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123 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Elements of Prescription: 1-4
(question on Final Exam Review) |
1.- 4. Bona Fides of Prescribing Dr.
Name Title Address Phone Number |
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Elements of Prescription: 5
(question on Final Exam Review) |
Elements of Prescription: Date Rx is written
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Elements of Prescription: 6-7
(question on Final Exam Review) |
Patient Identity by Name, address, age and weight
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Elements of Prescription: 8-11
(question on Final Exam Review) |
Specify Medication, Strength, Quantity dispensed, Dosage, Directions
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Elements of Prescription: 12-14
(question on Final Exam Review) |
Refill info, waiver of child-proof container, additional labeling instructions (eg: may cause drowsiness) and in some states may offer generic drug substitution or specify dispense as written (DAW)
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Elements of Prescription: 15-17
(question on Final Exam Review) |
Prescriber's information and other identification data
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Prescribing errors
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Rx errors legibility, ambiguous, not dated/timed, signature
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Diabetes mellitus
(question on Final Exam Review) |
not a single disease. heterogeneous group of syndromes all characterized by elevation of blood glucose caused by a relative or absolute deficiency in INSULIN.
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Cause of Diabetes Mellitus
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relative of absolute deficiency of insulin
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2 types of Diabetes
(question on Final Exam Review) |
IDDM/insulin dependent diabetes mellitus or Type I
NIDDM/non-insulin dependent diabetes mellitus or Type II |
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IDDM/insulin dependent diabetes mellitus or Type I
(question on Final Exam Review) |
onset in childhood
frequently malnourished 10-20% of diagnosed diabetics Moderate genetic disposition (maybe mother contracted virus) Beta cells destroyed (no more insulin made) |
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NIDDM/non-insulin dependent diabetes mellitus or Type II
(question on Final Exam Review) |
Frequently over 35 (now age lowering to high school kids)
Obesity present (exercise and diet can help) 80-90% off diagnosed diabetics very strong genetic predisposition Inability of Beta cells to make proper levels of insulin (little or none) Insulin resistance other unknown defects |
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Sources of insulin
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isolated from pork or beef pancreas
E Coli making human insulin (differing by one amino acid) |
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Hypoglycemic
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too much insulin
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Role of insulin
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binds to receptor to allow Glucose (CHO) to enter
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Admin of insulin
(question on Final Exam Review) |
SubQ (bc GI degrades the protein)
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Examples of Insulin Treatment
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Treatment burst of insulin
a) Rapid b) Short-acting Background a) Steady amount, combine 70% Long acting 30% Rapid acting (most common) |
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Oral Hypoglycemic Agents
(question on Final Exam Review) |
agents used for NIDDM pts who cant manage with diet...those who are over age 40 and have had diabetes for less than 5 years respond well. patients with long standing disease may require a combo of hypoglycemic drug and insulin to control hyperglycemia
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Sulfonureas
(question on Final Exam Review) |
-Not insulin, non-injection: oral
-increase insulin made, increase insulin binding or sensitivity to insulin -reduce glucagon binding. -can cause hypoglycemia |
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Byetta
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injectable medicine to improve blood sugar (glucose) control in adults with type 2 diabetes mellitus, when used with a diet and exercise program
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Rheumatoid arthritis
(question on Final Exam Review) |
Genetic autoimmune/immunological disease (body attacks synovial lining of joint)
Methotrexate gold salts in the synovial capsule/fluid Trx: COX II Inhibitor [Celebrex but not Vioxx(liars!)] NSAID |
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Osteoarthritis
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injury to joint
Trx: NSAIDS and COX II inh not reversible/no cure...just Physical Therapy |
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Gout
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-disease that attacks tissues and joints
-Big toe swollen) first (skips hips and shoulders) -Monosodium Urate crystals build up rubbing against the bone -Genetic predisposition (defect in metabolism of purine/nitrogen containing compounds) worse with a high protein diet -Trx: NSAIDS (except aspirin), Colchacine (but narrow margin of safety) -aspirin prevents kidneys from releasing uric acid |
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GRH
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Gonadotropin Releasing Hormone-tells pituitary what to do / release
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FSH
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Follicle Stimulating Hormone - release egg
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LH
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Leutenizing Hormone- released after endometrium reaches certain stage
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NSAIDS
(question on Final Exam Review) |
Non-steroidal Anti-Inflammatory Drugs
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COX1
(question on Final Exam Review) |
cyclooxygenase type one
Protects stomach lining ex Aspirin or Ibuprofen |
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COX2
