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219 Cards in this Set
- Front
- Back
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2 hormones work better at night |
growth hormone adrenocorticotropoid hormone (increases blood sugar) |
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up regulation |
increase in receptor numbers, decrease in hormone levels |
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down regulation |
decrease in receptor # increase in hormone levels |
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you will see increasing TSH levels in a patient with |
hypothyroidism |
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you will see a decreasing TSH level (too little?) with : |
hyperthyroidism |
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how to you test for TSH? |
serum thyroid stimulating hormone test: serum T4 txt serum T3 test |
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clinical presentation in adults for hypothyroidism |
pale, puffy, expressionless face cold dry skin brittle hair/ hair loss low HR, low body temp lethargy/fatigue intolerance to cold impaired mentality |
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In children, hypothyroidism = |
cretenism |
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in adults, hypothyroidism (sever)= |
myxedema |
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causes of hypothyroidism |
-primary hypothyroidism -hashimotos' disease (autoimmune) -insufficient iodine -surgical removal/destruction of thyroid -insufficient secretion of TSH or TRH |
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normal TSH (micro units/mL) |
0.3- 6 |
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hyperthyroidism TSH levels |
under 0.3 |
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hypothyroid TSH level |
over 6 |
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normal total T4 |
4.5 to 12.5 |
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normal free T4 |
0.9 to 2 |
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normal total T3 |
80 - 220 |
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normal free T3 |
230-620 |
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exophthalmos |
bulging eyes (can be caused by hyperthyroid) |
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6 s/sx of hyperthyroidism |
-weight loss -anxiety -insomnia -tachycardia -hyperreflexive state -exophthalmos |
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3 groups of meds given to relieve s/sx of hyperthyroidism |
-beta blockers (decrease workload/decrease oxygen consumption) -sleep aids -anti anxiety meds |
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cause of thyrotoxic crisis (thyroid storm) |
thyrotoxicosis triggered by significant stress- surgery, illness, etc. |
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can thyrotoxic crisis be dx with lab testing? |
no, sometimes no rise in thyroid hormone |
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s/sx of thyrotoxic storm |
-hyperthermia (105 degrees plus) -severe tachycardia -restless/agitated -tremor -loss of consciousness/coma -hypotension -hf |
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tx of thyrotoxic crisis/thyroid storm |
-potassium iodide -propylthiouracil (PTU) -beta blocker -sedation -cooling -glucocorticoids -IV fluid |
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coryza |
runny nose |
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# of americans with diabetes |
25.8 million |
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5 of US population with diabetes |
8.3% |
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# of people considered pre-diabeteic |
79 million |
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3 diseases that DM increases risk for |
CAD Stroke CKD |
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how much of glucose ingested is stored in liver |
2/3 |
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beta cells |
secreted insulin |
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alpha cells |
secrete glucagon |
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islets of langerhans secrete |
hormones into the blood |
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acini secrete |
digestive juices |
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delta cells |
secrete somatotropin (controls both insulin and glycogen) |
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how many americans have type II diabetes |
approx 22 million |
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long term complications of diabetes |
-macrovascular damage -heart disease -stroke -hyperglycemia -altered lipid metabolism -gastroparesis -amputation secondary to inf. |
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what psych meds cause metabolic syndromes |
2nd generation antipsychotic |
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metabolic syndrome can include |
-obesity -elevated TG -low HDL -HTN -DM type 2 |
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3 tests for diabetes |
-FPG: no food 8 hrs prior to test -CPG: casual finger stick -OGTT: oral glucose tolerance @ 2hrs |
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normal OGTT |
less than 140 |
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OGTT indicating prediabetic |
141 to 199 |
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OGTT indicating diabetic |
greater than 200 |
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CPG indicating diabetic |
