Term
|
Definition
Nicotine agonist, (blocker)
metabolized and excreted rapidly
insecticide, cigarettes |
|
|
Term
|
Definition
Nicotine antagonist
not orally active
hypertensive emergencies
controled hypotension during surgery
short duration of action
S: PHT, mydriasis |
|
|
Term
|
Definition
Nicotine antagonist
active orally
longer acting than trimethapan
S: PHT, mydriasis |
|
|
Term
|
Definition
depolarizing agonist
Fasiculations
Non reversible
rapid onset, 1-2 min
brief duration 5-10 min due to breakdown by pseudocholinesterase
SE: atypical AchE, malignant hyperthermia, hyperkalemia (in burn/trauma patients 2-3 days later) |
|
|
Term
| What are the two types of neuromuscular blocking agents |
|
Definition
1. Non depolarizing (competitive)
-Tubocurarine (curare)
-Rocuronium, Pancuronium,
cisAtracurium
2. depolarizing (non competitive) |
|
|
Term
| These compete with Ach for binding to the receptor. The muscle can still be stimulated directly by increasing the concentration of Ach. They cause flaccid , relaxed paralysis |
|
Definition
| Competitive (non depolarizing ) neuromuscular blocking agents |
|
|
Term
| How are competitive, non depolarizing neuromuscular blocking agents reversed |
|
Definition
| cholinesterase inhibitors such as neostigmine |
|
|
Term
| What are the 3 side effects of succinylcholine |
|
Definition
1. Malignant hyperthermia
2. Hyperkalemia (trauma/burn patients due to upregulation of N-receptors)
3. prolonged paralysis due to atypical pseudocholinesterase |
|
|
Term
| Can succinylcholine be reversed? |
|
Definition
| No, can only give mechanical breathing support |
|
|
Term
| What breaks down succinylcholine |
|
Definition
|
|
Term
|
Definition
Not orally transmitted
long onset 4-6 mins, long acting 80-120 min
histamine release (cause bronchospasm) |
|
|
Term
|
Definition
longer lasting and cleaner than tubocurarine
more potent than tubocurarine (x5)
less histamine release! |
|
|
Term
|
Definition
fast onset 1-2 min
short intermediate durationof 30-40 min
good substitute for succinylcholine |
|
|
Term
|
Definition
Hoffman degradation
organindependent and has less risk in patients with liver or renal disease |
|
|
Term
| What drug is give to those who have atypical pseudocholinesterase or cannot have succinylcholine |
|
Definition
|
|
Term
| what neuromuscular blocking agent is given to someone who has liver or renal disease |
|
Definition
| rocuronium, due to Hoffman degradation |
|
|
Term
| This is the DOC given to prevent malignant hyperthermia due to succinylcholine |
|
Definition
|
|
Term
| The ganglionic nicotinic receptor is a ______. ___ goes inward while ____ goes outward |
|
Definition
pentamer ion channel
Na+
K+ |
|
|
Term
| What happens when nicotine reaches a toxic level |
|
Definition
NMJ paralysis due to depolarizing blockade
hypertension initially followed by hypotension due to depolarizing block, cardiac arrhythmias
convulsions, vomiting, CV |
|
|
Term
| What is the treatment for nictotine toxicity |
|
Definition
treatment is symptom directed
1. muscarinic excess- anticholinergic (atropine)
2. NMJ blockade- mechanical respiration
3. CNS stimulation: anticonvulsant (diazepam) |
|
|
Term
| Toxicity by ganglionic blocking agetns causes |
|
Definition
hypotension, posteral hypotension
give presser agent to counter hypotension actions |
|
|
Term
|
Definition
|
|
Term
| Can the effects of succinylcholine be overcome? |
|
Definition
No, trying to over come the effects will only make it worst.
Mechanical respiration is the only treatment |
|
|
Term
| True or false: succinylcholine has a shorter duration than Ach |
|
Definition
|
|
Term
| What is the most important factor in regulating BP |
|
Definition
|
|
Term
| What are reasons for secondary HT and treatment |
|
Definition
-cortisol overproduction
-aldosterone overproduction
-renal artery stenosis
-pheochromocytoma
**treat the disease, and HT will be treated |
|
|
Term
| What are reasons for primary HT and treatment |
|
Definition
genetics, stress, obesity, smoking, salt intake, age, caffeine, and alcohol.
