NURS 5663 - Pharm – Exam #2
Video lecture #1 –
Antihistamines – 1st / 2nd generation. Allergy symptom relief. 1st gen – cause sedation, cross BBB. 2nd gen – very little
sedation associated.
FIRST GENERATION ANTIHISTAMINES (BPHD) SECOND-GENERATION ANTIHISTAMINES (FCL)
Use: reduce allergies symptoms Use: reduce allergies symptoms
Promethazine for motion sickness
S/E: sedation, GI disturbances, weak S/E: minimal sedation and anticholinergic effect.
anticholinergic effects d/t does not cross BBB, and low affinity for H1
Promethazine has a BBW for resp depression receptors in the CNS
Ex: diphenhydramine, brompheniramine, Ex: fexofenadine, cetirizine, loratadine
promethazine, hydroxyzine, doxylamine FCL
succinate
(BPH to Death) (Death by BPH) Common OTC agents
SSRIs – Selective serotonin reuptake inhibitor. SSRI block reuptake on presynaptic cleft, keeps more serotonin in
synapse. Can be bad, lead to serotonin syndrome, though rare. Quite serious! 2-72hr after treatment onset. (More
meds than just the SSRI can have serotonergic activity).
• CNS – AMS, agitation, disorientation, hallucinations, anxiety
• MSK – Incoordination, myoclonus, hyperreflexia, tremors
• Fever, excessive sweating, tachycardia, diarrhea
Avoid / separate by at least 2 weeks: MAOI’s (monoamine oxidase inhibitor)
• Isocarboxazid
• Phenelzine
• Selegiline
Random medications that have serotonergic activity –
• Fentanyl, tramadol
• Odansetron
• Sumatriptan
• Linezolid (antiinfective)
• ginseng
Arachidonic acid –
Phospholipase A2 breaks down fatty acids, into arachidonic acid
Can then go down 2 pathways – one the COX pathway, another 5-HPETE pathway.
• Arachidonic acid → Cyclic endoperoxides → prostacyclin / prostaglandins / thromboxane (platelet formation)
• Arachidonic acid → 5-HPETE → leukotrienes (cause bronchoconstriction).
COX enzymes – COX 1 & COX 2, ASA. Celecoxib selective for only COX 2.
Leukotriene inhibitor (montelukast/singular) causes bronchodilation, useful for asthma.
,COX 1 vs COX 2 –
COX 1 – protective effects: GI protective (unregulated acid secretion, decreased mucus production, decreased platelet
aggregation), renal protective (renal perfusion, renal function)
COX 2 – pathologic effect: inflammatory mechanism
Nonselective COX inhibitors (NSAIDS):
• Ibuprofen, naproxen, ketorolac, diclofenac
Selective COX2 inhibitors:
• Celecoxib (most selective) and meloxicam
How medications promote bronchodilation – can be achieved by promoting dilation, or by inhibiting constriction
Promote dilation –
• Beta agonist (albuterol) – promote cAMP synthesis
• Theophylline – inhibit cAMP degradation
Prevent constriction –
• Muscarinic antagonist (ipratropium) – acts on ACh to inhibit constriction, and mucous secretion
• Theophylline – acts on adenosine to inhibit constriction
Treatment of asthma / COPD –
ICS (inhaled corticosteroids) is 1st line in asthma, as it is more of an inflammatory disease. Reserved for more severe
cases of COPD as it is a ‘different type of inflammation’ that does not respond well to ICS versus asthma.
SABA (short acting beta agonists) – are ‘rescue med’ most often used for asthma, but sometimes in less severe COPD.
LABA (long-acting beta agonists) – should not be used alone for asthma, due to no anti-inflammatory effects. LABA is a
mainstay of treatment for COPD.
SAMA is most often used in combo with SABA for emergency asthma treatment or less severe COPD.
LAMA is typically not used for asthma; LAMA is a mainstay of treatment for COPD.
Osmosis videos:
Antihypertensives, by category:
• ACE inhibitors, ARBs and direct renin inhibitors
• Thiazide and thiazide-like diruretics
• Calcium channel blockers
• Adrenergic antagonists: Beta blockers
, #1: ACE Inhibitors, ARBs, and direct renin inhibitors: ALL ARE CATEGORY X
Angiotensin and renin antagonists are classes of
medications that work at different levels of the renin-
angiotensin-aldosterone system (RAAS). Three main
classes of medications include renin inhibitors, ACE-
inhibitors, and angiotensin receptor blockers (ARBs).