200 w/ postive signs: -polydipsia -polyfagia -polyuria -weight loss |
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FPG Normal Diabetes type I |
Normal: less than 100 Diabetes Type I: greater than 126 |
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Hemoglobin A1C |
excellent test to see how well patient is controlling glucose: anything greater than 6.5% means they are not under good control. |
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how many positive tests must you have to diagnose diabetes |
2 |
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pre diabetes FBG |
between 100 and 125 mg/dL |
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diet for diabetes 1, what is important to note about carbs? |
the total # of carbs matters, not the type (better to eat a small amount of high glycemic index food than a large amount of low glycemic index food.) |
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3 short duration: rapid acting insulins |
-Lispro (Humolog) -Aspart (Novolog) -Glulisine (Apidra) (LAG) |
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Short duration: slower acting insulin |
-Regular insulin (Humalin R, Novolin R) |
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2 Intermediate duration insulins |
Neutral protamine Hagedorn (NPH) Insulin detemir (Levemir) |
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NPH |
Intermediate duration insulin |
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Insulin detemir (Levemir) |
Intermediate duration |
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Long duration insulin |
Insulin glargine |
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Insulin glargine |
Long duration |
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Lispro (Humalog) onset peak duration |
onset: 15-30 min peak: .5 - 2.5 hours duration: 3 - 6.5 hours |
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onset: 15-30 min peak: .5 - 2.5 hours duration: 3 - 6.5 hours |
Lispro (Humalog) Rapid acting/short duration |
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Aspart (Novolog) onset peak duration |
onset: 10-20 minutes peak: 1-3 hours duration: 3-5 hours |
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glulisine (apidra) onset peak duration |
onset: 10-15 minutes peak: 1-1.5 hours duration: 3-5 hours |
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compare and contrast onset, peak, duration between Lispro, Apart, Glulisine |
Lispro- slowest to act, fastest to peak, longest duration of rapid acting/short duration insulins. Aspart- onset 10-20min like glulisine, slowest to peak (up to 3 hours), duration 3-5 like glulisine. Glulisine- onset 10-20 min like aspart, moderate to peak, duration 3-5 hrs like aspart. |
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5 delivery options for short duration/slower acting insulin (Regular) |
-sub cut -infusion pump -IV (ONLY W/ REGULAR) -IM (never seen) |
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type of insulin you will give in emergency |
Regular |
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2 measurements of Regular insulin |
U100 in 1 mL U500 in 1 mL |
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onset, peak, duration Humulin R Novolin R Exubera |
Humulin R: onset: 30-60min, peak: 1-5hr, dur: 6-10hr Novolin R: onset: 30-60 min, peak: 1-5hr, dur: 6-10 Exubera: onset: 15-30 min, peak: .5-1.5, dur: 6.5 |
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NPH- onset, peak, duration Humulin N Novolin N |
Humulin N: onset: 60-120min, peak: 6-14hr, dur:16-24hr Novolin N: onset: 60-120min, peak: 6-14hr, dur: 16-24hr |
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do you give NHP at mealtime? |
No. |
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can you mix long acting insulin with other insulins? |
No. |
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Long acting insulin example: |
Glargine (Lantus) |
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Glargine onset, peak, duration |
onset: 70 minutes peak: none duration: 24 hours |
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how to store insulin vials? how long after opening can they be kept? |
store in fridge, do not freeze. after opening, can keep for up to 1 month (room temp) or 3 months (under refrigeration). |
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how long can you keep mixtures of insulin in pre filled syringes |
stored in fridge for at least 1 week and should be kept vertically w/ needle pointing up. |
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4 categories of oral hypoglycemic agents AKA antidiabetics |
-Biguanides -Sulfonylureas -Thiazolidinediones (Glitazones) -Meglitinides (Big Suckers Take Meth) |
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Biguanides |
Metformin (Glucophage) |
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2 Thiazolidinediones (Glitazones) |
Rosiglitazone (Avandia) Pioglitazone (Actos) |
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2 Meglitinides (glinides) |
-Repaglinide (Prandin) -Nateglinide (Starlix) |
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how to biguanides work |
decrease glucose production by the liver & increase glucose uptake by muscle |
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Metformin (Glucophage) side effects |
-GI symptoms -diarrhea -Lactic acidosis -WILL NOT CAUSE HYPOGLYCEMIA |
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Indication for Metformin |