(question on Final Exam Review) |
cyclooxygenase type two
PAIN Ex: Celecoxib |
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Cell Phases
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PMAT
Prophase Metaphase Anaphase Telophase and a LOOONG Interphase |
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Ultimate goal of cancer treatment
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is to cure neoplastic cells. they need to be eradicated
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Surgery/Radiation
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reduce/remove tumor "de-bulking"
"remove neoplastic bulk" if surgery not possible or surgery then radiation |
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Adjuvent Therapy
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(after surgery) Chemotherapy
Micrometastosis High growth tumors de-undifferentiated or when surgery makes little or no sense |
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palliative care
(question on Final Exam Review) |
drugs less toxic for pts to live normal life
alleviate symptoms and avoid toxicity Palliative care is specialized care focused on the pain, symptoms and stress of serious illness related to hospice care which is for patients with terminally ill diagnoses (6months or less to live) |
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Cell Cycle
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PMAT Prophase (Nuclear membrane transparent), Metaphase (chromosomes line up), Anaphase (pull apart), Telophase (cleavage)
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? Cell Cycle Specific Cancer Treatment
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Antimetabolites- Cannot make DNA (high growth/leukemia/blood disease)
Antibiotics - Interfere directly with DNA Microtubule inhibitors |
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? Cell Cycle Nonspecific Cancer Treatment
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-Alkalating agents: most toxic combination, short bursts
-Makes parts of cell bind together (glued together and can't work) -works on whole thing even interphase from mustard gas (1st type and most effective)toxic when cell divides, but also on whole cycle, even on slow growth/solid tumors |
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Leukemia cells find sanctuary in the CNS because of the blood brain barrier T/F
(question on Final Exam Review) |
TRUE
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Essay question? Cancer Treatment
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Palliative/curative & changes of drugs
Radiation, Surgery, Debulking (Chemotherapy) |
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Nonspecific Anticancer Treatment
(question on Final Exam Review) |
Alkalating agents: most toxic combination, short bursts
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? Toxicity and Drug resistance
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Acute Lymphocytic Leukemia -Pregnasome
Oncavin Methotrexate Purinothol/mercaptopurine |
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? Cancer Treatment
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Palliative/curative & changes of drugs
Radiation, Surgery, Debulking (Chemotherapy) |
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Drug problems
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multidrug resistance
toxicity: side effects: losing hair, vomiting, treatment induced tumors |
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Myelo-suppression
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bone marrow activity is decreased, resulting in fewer red blood cells
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Helicobacter pylori
(question on Final Exam Review) |
cause of peptic ulcers. lives in mucus lining of the stomach
(gastric ulcer) |
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Ulcer management
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avoid nicotine/alcohol/caffenine
get alternatives for aspirin/NSAIDS stress management modify eating habits manage use of antacids |
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Peptic Ulcer disease requires medical treatment which includes
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antibiotics
bismuth (pepto-bismol) Proton pump inhibitors Antacids/H2 antagonists |
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Peptic ulcer types
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Duodenal and gastric
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Duodenal ulcers
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ulcer in the duodenum
causes burning/gnawing/aching sensation in area of stomach symptoms of pain occur closely after eating. Tarry stool (blood) |
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Gastric ulcer
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ulcer situated in the stomach. causes same symptoms as duodenal ulcer but also includes: nausea and vomiting
Treat by: 2 antisecretory and/or bismuth 1. Antisecretory PPI / H2 inhibit Rantidine (Zantac) / Cimetadine (Tagamet) 2. Bismuth 3. reduce/neutralize acid lansoprazole (Prevacid)/ omeprazole (Prilosec) |
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Gram positive stain results
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pink for Gram negative
(peptidoglycan cell wall covered by outer membrane) purple for Gram positive (peptidoglycan cell wall on outside) |
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Gram positive cell wall sensitivity
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Gram positive cell walls are sensitive to lysozyme and penicillin
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Empiric therapy (initial)
(question on Final Exam Review) |
Coverage by a combo of antibiotics to kill gram+, gram- and anaerobes
or a single broad spectrum antibiotic *also get culture report |
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Empiric therapy (after culture)
(question on Final Exam Review) |
Gr+: continue Gr+ coverage
discontinue anaerobic and Gr- trx Gr-: continue Gr- coverage discontinue anaerobic and Gr+ trx Anaerobic: continue anaerobic coverage disc Gr+ and Gr- trx mixed: continue therapy as initiated |
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Diabetes Statistics
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affects 5% or 10 Million in US. 8th leading cause of death in US.
