Glucose, magnesium, phosphate and proteins Flashcards

1
Q

Glucose draw, range, location and general function

A

Glucose concentration in extracellular fluid is closely regulated so that a source of energy is readily available to tissues.

Draw tube: SST (as part of chem -7 panel), PPT, gray (if drawing only glucose)

Normal range: 60–110 mg/dL
Panic values: < 40 or > 500 mg/dL

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2
Q

Conditions and drugs causing Hyperglycemia

A

Diabetes mellitus, Cushing syndrome (10–15%), chronic pancreatitis (30%)

corticosteroids,phenytoin, estrogen, thiazides

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3
Q

Conditions and drugs causing Hypoglycemia

A

Hypoglycemia seen with insulinoma, adrenocortical insufficiency, hypopituitarism, diffuse liver disease, enzyme deficiency diseases (eg, galactosemia).

Drugs:insulin, ethanol,propranolol; sulfonylureas,tolbutamide, and other oral hypoglycemic agents.

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4
Q

DIABETES MELLITUS Diagnosis components

A

Diagnosis of diabetes mellitus requires:

A fasting plasma glucose of > 126 mg/dL on two or more occasions

Spot plasma glucose level ≥200 mg/dL

HbA1c≥ 6.5% along with symptoms of diabetes.

Patients with fasting blood glucose levels 110 mg/dL to 126 mg/dL are considered to have impaired fasting glucose.

Glycosylated hemoglobin levels (HbA1c ) are favored to monitor glycemic control in patients with diabetes mellitus.

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5
Q

Calcium function skeletally

A

CA PROVIDES STRENGTH & STABILITY FOR THE COLLAGEN & GROUND SUBSTANCES THAT FORMS THE STRUCTURAL MATRIX OF THE SKELETAL SYSTEM & IS A HUGE RESERVOIR FOR MAINTAINING BLOOD LEVELS OF CALCIUM

Bulk of Ca++ is stored in the skeleton

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6
Q

Anion Calcium integration

A

ANIONS (BICARBONATE, LACTATE, & CITRATE)
CA USED IN MUSCULAR CONTRACTIONS, CARDIAC FUNCTION, TRANSMISSION OF NERVE IMPULSES, & BLOOD CLOTTING

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7
Q

Albumin influence on calcium

A

DECREASES OR INCREASES IN ALBUMIN WILL AFFECT THE TOTAL CALCIUM LEVEL, BUT WILL NOT AFFECT THE IONIZED PORTION

Amount of protein in blood will affect Ca++ levels

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8
Q

Muscular system, cardiac, nervous and heme calcium roles

A

CA USED IN MUSCULAR CONTRACTIONS, CARDIAC FUNCTION, TRANSMISSION OF NERVE IMPULSES, & BLOOD CLOTTING

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9
Q

Total Ca++ is made up of 3 fractions

A

Protein bound (∼40%)
Anion bound (∼10%)
Ionized “free” (∼50%) (metabolically active)

Only the ionized Ca++ can be used by the body for vital cellular processes

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10
Q

Calcium regulation

A

controlled by PTH, calcitonin, vitamin D & renal reabsorption

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11
Q

Ionized calcium functions

A

Participates in enzyme reactions
Important intracellular second messenger for “amplification”

Contributes to membrane potentials & neuronal excitability

Exocytosis of neurotransmitters at NMJ & CNS
Muscle contraction (skeletal, smooth, cardiac)

Participates in hormone release
Influences cardiac automaticity
Required for coagulation in intrinsic pathway

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12
Q

SERUM CALCIUM uses

A

Evaluating pts with known or suspected hyper/hypocalcemia

Evaluating electrolyte status in pts receiving IV fluids

Procedure:
Obtain 5ml of venous blood collected in red, yellow or speckled top tube

Reference range:
Varies considerably throughout adolescent years
Normal adult values: 8.9-10.1 mg/dl

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13
Q

Interfering factor in calcium

A

Thiazide diuretics
Large amount of blood transfusions
Pts undergoing dialysis

Excessive laxative use
Acid base disorders
Increased or decreased protein levels

Calcium levels are inversely related to phosphate levels

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14
Q

HYPERCALCEMIA

A

total Ca++ >12 mg/dl

Etiology:
Hyperparathyroidism
Malignancy (PTHrP producing tumors)
Granulomatous diseases

Thyrotoxicosis
Paget’s disease of bone
Bone fractures

Prolonged immobilization
Excessive intake of vitamin D

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15
Q

Clinical Manifestations of Hypercalcemia

A

Increased thirst
Polyuria, flank pain, signs of kidney stones or renal insufficiency

Anorexia, nausea, vomiting, constipation
Muscle weakness, atrophy, ataxia & loss of muscle tone

