most active organ in the body in steroid production

-        Governed by ACTH

-        CORTICOSTEROIDS: most important group of adrenal steroids

-        Glucocorticoids: cortisol, corticosterone

§  Produces metabolism and catabolism

§  Increase lipolysis

§  Inhibits Vitamon D activity

§  Mediates STRESS LEUKOGRAM

-        Mineralocorticoids: Aldosterone

§  Electrolyte regulation

§  Raises BP

-        Sex hormone    

-        DISEASES OF ADRENAL CORTEX

-        1. Cushing’s Syndrome

-        - unregulated excessive production of corticosteroid

-        - C.S: polyuria, polydipsia. Symmetrical alopecia; pendulous abdomen; enlarged clitoris; osteoporosis, testicular atrophy

-        - Lab findings: STRESS LEUKOGRAM, Increase SAP, low SPG, increase blood glucose level