1-2 million with IDDM (Type I) and 8-9 million with NIDDM (Type II) |
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Normal insulin activity
(question on Final Exam Review) |
after eating high sugar level in the blood. Beta cells in the Islets of Langerhans of the Pancreas create insulin.
Insulin binds to receptors on the cells allowing Sugar to enter. Without Insulin the Sugar molecule would be too large to pass through the membrane |
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Diabetic insulin activity
(question on Final Exam Review) |
IDDM/Type I: Patient cannot make insulin on own. must depend on outside sources of insulin
NIDDM/Type II: Beta cells cant make enough insulin or the insulin is ineffective. (Patient's cells may be resistant to insulin being produced) |
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Treatment of Type I diabetes
(question on Final Exam Review) |
relies on injected insulin to control hyperglycemia. maintain blood glucose levels while avoiding swings in concentration. Use portable glucose analyzers
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Treatment of Type II diabetes
(question on Final Exam Review) |
-Maintain glucose concentrations within normal limits.
-weight reduction, exercise and dietary modifications decrease insulin resistance and correct hyperglycemia. -Most commonly, use pharmacological intervention w oral hypoglycemic agents for Type II patients who fail dietary control -sulfonylureas: this stimulates pancreas for insulin production. and increase sensitivity to insulin -insulin therapy may be required - not for pregnant females, makes high risk obstetrics |
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American Diabetics Association:
Insulin Basics |
3 characteristics: types of Insulin vary by how quickly they work, when they peak and how long they last
different strengths. most common U-100 |
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American Diabetics Association:
Types of Insulin |
Rapid acting insulin
Regular/short acting insulin Intermediate acting insulin Long-acting insulin |
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American Diabetics Association:
Types of Insulin/How long will it take to work? Rapid acting insulin |
insulin lispro (eli lilly)
insulin aspart (novo nordisk) insulin glulisine (sanofi-aventis) all start working 5 min after injection. peaks in about 1 hour. continues for 2-4 hours |
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American Diabetics Association:
Types of Insulin/How long will it take to work? Regular/short acting insulin |
(human) reached blood in 30 min after injecting. peaks2-3 hrs after injecting. effective for 3-6 hrs
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American Diabetics Association:
Types of Insulin/How long will it take to work? Intermediate acting insulin |
(human) reaches blood in 2-4 hrs after injection. peaks 4-12 hours later. effective for 12-18 hrs
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American Diabetics Association:
Types of Insulin/How long will it take to work? Long-acting insulin |
(ultralente) reached blood 6-10 hrs after injecting. effective for 20-24 hrs.
two long acting insulin analogues:glargine and detemir |
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American Diabetics Association:
effectiveness of insulin analogues:glargine and detemir |
fairly even over a 24 hr period with less of a peak of action than ultralente
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American Diabetics Association:
insulin's added ingredients |
prevent bacteria from growing and help maintain a neutral balance (acids/bases). also Zinc which helps prolong their actions (keep from being absorbed too quickly)
sometimes bring on allergic reactions |
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American Diabetics Association:
US vs foreign insulin |
different strengths. most common U-100 (100 units/mL fluid) also comes in U-40 (Europe Latin America)
FDA: US only has insulin manufactured in lab. but you can import animal insulin for personal use |
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self administration of insulin
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after training can self admin insulin by sub q injection.
no inhalers at present time because of inability to get a constant amount of insulin through an inhaler |
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Corticosteroids
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Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex next to the kidney
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Prostaglandin
(related to question on Final Exam Review) |
family of potent chemical messenger/arachidonic acid metabolites which modulate some components of inflammation/ temperature/ pain/ platelets etc (or call in the immune response)
They are released on demand and are rapidly degraded sensitizes neurons to pain (among other things) |
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NSAIDS
(question on Final Exam Review) |
non-steroidal anti-inflammatory drugs penetrates joint space and inhibits cyclooxygenase synthesis, which is vital to prostaglandin production
ex: Aspirin, ibuprofen but not acetaminophen (not anti-inflammatory) |
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Prostaglandin production
(question on Final Exam Review) |
-COX-1 is responsible for the baseline levels of prostaglandins.