Basic patho: Renin>AGT1>AGT2>Aldosterone. BP low, =
decreased renal perfusion. Kidneys release renin. Renin
breaks down protein produced in liver called
angiotensinogen (so liver failure = BP regulation issues,
among other things) to angiotensin I. AGT1 to lungs,
converted to AGT2 by enzyme called angiotensin
converting enzyme (ACE). AGT2 binds to receptors in vascular smooth muscle, = constriction = ↑ BP. Also, AGT2
stimulates release of aldosterone by adrenal glands. Aldosterone works in kidneys to cause Na reabsorption, which also
increases water reabsorption, = ↑ BP.
ACE inhibitors and ARBs can also be used to treat heart failure and MI, but ACE inhibitors can cause coughing and
angioedema (d/t accumulation of bradykinin as ACE typically breaks down bradykinin). None of these medications
should be given during pregnancy.
Pts on ACE inhibitors should avoid a high potassium diet, d/t decreased aldosterone production, which = less potassium
excretion in the urine.
Angiotensin II receptor blockers, or ARBS, bind to angiotensin receptor 1 on vascular smooth muscles and the adrenal
glands, which prevent angiotensin II from binding (antagonism). This results in decreased vasoconstriction and
decreased aldosterone synthesis respectively.
Textbook:
Cardiovascular disease risk doubles with each increment of 20/10 mm Hg
Risk factors include smoking, including exposure to secondhand smoke; diabetes; metabolic syndrome including obesity,
dyslipidemia; physical inactivity; manifestations of end-organ damage at the time of
diagnosis; and a family history of cardiovascular disease
A specific cause of hypertension can be established in only 10–15% of patients. Patients in whom no specific cause of
hypertension can be found are said to have essential or primary hypertension. Patients with a specific etiology are said
to have secondary hypertension. Assessment of renal function and the presence of proteinuria are useful in
antihypertensive drug selection.
Epidemiologic evidence points to genetic factors, psychological stress, and environmental and dietary factors (increased
salt and decreased potassium or calcium intake) as contributing to the development of hypertension. Increase in blood
pressure with aging does not occur in populations with low daily sodium intake.
Video lecture #1 –
Antihistamines – 1st / 2nd generation. Allergy symptom relief. 1st gen – cause sedation, cross BBB. 2nd gen – very little
sedation associated.
FIRST GENERATION ANTIHISTAMINES (BPHD) SECOND-GENERATION ANTIHISTAMINES (FCL)
Use: reduce allergies symptoms Use: reduce allergies symptoms
Promethazine for motion sickness
S/E: sedation, GI disturbances, weak S/E: minimal sedation and anticholinergic effect.
anticholinergic effects d/t does not cross BBB, and low affinity for H1
Promethazine has a BBW for resp depression receptors in the CNS
Ex: diphenhydramine, brompheniramine, Ex: fexofenadine, cetirizine, loratadine
promethazine, hydroxyzine, doxylamine FCL
succinate
(BPH to Death) (Death by BPH) Common OTC agents
SSRIs – Selective serotonin reuptake inhibitor. SSRI block reuptake on presynaptic cleft, keeps more serotonin in
synapse. Can be bad, lead to serotonin syndrome, though rare. Quite serious! 2-72hr after treatment onset. (More
meds than just the SSRI can have serotonergic activity).
• CNS – AMS, agitation, disorientation, hallucinations, anxiety
• MSK – Incoordination, myoclonus, hyperreflexia, tremors
• Fever, excessive sweating, tachycardia, diarrhea
Avoid / separate by at least 2 weeks: MAOI’s (monoamine oxidase inhibitor)
• Isocarboxazid
• Phenelzine
• Selegiline
Random medications that have serotonergic activity –
• Fentanyl, tramadol
• Odansetron
• Sumatriptan
• Linezolid (antiinfective)
• ginseng
Arachidonic acid –
Phospholipase A2 breaks down fatty acids, into arachidonic acid
Can then go down 2 pathways – one the COX pathway, another 5-HPETE pathway.
• Arachidonic acid → Cyclic endoperoxides → prostacyclin / prostaglandins / thromboxane (platelet formation)
• Arachidonic acid → 5-HPETE → leukotrienes (cause bronchoconstriction).
COX enzymes – COX 1 & COX 2, ASA. Celecoxib selective for only COX 2.
