Week 3 Review Pharmacology
Ch’s 36, 47, 48 Response Modifiers, Endocrine Agents, Antidiabetic Agents
Ch. 36
BRM’s fx:
1. enhance immunologic fx
2. destroy or interfere w/ tumor activities (cytotoxic)
3. promote differentiation of stem cells (other biologic effects)
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Recombinant DNA & hybridoma technologies (monoclonal antibodies) have led to mass
production of BRM’s
Echinacea, Ginseng, Goldenseal interfere with action of Biologic Response Modifiers
Interferons interfere with DNA, ex. helps 40% of liver that is still functioning
 Usually taken 3x/wk injections,
 newer one taken 1x/wk= “Intron A” pegolated=time release
 Mostly interferon alpha used (there is also beta and gamma)
 Used for kaposi’s sarcoma, some leukemias, acute MS (lessen excaserbations & lengthen time
between attacks)
 #1 reason people quit taking = side effects
 flulike syndrome with chills/fever, headache (myalgias), nausea, etc.
 often premedicate with Tylenol, benedryl, Demerol
 standard dose = 3-4 million IU/ml based on blood values
Colony-Stimulating Factors hematopoietic CSF’s are proteins that stimulate or regulate growth maturation,
and differentiation of bone marrow stem cells.
 Erythropoietin (EPO) =aka Procrit, Epogen produced by kidney, stimulates RBC production
 EPO used for end-stage renal failure, chemo, AZT patients
 Side-effects=nausea, injection site skin reaction (more p. 521)
 Dosing- depends on hematocrit (RBC count), <30=anemic, get it IC, SC, or thru dialysis
 Dose should be reduced when the Hct reaches the 30%-33% range
 If client doesn’t respond to EPO or maintain response:
 Iron deficiency
 Occult blood loss
 hemolysis
 Not mentioned in class: underlying infx, malignancy, hematologic disease, folic acid or
vitamin B12 deficiency, aluminum intoxication, osteitis fibrosa cystica
 Warm vial to room temp to administer, don’t use same needle to draw med into syringe and to
inject med – use new needle to inject. Chill needle first if it’s always painful.
 Neupogen/(Granulocyte Colony Stimulating Factor) =>WBC (a chemo side effect)
 Much the same info as above, shot etc.
Neumega = > WBC
Interleukins –proteins produced by WBC’s, the lymphocytes
 Interleukin 2 =Proleukin for renal cancer
 Side-effect= hypotension
 Hold if HR irregular, atrial fib, slow HR, slow BP/systolic <90, or >creatinine b/c it’s
nephrotoxic
Monoclonal antibody
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Trastuzumab (Herceptin) for tx of metastatic breast cancer – allows chemo to work by not
rejecting it.
Blocks WBC’s (T cells) from recognizing foreign (chemo, organ transplant
Chimerism = 2 bodies “get along”
Rituximab (Rituxan) certain non-Hodgkin’s lymphoma
Nurse should obtain:
 *drub and herb hx from pt
 baseline physical info: ht, wt (primarily), vitals, labs: CBC, electrolytes, creatinine, liver fx
Ch. 47
Anterior pituitary secretes:
 GH – growth in tissue & bone
 Somatropin/Protropin for dwarfism
 Parlodel for giantism (suppress GH)
 Sandostatin to suppress GH, for cancer also
 TSH
 for diagnosing cause of hypothyroidism
 atrial fib common in hyperthyroidism
 ACTH – stimulates adrenal gland to get cortisol (sleep/wake cycle)
 Stresses like surgery, sepsis and trauma override the diurnal rhythm causing an increase
in ACTH and cortisol
 Corticotropin (Acthar) to diagnose adrenal gland disorders
 Gonadotropins (FSH & LH)
Posterior pituitary secretes:
 ADH (vasopressin, desmopressin/DDAVP intranasal or by injection)- promotes water
reabsorption from tubules to maintain water balance in the body fluids
 ADH deficiency = diabetes insipidus
 Released if BP is <
Hypothyroidism
 Myxedema –severe adult hypothyroidism:
o Lethargy, edema of eyelids/face, cold intolerance, wt. Gain; not mentioned in class: apathy,
memory impairment, emotional changes, slow speech, deep coarse voice, slow pulse,
constipation, abnormal menses.
o In children = cretinism, congenital
o Levothyroxin(Synthroid) usually 25-50mcg/day, don’t mix generic & brand name
Hyperthyroidism = > in T4 and T3, overactive thyroid
 Tx: Surgery / radioiodine therapy (results in hypothyroidism)
Parathyroid glands = PTH regulates Ca+ levels in blood
Calcitriol = vitamin D analogue promotes Ca+ absorption in GI and secretion of Ca+ from bone to
bloodstraeam, can interact with Digoxin so ck dig levels
Adrenal glands
 Adrenal cortex produces 2 hormones/corticosteroids which promote Na+ retention and K+ secretion:
1. glucocorticoids (cortisol)
o methylprednisolone (Solu-medrol) decreases cortisol levels with long-term use but side effect =
upper
o *Ginseng and steroids = upper, can = insomnia if taken hs
o *Echinacea may counteract effects of corticosteroids
2. mineralocorticoids (aldosterone)
Ch. 48
Diabetes= insufficient insulin secretion from beta cells resulting in > blood sugar
FX – insulin released by beta cells of the islets of Langerhans in response to increase in blood glucose. Insulin
promotes the uptake of glucose, amino acids, and fatty acids and converts them to substances that are stored in
body cells.