-COX-2 produces prostaglandins through stimulation. |
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NSAID problems
(question on Final Exam Review) |
because large doses of aspirin NSAIDs can irritate the GI/stomach and create ulcers acetaminophen can be used which work similar pathways but is not inflammatory
or can prescribe antiulcer treatment along with NSAIDs to prevent gastroduodonal mucosa damage or prescribe COX II inhibitor to ease inflammation and avoid GI irritation |
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Arthritis characteristics
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pain in joint
joint inflammation tissue damage |
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Anti-arthritis drugs
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-ability to reduce inflammation
-ability to reach therapeutic levels in the joint capsules without reaching toxic levels ex: NSAIDS like Celebrex Cox2 inhibitor (doesnt block Cox1, less GI side effects)...can be prescribed with antacids/H2 blockers/prostaglandin analogs to prevent or reverse damage to GI mucosa |
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?Anti-gout drugs
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NSAIDS: Tylenol or Aleve to treat
-Sodium urate crystals in joint inciting inflammation -aspirin may relieve symptoms but main focus to lower uric acid levels -uric acid from purine metabolism -inhibit xanthane oxidase and thus uric acid production/reuptake in urine ex: Colchicine (but has narrow therapeutic index) |
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Immuno-modulating:
Immuno-suppressants |
-to prevent rejection of transplanted organs/bone marrow/rejection of fetal blood cells
-are antibodies (produced by nonhuman animals) and not drugs directed at human immune system -used in multiple schlerosis, rh arthritis, crohns disease example: Interferon |
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interferon
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-future of autoimmune disease treatment
-enhance activity of cytotoxic T cells, natural killer cells and macrophages -inhibits tumor cells, and suppress graft rejection -takes 17 yrs to purify (too expensive) |
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Anithistamine treatment
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-Allergies (bee stings/pollen) cause potentially fatal immune responses.
-Histamine, a chem produced in human tissue, mediates these responses and they're released by mast cells and basophils -Use H1 histamine receptor blockers to prevent bronchial smooth muscle contraction/histamine induced vasodilatioin -can also use histamine inhibitors prophlactically |
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Corticosteroids
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Prednisone equivalent for rheumatoid arthritis and osetoarthritis
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nonsulfonylureas
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less likely to cause hypoglycemia
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NIDDM treatment order
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those who fail dietary control AND oral hypoglycemic agents progress to insulin dependency
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Hypoglycemic drugs: nonsulfonylureas
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Metformin (Glucophage)
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Birth Control Pills prevents pregnancy by ...
(question on Final Exam Review) |
-increasing the Estrogen and Progesterone
-lowering GRH, FSH and LH (negative feedback loop) -making the body think that it's already pregnant |
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Birth Control Examples
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the Pill*, the Patch, the Ring
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Types of Birth Control Pill regimens
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-Monophasic
-Biphasic -Triphasic |
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Monophasic Oral Contraceptives
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Fixed amount of Progesterone/Estrogen
ex: 21 days of fixed Progesterone/Estrogen and 7 days of no pills/sugar pills (28 days total) |
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Biphasic Oral Contraceptives
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14 days fixed Progesterone/Estrogen
14 days increased Progesterone/fixed Estrogen to mimic whats going on in the body |
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Triphasic Oral Contraceptives
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7 days Fixed amount of Progesterone/ Estrogen
7 days increase of either Progesterone or Estrogen 7 days increase of both Progesterone and Estrogen |
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Patch / Ring
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Fixed ratio of Progesterone /Estrogen
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RU 486
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"Morning After Pill"
Stop pregnancy (abortifacent) opposite of birth control pill antagonist to progesterone synthetic steroid causes endometrium to slough off/break down/causes contractions side effect: a LOT of bleeding |
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Effectiveness of birth control
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98% effective
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Biggest problem with birth control / biggest side effect of taking more estrogen
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clots more easily
more visits to vascular surgeons so, take with aspirin |
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Hormone
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chemical produced by a gland that goes through the blood
(hormones link adrenaline very similar to neurotransmitters like epinephrine) |
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Examples of negative feedback loops
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Breast feeding
Birthing Egg release |