Lethargy, personality/behavioral changes, stupor or possible coma

HTN, shortening of QT interval & possible AV block

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16
Q

HYPOCALCEMIA

A

total Ca++ <8.5 but true hypocalcemia is ionized Ca++ <4.0 mg/dl

Etiology:
Pseudohypocalcemia
0.8 (nl alb - measured alb) + reported Ca
Hypoparathyroidism

Hyperphosphatemia
Malabsorption syndromes & malnutrition
Pancreatitis

Alkalosis
Vit D deficiency (rickets or osteomalacia)
Alcoholism & cirrhosis

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17
Q

Clinical Manifestations of Hypocalcemia

A

Paresthesias
Skeletal muscle cramps, abdominal spasms & cramps
Hyperactive reflexes, + Chvostek’s & Trousseau’s signs, tetany & laryngeal spasm

Hypotension, cardiac insufficiency, no response to drugs with Ca-mediated mechanism
Osteomalacia, bone pain, deformities & fractures

18
Q

IONIZED CALCIUM uses and procedure

A

Particularly helpful during any surgical procedure that requires rapid & multiple whole blood transfusions

Second order test in the evaluation of pts with abnormal Ca++ levels

Neonatal calcium measurement

Assessing Ca++ levels in critically ill pts

Procedure:
5ml of venous blood in red, yellow, or speckled top tube

19
Q

IONIZED CALCIUM LEVEL

A

Reference range:
Normal: 4.75-5.20 mg/dl
Panic values: <2.0 mg/dl may produce tetany or life-threatening complications, levels >7.0 mg/dl may cause coma

Increased levels:
Hyperparathyroidism
Ectopic PTHrP tumors
Increased vitamin D intake

20
Q

Ionized calcium decreased levels and Interfering factors

A

Decreased levels:
Hypoparathyroidism
Vitamin D deficiency

Pts receiving bicarbonate to control metabolic acidosis
Acute pancreatitis

Hyperventilation to control increased ICP
Magnesium deficiency
Multiple organ failure

Interfering factors:
Improper specimen collection in EDTA

21
Q

SERUM PHOSPHATE functions

A

85% of the body’s total phosphorus is combined with Ca+ inside bone; 14% resides within cells; 1% is the the extra-cellular compartment

Multiple functions – bones, glucose, lipids, acid-base balance, storage & energy transfer

Moves into cells after carbohydrate ingestion & therefore is lowered in the plasma
Inversely related to Ca++

22
Q

SERUM PHOSPHATE functions 2

A

Major role in bone formation (bone matrix)
Essential for certain metabolic processes (ATP formation, building of enzymes for glucose, fat, & protein metabolism)

Cell structure (nucleic acids of DNA/RNA, membrane phospholipids

Serves as a acid-base buffer in the ECF & in the renal excretion of H+ ions

O2 delivery by RBCs through organic phosphates & 2,3 diphosphoglycerate

23
Q

Serum phosphate uses

A

Evaluating pts with CKD or hyperparathyroidism
Evaluating alcoholic & malnourished pts or pts receiving TPN

Evaluating status of pts recovering from diabetic ketoacidosis or pts receiving IV fluids containing phosphorus

Evaluating pts with hyperparathyroidism
Procedure: same as other electrolytes

Reference range: 2.5-5.0 mg/dl
Interfering factors: hemolysis

24
Q

HYPERPHOSPHATEMIA

A

Definition: >5 mg/dl

Etiology:
Decreased excretion due to renal failure
Hypoparathyroidism
Adrenal insufficiency & acromegaly
Increased intake & absorption
Redistribution/cellular release
Hypocalcemia
Bone tumors & cancer metastases

25
Q

Clinical Manifestations of Hyperphosphatemia

A

Manifestations are usually related to the reciprocal changes that are seen in calcium (hypocalcemia)

Paresthesia’s, tetany, Chvostek’s and Trousseau’s signs
Hypotension and cardiac dysrhythmias

Skeletal muscle cramps, abdominal spasms & cramps
Bone pain

26
Q

HYPOPHOSPHATEMIA

A

Definition: <2.5 mg/dl

Etiology:
Hyperparathyroidism
Diabetic ketoacidosis
Antacids
Severe diarrhea
Vitamin D deficiency
Alkalosis
Alcoholism, malnutrition, and TPN
Renal tubular absorption defects

27
Q

Clinical Manifestations og Hypophosphatemia

A

Manifestations usually related to reciprocal calcium changes (hypercalcemia)