-Polycystic Ovary Syndrome -Hyperglycemia w/ type II diabetes |
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don't give this oral hypoglycemic agent to a patient w/ renal insufficiency or a patient getting IV con |
Metformin (Glucophage) |
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how to sulfonylureas work |
promote insulin secretion by the pancreas, may also increase tissue response to insulin |
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Which oral hypoglycemic agent promotes insulin secretion by the pancreas, may also increase tissue response to insulin |
Sulfonylureas |
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what class of drug is commonly added to metformin to improve glucose control w/ a reduction of 1-2% of A1C? |
Sulfonylureas |
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What group of drugs stimulates insulin secretion regardless of blood glucose levels |
Sulfonylureas |
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what class of drug may accelerate disease (diabetes) progression by inducing B cell exhaustion |
Sulfonylureas |
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2 second generation Sulfonylureas |
-Glipizide (glucotrol) -Glimepiride (Amaryl) |
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Benefit/drawback of using Glipizide (Glucotrol) |
This second generation Sulfonylureas has less drug/drug interactions but cannot be used in pregnancy. |
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Glinides /Metiglinides act by |
stimulation of pancreatic insulin release |
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2 drugs that are M-Glinides |
-Repaglinide (Prandin) -Nateglinide (Starlix) |
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-glinide |
M-glinides |
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what is difference between m-glinides & sulfonylureas |
pharmacokinetics- m-glinides are faster acting |
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prototype m-glinide: |
Repaglinide (Prandin) |
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Repaglinide (Prandin) |
Prototype m-glinide |
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should a patient take Repaglinide (Prandin) w/ or w/out meals? |
MUST give with meals/ eat within 30 minutes of taking med. |
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peak for Repaglinide |
1 hour of PO |
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metabolism for Repaglinide (Prandin) |
hepatic |
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adverse effects of Repaglinide (Prandin) |
hypoglycemia |
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concern when giving patient w/ liver disease Repaglinide (Prandin) |
yes, stays in body longer, increases hypoglycemia risk. |
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action for TZDS |
decreases insulin resistance, increases glucose uptake by cells of muscle, decreases glucose production by liver |
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2 drugs that are TZDS |
-Rosliglitazone (Avandia) -Pioglitazone (Actos) |
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where are incretin hormones released from |
gut |
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what are incretin hormones released in response to? |
food intake |
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what do incretin hormones do? |
potentiate glucose induced insulin secretion |
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2 incretin hormones |
-glucagon like peptide 1 (GLP-1) -glucose dependent insulinotropic polypeptide (GIP) |
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these hormones contribute to insulin secretion from the beginning of a meal and their effects are progressively amplified as plasma glucose concentrations rise |
Incretin hormones |
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3 ways GLP-1 AGONIST decreases postal glycemia |
-stimulates insulin production from pancreatic beta cells -decreases glucagon secretion by pancreas -slows gastric emptying, delays nutrient absorption and decreases food intake. |
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this enzyme degrades incretin hormones |
DPP-4 |
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how do DPP 4 inhibitors act? |
prevent the degradation of released incretin hormones and prolongs their actions |
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2 complications of poor glycemic control |
-DKA -Hyperglycemic hyper osmotic nonketotic syndrome (HHNS) |
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what is the most common complication in pediatric patients with diabetes and the leading cause of death? |
diabetic ketoacidosis |
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5 characteristics of diabetic ketoacidosis |
-hyperglycemia -ketoacids -hemoconcentration -acidosis -coma |
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5 tx for diabetic ketoacidosis |
-insulin replacement -bicarbonate -water & sodium replacement -potassium replacement -normalization of glucose levels |
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preferred tx for hypoglycemia |
IV glucose |
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if preferred tx (IV GLUCOSE) is not available & your patient is hypoglycemic, give them: |
-parental glucagon -candy, life saver, apple juice -then carbohydrate snack |
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principle endogenous estrogen |
estradiol |
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principle progestational hormone: |