**Can lower HT with medication and lifestyle changes but HT will not be "cured" |
|
|
Term
| What are the treatment indications for pre hypertension |
|
Definition
|
|
Term
| what are the treatment indications for stage 1 hypertenison |
|
Definition
| use a single drug and lifestyle change |
|
|
Term
| what are the treatment indications for stage 2 hypertension |
|
Definition
| use a drug combination and lifestyle change |
|
|
Term
| What are the four front line drugs for treating HT |
|
Definition
1. Diuretics
2. Renin/A-II system (ACE1, ARBs)
3. Calcium antagonists
4. Beta receptor antagonists |
|
|
Term
| Which hypertension drug is recommended for an uncomplicated case |
|
Definition
|
|
Term
| patients with diabetes who have HT should use which front line hypertension drug |
|
Definition
| Renin/ A-II system/ ACE1 ARBs |
|
|
Term
| patients with a history of myocardial infarct should use which front line hypertension drug |
|
Definition
| beta receptor antagonists |
|
|
Term
| Where do thiazides take action and how |
|
Definition
| early distal tubule, inhibit Na-CL symporter to inhibit water/Na reabsorption. This decreased BP by depleting the body of Na |
|
|
Term
|
Definition
thiazide
treats hypertension, HF
decrease Na reabsorbtion in early distal tuble and decreases blood volume
SE: hypokalemia, decreased glucose tolerance, photosensitivity, hearing loss |
|
|
Term
|
Definition
thiazide
treats hypertension, HF
decrease Na reabsorbtion in early distal tuble and decreases blood volume
SE: hypokalemia, decreased glucose tolerance, photosensitivity, hearing loss |
|
|
Term
|
Definition
thiazide
treats hypertension, HF
decrease Na reabsorbtion in early distal tuble and decreases blood volume
SE: hypokalemia, decreased glucose tolerance, photosensitivity, hearing loss |
|
|
Term
|
Definition
thiazide
treats hypertension, HF
decrease Na reabsorbtion in early distal tuble and decreases blood volume
SE: hypokalemia, decreased glucose tolerance, photosensitivity, hearing loss |
|
|
Term
|
Definition
| Acts on collecting tube, no K+ loss, blocks aldosterone |
|
|
Term
|
Definition
| Acts on collecting tube, no K+ loss, blocks aldosterone |
|
|
Term
|
Definition
| Acts on collecting tube, no K+ loss, blocks Na channels |
|
|
Term
| Angiotensin converting enzyme inhibitors end in |
|
Definition
|
|
Term
| This is a potent vasocontrictor peptide which increases the production of aldosterone |
|
Definition
|
|
Term
| What are the steps in the making of Angiotensin II |
|
Definition
| Angiotensinogen converted to angiotensin I by renin. angiotensin I converted to angiotensin II by ACE |
|
|
Term
| What drug blocks the conversion of angitensinogen to angiotensin I |
|
Definition
|
|
Term
|
Definition
Treatment of hypertension
direct renin inhibitor
decreases angiotensin I
NO DRY COUGH
hyperkalemia, altered taste (Zn), glossitis, angioedema, dry mouth |
|
|
Term
|
Definition
treats hyptertension, heart failure
ACE inhibitor
decreasess angiotensin II and aldosterone, which decreases TPR
SE: increases bradykinin which causes a dry cough
other side effects: hyperkalemia, altered taste (Zn), glossitis, angioedema, dry mouth |
|
|
Term
|
Definition
treats hyptertension, heart failure
ACE inhibitor
decreasess angiotensin II and aldosterone, which decreases TPR
SE: increases bradykinin which causes a dry cough
other side effects: hyperkalemia, altered taste (Zn), glossitis, angioedema, dry mouth |
|
|
Term
|
Definition
treats emergency hyptertension, heart failure
prodrug with a half life of 6 hours
ACE inhibitor
decreasess angiotensin II and aldosterone, which decreases TPR
SE: increases bradykinin which causes a dry cough
other side effects: hyperkalemia, altered taste (Zn), glossitis, angioedema, dry mouth |