Ataxia, hyporeflexia, muscle weakness, joint & bone pain

Increased thirst, anorexia, N/V, & constipation

Lethargy, personality/behavioral changes, stupor or possible coma

POLYURIA, FLANK PAIN, SIGNS OF KIDNEY STONES OR RENAL INSUFFICIENCY

HTN, SHORTENING OF QT INTERVAL & POSSIBLE AV BLOCK

28
Q

SERUM MAGNESIUM

A

50% in bone, 49% in body cells, & 1% is dispersed within the serum

Mg is required as a cofactor for the production of cellular energy and function of cellular messenger systems

Along with Na, K, & Ca ions, Mg also regulates neuromuscular irritability and the clotting mechanism

The secretion, synthesis, & action of PTH is influenced by Mg

Mg & Ca are intimately linked in their body functions

29
Q

Serum Magnesium further functions

A

Cofactor for intracellular enzyme reactions (transfers phosphate groups)

Essential for all ATP reactions

Essential for every step related to replication & transcription of DNA & for translation of messenger RNA

Required for cellular energy metabolism, function of the Na+/K+/ATPase pump

Stabilizes membranes

Contributes to nerve conduction, ion transport, & calcium channel activity

30
Q

Serum Magnesium uses, procedure and Interfering factors

A

Evaluating renal function & electrolyte status in hospitalized patients

Pts with hypocalcemia or hypokalemia not responding to electrolyte correction

Identification of malabsorption disorders
Monitoring tx of pre/eclampsia

Procedure: same as other electrolytes

Reference range: 1.5-3.0 mEq/L
Interfering factors:
Hemolysis, lithium or salicylates use

31
Q

HYPERMAGNESEMIA

A

Definition: >3.0 mEq/L

Etiology:
Renal failure or dehydration
Treatment of pre/eclampsia

Rhabdomyolysis
Excessive use of antacids

32
Q

Clinical manifestations of Hypermagnesmia

A

Lethargy, hyporeflexia, muscle weakness
Depressed respiration, apnea, confusion

33
Q

HYPOMAGNESEMIA

A

Definition: <1.5 mEq/L

Etiology:
Alcoholism, malnutrition, malabsorption & starvation
Parenteral nutrition
Pancreatitis

Hypoparathyroidism

34
Q

Clinical Manifestations of Hypomagnesmia

A

Personality changes, tetany, nystagmus, Chvostek’s & Trousseau’s sign, TACHYCARDIA, HYPERTENSION, and CARDIAC ARRHYTHMIAS

Altered PTH secretion/action may occur

35
Q

SERUM PROTEINS functions

A

Source of nutrition
Buffer system
Immune function

Carrier proteins
Metabolic function
Chromosomal & DNA components

Cell membrane structure
colloidal osmotic pressure
Antiprotease

36
Q

Serum Albumin

A

Part of a diverse microenvironment which primarily maintains colloidal osmotic pressure

Source of nutrition & also part of a complex buffer system. It is a “negative” acute phase reactant

Useful for:
Evaluation of nutritional status, albumin loss in acute illness

Evaluation of pts with liver or renal disease, hemorrhage, burns or leaks in GI tract

37
Q

Serum Albumin

A

Reference range:
Normal: 3.5-4.8 g/dl

Increased levels:
Volume depletion or dehydration

Decreased levels:
Acute/chronic inflammation & infection
Cirrhosis, liver disease & alcoholism
Nephrotic syndrome
Crohn’s, colitis, malabsorption
Burns & severe skin disease

Procedure: same as electrolytes (red, yellow SST tube or plain red tube )

38
Q

Serum Albumin interferring factors

A

Pregnancy
Oral contraceptives (OCP) & estrogen replacement
Prolonged bed rest

IV fluids, rapid hydration or overhydration
Is not a good indicator of recent changes in nutrition due to prolonged half-life in serum

39
Q

SERUM PROTEIN ELECTROPHORESIS (SPEP)

A

Separates albumin & globulins with an electric field to differentiate the proteins according to size, shape & electric charge into 5 distinct fractions

[Albumin, alpha-1-globulin, alpha-2-globulin, beta-globulin, gamma-globulin]

Useful for:
Detection of monoclonal protein or monitoring size of monoclonal peak in multiple myeloma pts

40
Q

SPEP Interpretation

A

↑ & ↓ albumin
↑ in total serum protein
Volume depletion or dehydration
Multiple myeloma

Sarcoidosis & other granulomatous diseases
Any inflammatory state
↓ in total serum protein

Poor nutritional status, liver disease, alcoholism, burns, severe skin disease
Renal disease, Crohn’s, UC

41
Q

SPEP more interpretation

A

Increases in gamma-globulin protein
Multiple myeloma, leukemia & other cancers
Autoimmune disease, chronic infections

Decreases in gamma-globulin protein
Nephrotic syndrome
Hereditary aggamaglobulinemia

Increases in beta-globulin protein
Multiple myeloma, biliary cirrhosis, obstructive jaundice

Decreases in beta-globulin protein
Nephrosis