progesterone |
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estrogen is secreted from: |
ovaries |
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progesterone is secreted from: |
ovaries & placenta |
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Describe the menstrual cycle |
first day of menstrual cycle- period follicular phase- first half of cycle (day 1-14) luteal phase- day 15-28 |
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During the first half of the menstrual cycle, THIS HORMONE acts on the developing ovarian follicles, causing them to mature and secrete estrogens |
FSH |
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rising estrogen levels towards mid cycle suppress ___________. |
FSH |
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_______ levels rise abruptly at mid cycle, cause dominant follicle to swell and burst |
LH |
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after ovulation, the ruptured follicle becomes a corpus luteum and under the influence of _________ begins to secrete _________ |
LH progesterone. |
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where are estrogens made in men & women |
men: sm. Amt of testosterone converts to estradiol/estrone in testes, peripheral tissues: fat, liver, skeletal muscle women: ovary, follicles, placenta |
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decline in _________ brings on menstruation but decline in ___________cuases breakdown of endometrium |
estrogen progesterone |
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2 metabolic actions of estrogens |
-block bone reabsorption -@ puberty, increase in estrogen promotes epiphyseal closure |
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2 effects of estrogen on cholesterol |
-lowers LDL, increase HDL -increase cholesterol amount in bile |
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effects of estrogen on blood coagulation |
-suppress and promote coagulation -increase levels of coagulation factors -decrease levels that suppress coagulation |
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6 adverse effects of estrogen |
-endometrial hyperplasia/carcinoma -promotes growth of EXISTING breast cancer -ovarian cancer (post menopausal women) -cardiovascular events -nausea -adverse effects when used during pregnancy |
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3 therapeutic uses for estrogens |
-hormone therapy after menopause -female hypogonadism -acne |
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routes for estrogens |
oral, transdermal, intravaginal, parenteral (IM/Sub cut) |
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3 drugs whose effects are reduced by OCs |
-Warfarin -Insulin -Oral hypoglycemics |
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Drugs whose effects are increased by OCs |
-theophlline -tricyclic antidepressants -diazepam -chlordiazepoxide |
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drugs that elevate _________ should be avoided by patients on yasmin |
potassium |
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Plan B- high dose tablets of _______ |
progestin |
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androgens are produced in these three places |
-testes -ovaries -adrenal cortex |
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major endogenous androgen |
testosterone |
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primary clinical application for androgens |
management of androgen deficiency in males |
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2 principle adverse effects for androgens |
-virilization -hepatotoxicity |
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what is virilization |
in women: hair growth, menses irregular, acne, male pattern baldness |
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% of men over 75 with ED |
47% |
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COX1 (good COX) is present in all tissues but primarily acts on these 3: |
stomach- protects gastric mucosa Renal- renal synthesis of PGE2 & PG12 to increase blood flow. Platelets- promotes platelet aggregation |
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COX 2 "bad cox" is present in injured tissue and has these two main actions |
-mediate inflammation -sensitizes to pain |
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COX 2 acts primarily on these 4 tissues |
-brain- mediates fever & pain perception -kidney- supports renal function -blood vessels- increases vasodilation -colon- contribute to colon cancer |
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Inhibition of COX 1 causes |
BAD! -gastric erosion -renal impairment -bleeding |
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Inhibition of COX 2 causes |
GOOD: -suppression of inflammation -alleviates of pain -reduces fever -protects from colorectal cancer BAD: -renal impairment -promotes MI & stroke (2nd to decreased vasodilation) |
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2 broad classifications of COX inhibitors |
-NSAIDS (anti inflammatory) -NON anti inflammatory (acetaminophen) |
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2 generations of NSAIDS, examples of meds and difference between 2 generations |
1st generation: inhibit cox 1 & cox 2 -aspirin, ibuprofen 2nd generation: selective cox 2 inhibitors -celecoxib |
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# of people who die per year from NSAID induced ulcers: |
7000 to 10,000 deaths per year |