Leukotriene inhibitor (montelukast/singular) causes bronchodilation, useful for asthma.
,COX 1 vs COX 2 –
COX 1 – protective effects: GI protective (unregulated acid secretion, decreased mucus production, decreased platelet
aggregation), renal protective (renal perfusion, renal function)
COX 2 – pathologic effect: inflammatory mechanism
Nonselective COX inhibitors (NSAIDS):
• Ibuprofen, naproxen, ketorolac, diclofenac
Selective COX2 inhibitors:
• Celecoxib (most selective) and meloxicam
How medications promote bronchodilation – can be achieved by promoting dilation, or by inhibiting constriction
Promote dilation –
• Beta agonist (albuterol) – promote cAMP synthesis
• Theophylline – inhibit cAMP degradation
Prevent constriction –
• Muscarinic antagonist (ipratropium) – acts on ACh to inhibit constriction, and mucous secretion
• Theophylline – acts on adenosine to inhibit constriction
Treatment of asthma / COPD –
ICS (inhaled corticosteroids) is 1st line in asthma, as it is more of an inflammatory disease. Reserved for more severe
cases of COPD as it is a ‘different type of inflammation’ that does not respond well to ICS versus asthma.
SABA (short acting beta agonists) – are ‘rescue med’ most often used for asthma, but sometimes in less severe COPD.
LABA (long-acting beta agonists) – should not be used alone for asthma, due to no anti-inflammatory effects. LABA is a
mainstay of treatment for COPD.
SAMA is most often used in combo with SABA for emergency asthma treatment or less severe COPD.
LAMA is typically not used for asthma; LAMA is a mainstay of treatment for COPD.
Osmosis videos:
Antihypertensives, by category:
• ACE inhibitors, ARBs and direct renin inhibitors
• Thiazide and thiazide-like diruretics
• Calcium channel blockers
• Adrenergic antagonists: Beta blockers
, #1: ACE Inhibitors, ARBs, and direct renin inhibitors: ALL ARE CATEGORY X
Angiotensin and renin antagonists are classes of
medications that work at different levels of the renin-
angiotensin-aldosterone system (RAAS). Three main
classes of medications include renin inhibitors, ACE-
inhibitors, and angiotensin receptor blockers (ARBs).
Basic patho: Renin>AGT1>AGT2>Aldosterone. BP low, =
decreased renal perfusion. Kidneys release renin. Renin
breaks down protein produced in liver called
angiotensinogen (so liver failure = BP regulation issues,
among other things) to angiotensin I. AGT1 to lungs,
converted to AGT2 by enzyme called angiotensin
converting enzyme (ACE). AGT2 binds to receptors in vascular smooth muscle, = constriction = ↑ BP. Also, AGT2
stimulates release of aldosterone by adrenal glands. Aldosterone works in kidneys to cause Na reabsorption, which also
increases water reabsorption, = ↑ BP.
ACE inhibitors and ARBs can also be used to treat heart failure and MI, but ACE inhibitors can cause coughing and
angioedema (d/t accumulation of bradykinin as ACE typically breaks down bradykinin). None of these medications
should be given during pregnancy.
Pts on ACE inhibitors should avoid a high potassium diet, d/t decreased aldosterone production, which = less potassium
excretion in the urine.
Angiotensin II receptor blockers, or ARBS, bind to angiotensin receptor 1 on vascular smooth muscles and the adrenal
glands, which prevent angiotensin II from binding (antagonism). This results in decreased vasoconstriction and
decreased aldosterone synthesis respectively.
Textbook:
Cardiovascular disease risk doubles with each increment of 20/10 mm Hg
Risk factors include smoking, including exposure to secondhand smoke; diabetes; metabolic syndrome including obesity,
dyslipidemia; physical inactivity; manifestations of end-organ damage at the time of
diagnosis; and a family history of cardiovascular disease
A specific cause of hypertension can be established in only 10–15% of patients. Patients in whom no specific cause of
hypertension can be found are said to have essential or primary hypertension. Patients with a specific etiology are said
to have secondary hypertension. Assessment of renal function and the presence of proteinuria are useful in
antihypertensive drug selection.
Epidemiologic evidence points to genetic factors, psychological stress, and environmental and dietary factors (increased
salt and decreased potassium or calcium intake) as contributing to the development of hypertension. Increase in blood
pressure with aging does not occur in populations with low daily sodium intake.
