MLSC 4066 FINAL

pH reference range

7.35-7.45

pCO2 reference range

35-45 mmHg

HCO3 reference range

22-28 mmol/L

Total CO2 reference range

22-28 mmol/L

pO2 reference range

85-105 mmHg

What specimen is preferred for blood gases?

1-3 mL self-filling, plastic, disposable syringe, with heparin salts

How are blood gases affected by exposure to air bubble or room air?

False elevation in pO2 and pH, decrease in CO2

How are blood gases affected by sitting out for several hours without ice?

increased cell metabolism leads to falsely increased CO2, decreased pH and pO2

Right shift of the oxygen dissociation curve means

Decreased Hgb affinity for O2 (releases it readily):

Decreased pH

Increased temperature

Increased 2,3-DPG

Increased pCO2

What conditions result in a right shift on the oxygen dissociation curve?

anemia, cirrhosis, fever, high Co2

Left shift of the oxygen dissociation curve means

Increased Hgb affinity for O2

Increased pH

Decreased temperature

Decreased 2,3-DPG

Decreased pCO2

How is pO2 measured

amperometry (Clark electrode)

How is pH and pCO2 measured

potentiometry; change in voltage

4 forms of hemoglobin

Oxyhemoglobin

Deoxyhemoglobin

Carboxyhemoglobin

Methemoglobin

Affinity of CO for Hgb

200-250x greater affinity for hgb c/t oxygen

What oxidation state does Fe need to be in for binding of O2?

Ferrous state (Fe2+)

Transport of CO2 in blood

89% as bicarbonate in RBCs

11% as CO2 remains in plasma

four blood buffering systems

Bicarbonate, hemoglobin, phosphorus, and proteins

Bicarbonate buffer system

most important buffer system; carbonic acid-bicarbonate pair

Lungs control CO2

Kidneys control HCO3

Henderson-Hasselbalch equation using bicarbonate-carbonic acid pair

pH = 6.1 + log ([HCO3-]/[0.031*pCO2])

Normal ratio of bicarbonate to carbonic acid

20:1

Bicarbonate:carbonic acid ratio <20:1

seen in respiratory and metabolic acidosis

Bicarbonate:carbonic acid ratio >20:1

seen in respiratory and metabolic alkalosis

How does the body compensate for metabolic acidosis?

hyperventilation; expelling CO2 will normalize by reducing pCO2 and elevating the pH

How does the body compensate for respiratory acidosis?

hypoventilation and metabolic/renal processes; excreting H+ and retention of HCO3-

What is metabolic acidosis caused by?

severe diarrhea, diabetes, renal failure, pancreatitis, MUDPILES

What is respiratory acidosis caused by?

asthma, COPD, overdose of drugs that slow respiration, congestive heart failure

How does the body compensate for respiratory alkalosis?

excreting HCO3- in

the urine and reclaiming H+ to the blood through

decreased activity of the Na+-H+ exchange

How does the body compensate for metabolic alkalosis?

hypoventilation; this is erratic and can result in an increase in respiration. The primary cause needs to be corrected.

What is respiratory alkalosis caused by?

hyperventilation (anxiety or hypoxia), anemia, high altitude, aspirin intoxiation

Hemoglobin buffer system

Hgb binds to or releases hydrogen and carbon dioxide with little to no change in pH

Phosphate buffer system

primary buffer in urine; enables kidneys to excrete H+; NaH2PO4 neutralizes strong acids

Protein buffer system

primarily cellular buffer; ionizable side chains that pick up or release H+

Steroids are derived from

cholesterol

Properties of steroids

hydrophobic, reversibly bound to carrier proteins, half life 30-90 minutes

Properties of hormones derived from proteins

water-soluble, circulate freely, half-life <30 minutes

Tropic hormones

act on endocrine glands; TSH, ACTH, LH, FSH

Direct effector hormones

act directly on peripheral tissue; cortisol

Membrane receptors bind which hormones

protein/catecholamines (epinephrine)

Nuclear receptors bind which hormones

smaller molecules such as steroid/thyroid that diffuse across the plasma membrane

Negative feedback

increased stimuli will feedback upstream to decrease its production

Positive feedback

change in stimulus triggers mechanisms that amplify the stimulus; childbirth and oxytocin

Pituitary hormone secretion is controlled by

hypothalamus; releasing/inhibiting factors

Anterior pituitary secretes

GH

PRL

ACTH

TSH

LH

FSH

Posterior pituitary

Stores and releases hormones from hypothalamus; oxytocin and arginine vasopressin (AVP)

Thyrotropin-releasing hormone (TRH)

Promotes secretion of TSH and PRL

Gonadotropin-releasing hormone (GnRH)

Promotes secretion of FSH and LH

Corticotropin-releasing hormone (CRH)

Promotes secretion of adrenocorticotropic hormone (ACTH)

Growth hormone-releasing hormone (GHRH)

Promotes secretion of GH

Somatostatin

suppresses secretion GH and TSH

Dopamine

inhibits prolactin

ACTH acts on and promotes the synthesis of

adrenal cortex; glucocorticoids

FSH acts on and promotes the sythesis of

ovaries and testes; estrogen and spermatogenesis

GH acts on

liver and bone

LH acts on and promotes the production of

ovary and testes; ovulation, corpus luteum, progesterone and testosterone

Prolactin acts on and promotes

breast and lactation

TSH acts on and promotes the synthesis of

thyroid and thyroid hormones (T4 and T3)

AVP acts on and promotes

kidneys and osmotic homeostasis; regulates renal free water excretion; promotes release of clotting factors

Diabetes insipidus

deficiency of AVP characterized by polyuria and polydipsia

Oxytocin acts on and promotes

uterus and hemostasis and uterine contractions; positive feedbackk

GH deficiency causes and symptoms

genetic, tumors, injury; short stature common in children

acromegaly

GH disorder of middle-aged persons marked by elongation and enlargement of extremities and head bones

pituitary gigantism

leads to an abnormal growth of the long bones in children; caused by pituitary tumors

Diagnosis of pituitary gigantism

-IGF 1 levels (excess)

-Gold standard: GH suppression tests (oral glucose loading)

Prolactins major mode of regulation

tonic inhibition rather than intermittent stimulation; TRH, estrogen, and breastfeeding stimulate secretion

Hyperprolactinemia is associated with

hypogonadism by suppression of gonadotropin secretion

Sensitive indicator of pituitary dysfunction

prolactin; most frequently associated with pituitary tumors

Symptoms of hyperprolactinemia

amenorrhea, galactorrhea, loss of libido, infertility, headache, visual complaints

Hypopituitarism

failure of either the pituitary or hypothalamus results in loss of anterior pituitary function

GH is stimulated by

exercise, sleep, stress, low plasma glucose, sex hormones, norepinephrine

GH is inhibited by

Glucose loading, epinephrine, prychological stress, thyroxine deficiency

Primary aldosteronism (PA) should be suspected when patients present with

hypertension, hypokalemia, metabolic alkalosis, elevated urinary aldosterone and potassium

Excessive secretion of aldosterone seen in PA cannot be suppressed with

salt or volume replacement

Conn's syndrome

adrenal aldosterone-producing adenoma

Secondary Aldosteronism hallmark is

increased urinary aldosterone in the presence of increased plasma renin activity

Cushing's syndrome should be suspected when patients present with

hypertension, rapid unexplained weight gain, red/purple stretch marks, and proximal muscle weakness