*Normal values: 70-110 mg/dl serum glucose (sometimes 70-100)
Cultural occurances: native Americans, Hispanics, blacks 2-3x > incidence
SX: > blood sugar, “3 P’s”: polyuria(> urine), polydipsia (> thirst), polyphagia (> hunger)
Types:
1 Insulin dependant (IDDM)/ juvenile-onset: 10-12%
2 Non-insulin dependant (NIDDM) 85-90% (95% per Stecher), producing but not using effectively
3. Secondary diabetes (meds, hormonal) 2-3%
4. Gestational (GDM) – risk if: overweight, family hx in female side <1% (2-5% of pregnancies)
New category preDiabetic, hi BG but not yet type II
When more insulin is administered than is needed for glucose metabolism=
Hypoglycemic reaction or insulin shock, (upper) =
 SX: tachy, nervousness, trembling, lack of coordination, cold/clammy skin, headache, sweating, slurred
speech, memory lapse, confusion, seizures
Hypoglycemia risk:
1. long acting & non compliant
2. take too much insulin
3. right amount insulin but doesn’t eat
W/ inadequate insulin, sugar can’t be metabolized and fat catabolism occurs. Use of fatty acids (ketones) for
energy causes
Ketoacidosis/ hyperglycemic/ diabetic coma
 SX: Extreme thirst, polyuria (esp. at night), fruity breath (apples), kussmaul breathing, rapid/thready pulse,
dry mucus membranes, poor turgor, blood sugar > 250mg/dl
 Ketoacidosis is slow to develop, usually in undiagnosed diabetics “in slow motion”
Types of insulin:
1. rapid acting- regular, lispro(Humalog), Humulin R
2. intermediate acting- NPH, Humulin N, Lente, Humulin L
3. long acting Ultralente (don’t see much);
 Lantus (new) – basal reaction, works w/ metabolism, CLEAR, don’t mix w/ other insulin, peakless,
stable, and steady 24 hours Protamine zinc insulin should not be mixed
4. combinations- Humulin 70/30, 50/50, etc.
Triangle of management to consider with hypo/hyper glycemic reactions:
Insulin
Exercise
Diet
 Diabetes 5th leading cause death, leading cause blindness, 60% of amputees are diabetics, 75% also have
HTN so most get coronary disease and renal failure.
Insulin pen injectors > compliance with insulin regimen
Insulin pumps- two kinds:
1. implantable- delivers basal insulin infusion. There are fewer hypoglycemic reactions and the blood
glucose levels are controlled.
2. portable
Pump is set to a basal rate, but can be manually triggered to deliver additional insulin before each meal as
indicated by blood glucose level. Control is better than with multiple injections once the regimen stabilized.
Oral Antidiabetic Drugs  for non-insulin diabetics
Oral insulin criteria:
 Non-insulin dependant
 40 yrs.
 Diagnosed < 5 yrs.
 Normal or overwt.
 Fasting blood sugar about 200
 Normal renal and liver fx
1st and 2nd generation sulfonylureas = more problems than newest 2nd generations
Nonsulfonylurease (2nd generation)
Biguanides
Metformin (Glucophage)
 for type 2 when no response to sufonylureas
 acts by decreasing hepatic production of glucose from stored glycogen. This diminishes the
increase in serum glucose following a meal and blunts the degree of postprandial
hyperglycemia. Also < absorption of glucose from small intestine. Unlike sulfonylureas,
doesn’t produce hypo/hyperglycemia.
 * < blood sugar after meal eaten
 so less hypoglycemic responses
 is excreted thru kidneys so NOT for renal failure or CHF w/ diuretic;
 NOT for those who go into ketoacidosis
 some people with allergy to it
Thiazolidinediones (insulin-enhancing agents)
Avandia
 < insulin resistance, allows insulin to be used
 usually for someone who did good w/ metformin but still borderline so Dr. adds Avandia,
often secondary.
New way to manage with 1 unit insulin/15g. carbs:
 So, 60 carbs med- 4 units regular insulin needed
 Advantages:
 > compliance
 puts people in control of diet
 you can have dessert, etc.
Hyperglycemic drugs
Glucagon
 available for parenteral use (SC, IM, IV)
 not used much in hospitals anymore but for pt. who crashes on tennis court, etc… they can keep
it on hand just in case
Garlic p. 146 & 150
Reported to lower cholestrerol & triglycerides levels, < BP, reduce clotting capability of blood. Also acts as
ABX, oil for earache.
Garlic/ammonia smell thru skin could = liver problems (i.e. drinking problem?)
Chronic use:
 < hemoglobin cells
 increase antiplatelet (Plavix)
 < lipids
Juniper
o
o
o
o
o
o
< glucose levels
Ca+, magnesium
Who shouldn’t take it?  cardiacs
Capsule, liquid, oils, tabs
Most impt.  hypoglycemic effect for diabetes,
Diuretic effect for renal patients (only for mild CHF to get > urine output) – don’t give to
chronic renal failure to get more output for annuria (no urine), oliguria <400cc/24 hours