|
|
Term
| All Angiotensin II Type 1 Receptor Blockers (ARBs) end in |
|
Definition
|
|
Term
| What are the two receptors that angiotensin II affect. Which ones do ARBs affect? |
|
Definition
angiotensin II type I receptor
angiotensin II type II receptor
angiotensin II type I receptor |
|
|
Term
| Angiotensin II type I receptors mediate |
|
Definition
| production of aldosterone, anti diuretic hormone, increased TPR, increased sympathetic NS |
|
|
Term
| Angiotensin II type II receptors mediate |
|
Definition
| vasodilation, decreased TPR, increase NO |
|
|
Term
|
Definition
Treats Hypertension and heart failure
angiotensin II type I receptor blocker
treats hyptertension, heart failure
ACE inhibitor
decreasess angiotensin II and aldosterone, which decreases TPR
NO DRY COUGH
side effects: hyperkalemia, altered taste (Zn), glossitis, angioedema, dry mouth |
|
|
Term
|
Definition
Treats Hypertension and heart failure
angiotensin II type I receptor blocker
treats hyptertension, heart failure
ACE inhibitor
decreasess angiotensin II and aldosterone, which decreases TPR
NO DRY COUGH
side effects: hyperkalemia, altered taste (Zn), glossitis, angioedema, dry |
|
|
Term
| What are the two classes of calcium channel blockers |
|
Definition
Non dihydropyridines
Dihydropyridines (end in dipine) |
|
|
Term
| What is the effect of calcium channel blockers |
|
Definition
| bind to L type calcium channels in cardiace and vascular smooth muscle and causes dilation of vessels |
|
|
Term
| Nifidipine is a _____ and mainly causes ____ vasodilation and has little effect on ____. |
|
Definition
dihydropyridine calcium channel blocker
arteriole
cardiace tissue
commonly causes reflex tachycardia |
|
|
Term
| Verapamil is a ______ and has effect on _______ |
|
Definition
non dihydropyridine calcium channel blocker
cardiac tissues
causes brady cardia |
|
|
Term
Dilitazem is a _____ and has actions on ____ and _____.
Is it more similar to nifidipine or verapamil? |
|
Definition
non dihydropyridine calcium channel blocker
cardiac and vascular beds
verapamil action |
|
|
Term
|
Definition
treats hypertension and mainly acts on arterioles.
causes reflex tachycardia |
|
|
Term
| what are side effects of calcium channel blockers |
|
Definition
constipation (more so w/ non-DHPs)
cardiac depression, brady cardia (non DHPs)
hypotension (DHP)
gingival hyperplasia (esp with nifedipine) |
|
|
Term
| Beta blockers have a ____ hypotensive action. |
|
Definition
|
|
Term
| What are the possible mechanisms of action for beta blockers |
|
Definition
CNS effect to decrease sympathetic NS tone
inhibition of renin secretion: beta 1 receptors mediate renin release
block cardiac beta 1 receptors which causes a decrease in HR and cardiac output decreasing the BP |
|
|
Term
| Selective beta blockers have names beginning with ___ |
|
Definition
|
|
Term
| All beta blockers end in ___ |
|
Definition
|
|
Term
|
Definition
selective B1 blocker
No local anestetic action |
|
|
Term
|
Definition
Non selective B blocker with partial alpha blocker activity
local anesthetic action |
|
|
Term
|
Definition
selective B1 blocker
local anesthetic action |
|
|
Term
|
Definition
| non selective B blocker with local anesthetic action and partial agonist |
|
|
Term
|
Definition
| non selective B blocker with local anesthetic action |
|
|
Term
|
Definition
|
|
Term
| What are the 2 mixed alpha and beta recepter blockers that are used for acute and chronice hypertension |
|
Definition
|
|
Term
| What are the 2 mixed alpha and beta recepter blockers that are used for Heart Failure |
|
Definition
| carvedilol and metoprolol |
|
|
Term
| What antihypertensive agents cause hypokalemia |