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what is Reye's Syndrome |
from Aspirin: swelling in liver & brain, s/sx: confusion, seizures, changing LOC, fatty liver degeneration, encephalopathy, mortality 20-30% -most often affects children & teens recovering from viral infection, flu or chickenpox |
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What is salicylism |
from Aspirin: tinnitus, sweating, headache, changing acid base disturbance (respiratory alkalosis) |
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what is hypersensitivity to aspirin |
occurs with hx of asthma, rhinitis, nasal polyps: profuse watery rhinnorhea. |
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principle indications for non aspirin 1st generation NSAIDS |
RA and OA |
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-profen, -proxen, -fenac |
1st generation NSAIDS |
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3 classes of anti arthritic drugs |
-NSAID -DMARDs: disease modifying anirheumatic drug -Glucocorticoids: adrenal corticosteroids |
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most rapid acting DMARD |
Methotrexate |
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Methotrexate adverse effects |
hepatic fibrosis bone marrow suppression GI ulceration pneumonitis |
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how long does it take for methotrexate to take full effect? |
3 to 6 weeks |
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glucocorticoids physiologic effects low dose vs high dose |
low dose: modulation of glucose metabolism in adrenocortical insufficiency. High dose: suppression of inflammation |
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hyperuricemia men/women |
uric acid greater than 7mg/dL in men uric acid greater than 6mg/dL in women |
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meds for short term relief of Gout (infrequent flares fewer than 3x/yr) |
-NSAIDS (first line agents) -Glucocorticoids |
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long term gout is defined by- and treated with- |
3 or more flares per year uricosuric drugs |
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arthralgia |
pain in a joint, side effect of Febuxostat (Uloric) tx for chronic tophaceous gout. |
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calcium is critical to function of these systems |
skeletal, nervous, muscular, CV systems |
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what % of body stores of calcium are in the bones |
98% |
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total serum calcium should = |
10 mg/dL |
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where is calcium absorbed |
sm intestine |
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what 2 hormones in crease absorption of calcium |
PTH & vitamin D |
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what decreases absorption of calcium? |
glucocorticoids |
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what hormone causes excretion of calcium? |
calcitonin augments calcium elimination |
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symptoms of hypercalcemia |
usually asymptomatic |
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cause of hypercalcemia |
cancer, hyperparathyroidism |
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tx of hypercalcemia |
-promote urinary excretion -decrease mobilization from bone -decrease intestinal absorption -IV SALINE |
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s/sx of hypocalcemia |
-increased neuromuscular excitability -tetany -convulsions -spasm of pharynx -chvosteks sign: poke @ jaw and face twitches -trousseu's sign: hand flexes w/ BP pressure cuff |
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cause of hypocalcemia |
-PTH deficiency -vitamin D deficiency -calcium deficiency |
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tx of hypocalcemia |
-calcium supplements (calcium glutinate) -Vitamin D |
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most common disorder of calcium metabolism |
osteoporosis |
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primary prevention of osteoporosis |
calcium, vitamin d, lifestyle |
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2 ways to diagnose osteoporosis |
-measuring bone mineral density (BMD) -dual energy x ray absorbtiometry (DEXA) |
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what does antiresorptive therapy drugs like Estrogen (premarin), Raloxifine (Evista), Bisphosphonates (Alendronate (Fosamax), Risedronate (Actonel), Ibandronate (Boniva)) & Calcitonin-salmon nasal spray (Miacalcin) treat? |
Osteoporosis in women. |
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3 contributors to COPD |
-Chronic bronchitis (person is rotund) -emphysema (person is skinny) -asthma |
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5 goals of therapy for COPD |
-relieve symptoms -tx infections -control cough -relieve bronchospasm -STOP SMOKING |
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2 main pharmacologic classes of drugs for asthma |
glucocorticoids - anti inflammatory agents beta 2 agonists- bronchodilators |
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3 types of inhalation drug therapy |
Metered dose inhalers (MDIs) Dry powder inhalers (DPIs) Nebulizers |
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name 2 glucocorticoids used for asthma |
-budesonide -fluticasone |
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what are considered the most effective anti-asthma drugs available |