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Role of Hypothalamus in Pregnancy/menstrual cycle
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GnRH - gonadotropin releasing hormone tells pituitary what to do like release gonad chemicals
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Role of pituitary in Pregnancy/menstrual cycle
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releases FSH-follicle stimulating hormone
releases LH-leutenizing hormone |
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Role of follicle
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-Producing estrogen
-Releasing egg -Corpus Leuteum produces Progesterone thereby causing the endometrium to thicken and can create a mucus plug/inhibit uterine contraction. |
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Role of Mucus plug
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prevent more sperm entering and/or kill them as they try to enter
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Role of uterine contraction
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birthing
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Cause of 25% of deaths in US
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Cancer, or the uncontrolled division of cells
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Percentage of people that get cancer
(question on Final Exam Review) |
25% or 1 in 4
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Percentage of people that get cancer that are cured by surg. radiation
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6 out of 25
or 24% of the people that get cancer |
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Percentage of people that cannot be cured by surg. radiation that are cured or have a long remission
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2 out of 19
or ~10% of the people that cannot be cured by surg. radiation |
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Percentage of people that will have regression /complications /relapse /death
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17 out of 19
or ~80% of the people that cannot be cured by surg. radiation |
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5 Examples of carcinogens
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1. Tobacco
2. Radiation (luminescent paint) 3. Chemicals (Benzene) 4. Infectious disease (Human Pamploma Virus/Hepatitus) 5, Genetics (born with it/tumor) |
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Goal of Cell Cycle Specific Cancer Treatment
(question on Final Exam Review) |
-Interfere with DNA/RNA/Protein synthesis (like antibiotics ->used for cancer treatment)
-Inhibit microtubule formation |
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3 Adverse effects of Chemotherapy
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1. Resistance
2. Toxicity 3. Treatment Induced Tumors |
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Adverse effects of Chemotherapy: Resistance
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Short term intensive - intermittent break - short term intensive - break (repeat) cocktails/combos
Glycoprotein pump to get rid of anticancer /or other toxic substances |
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Adverse effects of Chemotherapy: Toxicity
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Hair loss - alopecia (only lasts during chemo)
No immune system - myelosuppression vomiting/nausea weight loss loss of appetite (sometimes a permanent effect on cardiac/pulmonary/bladder systems) |
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Adverse effects of Chemotherapy: Treatment Induced Tumors
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can cause cell to become mutagenic (secondary cancer after many years) can happen w/ alkalating agents
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? Hormonal cancer: Breast / testicular cancer
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-go through blood (slower)
-agonist hormones -antagonist hormones cancer with receptors with opposite competing hormones |
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POMP Cocktail
For all acute lymphocytic leukemia |
Prednasone
Oncosine/Vincristine* Methotrexate** Purinathol/Mercaptopurine |
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Pharmacological sanctuaries
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CNS-Blood-Brain barrier hard to treat
Solid Tumors Slime (protective) like bacteria and antibiotics |
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Immunomodulating drugs (modulate immune system)
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used for leukemia/lymphomas cancers of white blood cells immune cells
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Nukes
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Nucleo Restrictive Transferase Inhibitor
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Non-Nukes
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Non-Nucleo-Restrictive Transferase Inhibitor
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HAART
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Highly Active Anti Retro Viral Therapy:
Cocktail: 3 or more drugs used in combo NRTI + NNRTI + Protease Inhibitor |
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Retroviral Order
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RNA -> DNA -> Protein
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HIV patients usually die of:
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opportunistic infections like shingles, CMV, Carposy
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GERD
Gastro-Esophageal Reflux Disease |
inflammation of espohageal mucosa caused by reflux of acidic stomach acid past lower esophageal sphincter
Obesity and nicotein smoking exacerbates situation can be caused by H Pylori and NSAIDS |
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GERD Treatment
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1. H2 receptor antagonist
2. Proton Pump Inhibition 3. Bismuth 4. Tums Antacid 5. Gastric Emptying (erythromycin) |
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