|
Definition
|
|
Term
| what antihypertensive agents cause hyperkalemia |
|
Definition
|
|
Term
| What antihypertensive agents/CHF drugs are contraindicated for pregnant women? |
|
Definition
|
|
Term
| Define compensated heart failure |
|
Definition
resting cardiac function is ok
excessive stress or exercise is not ok |
|
|
Term
| Define congestive heart failure (CHF, decompensated) |
|
Definition
| resting cardiac function is inadequate for body's oxygen demand |
|
|
Term
| What are some symptoms of CHF |
|
Definition
venous pooling which causes edema especially in the lungs
dyspnea
neurohormonal storm |
|
|
Term
| Describe the neurohumoral storm |
|
Definition
| Decreased cardiace function leads to neuro-humoral activation which increases sympathetic NS activity and Renin angiotensin aldosterone system activity. This also leads to tissue remodeling (hypertrophy, decreased CO) |
|
|
Term
| are calcium channel blockers used for CHF? |
|
Definition
|
|
Term
| What is the site of action for cardiac glycosides |
|
Definition
|
|
Term
| What is the cardiac glycoside that we need to know for this test? |
|
Definition
|
|
Term
|
Definition
cardiac glycoside
has very narrow therapeutic range
contraindicated for women |
|
|
Term
| An increase in potassium concentration causes ________ of the alpha subunit of the Na/K ATPase pump causing cardiac glycosides to bind _______ |
|
Definition
dephosphorylation
less effectively |
|
|
Term
| An decrease in potassium concentration causes ________ of the alpha subunit of the Na/K ATPase pump causing cardiac glycosides to bind _______ |
|
Definition
phosphorylation
more effectively |
|
|
Term
| Do ACE inhibitors enhance or weaken the effects of cardiac glycosides |
|
Definition
|
|
Term
| Do thiazide diuretics enhance or weaken the effects of cardiac glycosides |
|
Definition
|
|
Term
| Describe the steps of how digoxin works |
|
Definition
| It inhibts the Na/K/ATPase which decreases the exchange of Na/K. the concentrat the Na/Ca exchanger to reverse or to become depolarized and the intracellular concentration of Ca increases, thus increasing the SR stores of Ca and increasing contractile force |
|
|
Term
| cardio glycosides have an ionotropic effect which means |
|
Definition
| it increases the influx of Ca stores which increases contraction |
|
|
Term
| How does digoxin affect the frank-starling graph |
|
Definition
| it will shift the line up and to the left (increase steepness of the curve) |
|
|
Term
| What effects are seen with cardiac glycoside toxicity |
|
Definition
| ventricular tachycardia, delirium, fatigue, weakness, dizziness, nausea, vomiting, vision/light disturbances (halo effect, mainly yellow and green ) |
|
|
Term
| what is the treatment for toxicity by cardiac glycoside |
|
Definition
discontinue cardiac glycoside or alter dose
administer K or discontinue K depleting diuretics |
|
|
Term
| What type of drug is used in IV form in acute emergency CHF NOT CHRONIC |
|
Definition
|
|
Term
| What 3 drugs are catecholamines used for acute emergency CHF |
|
Definition
| dobutamine, milrinone, Inamrinone |
|
|
Term
| These catecholamine inhibit phosphodiesterase III. Which increases cAMP levels and causes phosphorylation of Ca channel |
|
Definition
|
|
Term
| what vasodilator is a combination of isosorbide dinitrate and hydralazine and is good for treating African Americans with CHF |
|
Definition
|
|
Term
| Is propranolol recommended for CHF? |
|
Definition
|
|
Term
| Beta-type natriuretic peptide is also known as ____ |
|
Definition
|
|
Term
| Beta-type natriuretic peptide |
|
Definition
| Uses NO to Increase cGMP, leading to smooth muscle relaxation and vasodilation. works on both arteries and veins. |
|
|