anti inflammatory drugs: glucocorticoids: -budesonide -fluticasone |
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how to glucocorticoids like budesonide and fluticasone work |
-reduce bronchia hyperactivity, decrease airway mucus production, increase number of bronchial beta 2 receptors and increase their responsiveness to beta 2 agonists |
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how do glucocorticoids like budesonide and fluticasone work? |
inhalation (usually) IV PO |
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3 ways that glucocorticoids suppress inflammation |
-decrease synthesis & release of inflammatory mediators. -decrease infiltration & activity of inflammatory cells. -decrease edema of airway mucosa |
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adverse effects of glucocorticoids used for asthma |
-adrenal suppression -osteoporosis -hyperglycemia -.....others |
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patient with COPD will be on these two groups of drugs |
-bronchodilator -glucocorticoid |
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principle bronchodilators are (+name a bronchodilator) |
beta 2 agonist Albuterol |
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these asthma meds provide symptomatic relief but do not alter the underlying disease process (inflammation) |
bronchodilators. principle bronchodilator: beta 2 adrenergic agonists. i.e.: albuterol |
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3 methods for bronchodilators |
MDI, nebulizer, PO (rare) |
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3 beta 2 adrenergic agonists |
-albuterol -salmeterol -terbutaline |
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-albuterol-salmeterol-terbutaline- you can use these three beta 2 adrenergic agonists (bronchodilators) to tx what 2 issues |
-acute asthma attack -acute COPD |
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most effective drugs for relief of acute bronchospasm and prevention of exercise induced bronchospasm |
albuterol salmeterol terbutaline (bronchodilators: beta 2 adrenergic agonists) |
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prior to prescribing a bronchodilator, a nurse should know |
what a patient's normal HR is. |
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3 adverse effects of inhaled preparations of beta 2 adrenergic agonists |
systemic effects: -tachycardia -angina -tremor |
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4 classes of chronic asthma |
intermittent mild persistant moderate persistant severe persistant |
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this drug is a long acting, inhaled anticholinergic agent approved for maintenance therapy for COPD |
Tiotropium (Spiriva) |
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this drug is a leukotriene receptor blocker indicated for maintenance therapy of asthma. approved for children over the age of 1, no serious side effects |
Montelukast (Singulair) |
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2 anticholinergic asthma/copd treatments |
-Tiotropium (Spiriva) -Ipratropium (Atrovent) |
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-opium |
anticholinergics tx asthma or COPD |
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leukotriene inhibitor |
Montelukast (Singulair) |
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leukotrienes increase ____________ production |
mucus production |
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leukotriene inhibitors like Montelukast (Singular)do what |
decrease mucus production |
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4 emergency therapies for acute/severe exacerbations of asthma/copd |
-give oxygen (no more than 2L to start) -give systemic glucocorticoid (reduce inflammat.) -give nebulized high dose SABA (bronchodilate) -give nebulized ipratropium (LABA) |
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to control dust mites/ feces, wash all bedding and stuffed animals weekly in what temp water: |
hot water wash cycle- 130 degrees F |
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keep indoor humidity below _____% to reduce exposure to allergens & triggers |
50% |
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what is allergic rhinitis? |
inflammatory disorder of upper airway, lower airway, and eyes |
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s/sx of allergic rhinitis? |
-sneezing -rhinorrhea -pruritis -nasal congestion -for some: conjunctivitis, sinusitis, asthma |
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allergens bind to immunoglobulin _____ on mast cells |
Ig E |
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3 inflammatory mediators released |
-histamine -leukotrienes -prostaglandins |
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what class of meds do you give for allergic rhinitis? |
oral antihistamines |
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what are antitussives |
drugs that suppress cough |
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2 examples of opioid antitussives |
-codeine -hydrocodone |
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2 examples of nonopioid antitussives |
-dextromethorphan -diphenhydramine |
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OTC cold remedies usually combine two or more of the following: |
-nasal decongestant -antitussive -analgesic -antihistamine (for cholinergic actions) -caffeine (to offset effect of antihistamine) |
