pharmacology exam 3

bronchodilators

drugs that deal with respiratory disorders

rapid-acting dilators

rescue agents

• asthma patients need a drug that acts instantaneously

slow-acting

not beneficial in an asthma attack

• can be taken to prevent attacks 

beta 2 agonists

rapid acting is albuterol and slow acting drug is salmeterol

• bind to beta 2 receptors and an ANS drug

albuterol

given via inhaler

salmeterol

not a rescue agent and increases bronchodilation but slower

antimuscarinics

tiotropium - bronchodilator by blocking off Ach

• used in patients with COPD

• not a rescue agent

methyl xanthines

NOT an ANS drug

• theophylline

• has toxicity issues (small therapy index)

• direct bronchodilator

• caffeine falls into this category

antiinflammatories

decreases inflammation effects

• corticosteroids, leukotriene agonists, and mast cell stabilizers

corticosteroids

given in inhalation form and mimic cortisol

leukotriene antagonists

given orally; block effects of leukotriene

• montelukast (24 hr)

mast cell stabilizers

stabilizes cell membrane of mast cells

• mast cells are packed with inflammatory mediators and “vomits” their contents (typically in allergic reactions)

• cromolyn Na+ (inhaled or nasal spray)

peptic ulcer disorder

too much HCl production or not enough mucosal layer (eroded by peptic ulcer disease)

drugs that decrease HCl production

proton pump inhibitors and H2 receptor blockers

proton pump inhibitors (PPI’s)

targets the cells and decreases HCl production

• used to treat acid reflux disease (GERD) and peptic ulcer disease 

H2 receptor blockers

blocks H2 receptors and decreases HCl production

• treats GERD and peptic ulcer disease

drugs that increase mucosal protection

bismuth subsalicylate and sucralfate

bismuth subsalicylate

pepto bismol

• acts to protect lining (enhances mucosal protection)

sucralfate

large tablet, add H2O and forms into a gel that protects the mucosal lining

diarrhea

colon motility needs to decrease (slow down material in large intestine) or secreting too much H2O

loperamide

antimotility agent (imodium) and slows down peristalsis

bismuth subsalicylate

pepto bismol; decreases H2O secretion

constipation

needs to be treated with laxatives

laxatives

increase colon motility

bulk-forming laxatives

dietary fiber (natural)

• absorbs water and stool becomes bulkier, which increases peristalsis

• this will not work without water

• FIBER WITH WATER

stimulants

stimulate the gut to contract

osmotic laxatives

polyethylene glycol (PEG)

• taken after a colonoscopy; water follows the PEG and creates an osmotic effect

• miralax

opioid analgesics

used to treat moderate/severe pain

• bind to opioid receptors (mu)

how an opioid analgesic works

• decreases ascending pain transmission

• increases descending pain inhibition activity

• alter brain’s perception of pain

strong agonists

morphine and fentanyl

moderate agonist

hydrocodine

analgesic

decreases pain

true

T OR F

• strong and moderate agonists both have a tolerance and dependence factor which causes an addiction if abused

unwanted side effects of opioid analgesics

• respiratory depression (most lethal)

• decreases GI motility

• nausea and vomiting

• euphoria (not universal)

non-opioid analgesics

used to treat moderate pain

• don’t bind to mu receptors and majority don’t treat severe pain

acetaminophen

NOT an anti inflammatory

• it’s an analgesic and antipyretic (reduces fever)

• therapeutic index is very large

  • it’ll destroy liver if you got into a toxic dose (24 hr window)

NSAIDS

ex. aspirin and ibuprofen

• inhibit the cyclooxygenase pathway (COX)

  • yield products that cause pain, fever, inflammation etc.

products of the COX pathway

prostaglandins (PG’s) and thromboxane A2 (TXA2)

prostaglandins (PG’s)

increases pain, fever, inflammation, and mucosol protection

thromboxane A2 (TXA2)

increases platelet aggregation (pro platelet aggregation)

COX enzymes

COX 1 and COX 2

cox 1

• catalyzes PG’s that are mucosal protectants

• catalyzes TXA2 (increases platelet aggregation)

cox 2

• catalyzes PGs that cause pain, fever, inflammation

• catalyzes prostacyclins that prevents platelet aggregation

non-selective NSAIDS

they inhibit both enzymes

NSAID targeting COX 1

GI bleeding/ulcer risk and antiplatelet effect

why? PGs and TXA2 aren’t produced

NSAIDS targeting COX 2

analgesic/antipyretic/anti inflammatory

corticosteroids

anti inflammatory

• suppress COX 2

• increase release of anti inflammatory chemicals

• inhibit release of inflammatory mediators

• decrease phagocyte function - increase in infection risk

• have immunosuppressive effects

• act as cortisol

• raise blood sugar (hyperglycemia)

true

T or F

• inflammation is a prerequisite for wound healing

yes

would wound healing be delayed if anti inflammatory effects took place?

yes

are corticosteroids catbolic?

side effects of corticosteroids

• increase in artherosclerotic plaque formation

• can cause fluid retention

• increase cataract formation (cloudy lenses)

• GI bleeding risk increases

• increase of ulcer risk

these are likely to occur with higher doses and longer uses

type 1 diabetes

absolute insulin deficiency - no insulin is producedt

type 2 diabetes

relative insulin deficiency (decrease in insulin) and tissue resistance to insulin

insulin

decreases blood glucose

• mainly used for type 1 diabetes

• super important to eat after taking this drug

• can cause weight gain because it has an anabolic effect

hypoglycemia

a side effect for taking insulin is…

type 2 diabetes drugs

drugs that increase insulin secretion and increase insulin sensitivity

drugs that increase insulin secretion

semaglutide (ozempic) and DPP-4 inhibitors (sitagliptin)

semaglutide

Ozempic

• mimics the effect of incretin

• GLP 1 agonist

• used for weight loss but treats type 2 DM

incretin

a chemical that tells beta cells to make more insulin in pancreas

DPP 4 inhibitors

sitagliptin

• prevents the breakdown of incretins

• any drug that ends in gliptin

biguanides

metformin

• increases insulin sensitivity by making the body sensitive to insulin

• decreases production of glucose in the liver

true

T or F

• a patient isn’t likely to develop hypoglycemia just taking the type 2 DM drugs by themselves

no

are taking the type 2 dm drugs beneficial for type 1 patients?

SGLT2 inhibitor

dapagliflozin - Farxiga

• not front-line therapy for type 2 DM

• decreases renal reabsorption of glucose → increases in urinary excretion of glucose (you pee off more glucose)

• blood sugar decreases

increased risk of UTI’s

side effect for taking SGLT2 inhibitor