anti HTN drugs (part 2-guest lecturer)

Question 1

womens heart health facts:

Answer 1

1. one in 4 women die from heart disease

2. 23% of women die within 1 year of having an MI

Question 2

hypertension

1. how does htn rank in causes of cardiac disease?
2. what is considered hypertension
3. what is HTN when no cause is apparent?
4. what is HTN caused by another disease?

Answer 2

1. number 1 cause of CV disease
2. HTN is 140/90
3. primary or essential hypertension
4. secondary hypertension

Question 3

1. how many millions suffer from chronic hypertension?
2. what percent are underdiagnosed?
3. what percent are untreated?
4. what percent are undertreated?

Answer 3

1. 73 million
2. 16%
3. 27%
4. 45%

Question 4

what are the major cardiovascular risk factors (9 things)?

Answer 4

• hypertension
• cigarette smoking
• obesity (BMI>30 kg/m2)
• sedentary lifestyle
• dyslipidemia
• diabetes
• microabluminemia or GFR < 60mL/min
• age (men <65)
• family history of premature CV disease

Question 5

diseases, conditions or “activities” that cause hypertension (9 things):

Answer 5

• sleep apnea
• drugs
• chronic kidney disease
• primary aldosteronism
• renal-vascular disease
• chronic steroid therapy/cushings syndrome
• pheochromocytoma
• coarctation (dissection) of aorta
• thyroid/parathyroid disease

Question 6

what is involved with a hypertensive crisis (5 things)?

Answer 6

1. acute elevation of BP associated with end organ damage (kidneys (renal arteries), liver, eye (retinal arteries)& mural cardiac muscle
2. BP 190/100 x2 consectutive readings
3. hypertensive crisis, hypertensive emergency, malignant hypertension
4. potentially fatal
5. 4-35% of patients suffer from post op hypertension (2-4% of this group is hypertensive crisis)

Question 7

1. when will symptoms be seen in hypertensive crisis?
2. which persons have less of a chance of developing symptoms?
3. which have greater chance of developing symptoms?

Answer 7

1. when diastolic >130 mmhg
2. persons with longstanding hypertension
3. children and pregnant women

Question 8

what are symptoms of hypertensive crisis (6 things)?

Answer 8

• hypertensive encephalopathy
• acute aortic dissection
• acute MI
• acute CVI
• acute renal failure
• acute CHF

Question 9

what are the common causes of hypertensive crisis?

1. med changes such as…
2. _____ hyperactivity
3. diseases such as______
4. _____ artery ______
5. _____ trauma that causes _____?
6. what type of cancer?
7. what pregnancy condition?
8. what recreational drugs?

Answer 9

1. abrupt withdrawl of clonidine (or even propanolol)
2. sympathetic (autonomic) hyperactivity
3. collagen vascular disease such as scleroderma
4. renal artery stenosis
5. head trauma that causes loss of consciousness >30 min
6. renal neoplasm
7. pre eclampsia leading to seizures
8. recreational drugs like cocaine

Question 10

evaluation of hypertensive crisis patient:

1. what histories should be explored?
2. what should be assessed (physically palpated)?
3. what diagnostics?
4. what meds to treat it?
5. what is goal with these patients?

Answer 10

1. medical history (renal, cardiac, medication), rec. drugs
2. pulses x4 (differences in pulses may be coarctation of aorta)
3. cbc, lytes, bun,creat, UA, cxr, head ct, EKG
4. Meds:
   
   • Nipride (direct acting arterial vasodilator)
   • nifedipine (ca++ channel blocker)
   • labetolol (Beta blocker (some alpha blocker activity)
   • esmolol (beta blocker)
   • diazoxide (potassium channel ACTIVATOR)
   • minoxidil- vasodlator
5. prompt recognition and immediate treatment to halt vascular damage

Question 11

hypertension: effects on body:
1. increased risk of what? also causes what related conditions?
2. damage to what organ accelerates with HTN?
3. what does HTN do to cause stroke and heart attack?
4. why is HTN called the silent killer?

Answer 11

1. stroke and heart attack risk increases dramatically with blood pressure increases, also causes TIAs, PEs, CAD.
2. kidneys
3. plaque in vessel walls ruptures more easily with increased BP
4. HTN silently causes all these conditions which all have high mortality rates.

Question 12

how do you calculate blood pressure?

Answer 12

cardiac output x peripheral vascular resistance

Question 13

what are the classes of antihypertensive drugs (7 types)?

Answer 13

1. diuretics
2. ACE inhibitors
3. ARBs
4. Ca++ channel blockers
5. Beta blockers
6. Alpha blockers
7. centrally acting antihypertensives

Question 14

what 2 things regulate blood pressure & how?

Answer 14

1. baroreceptors-modulate sympathetic stimulation of cardiac output and HR and adjust the BP in response to postural changes and altered physical activity (short term regulation of BP via sympathetic nervous system)
2. kidneys-regulate plasma volumes and renin-angiotensin II and aldosterone
3. keep blood pressure within narrow range (homeostasis)

Question 15

diuretics:
1. what do diuretics do?
2. how do they work?

Answer 15

1. work at varius sites in nephron to increase urine output

2. use changes in osmotic gradients to eliminate water (blocks sodium reabsorption; where sodium goes, water goes).

Question 16

clinical uses for diuretics (7 things)

treatment of:

Answer 16

1. cardiovascular disease
2. HTN
3. renal disease
4. endocrine abnormalities
5. glaucoma
6. increased ICP
7. treat metabolic alkalosis or to alkalyze urine

Question 17

Diuretics:classification

4 types, give examples

Answer 17

1. high ceiling or LOOP diuretics (LASIX)
2. thiazide diuretics (HCTZ)
3. Potassium sparing diuretics
   
   • aldosterone (ALDACTONE)
   • non-aldosterone (TRIAMTERENE)
4. Others:
   
   • carbonic anhydrase inhibitors (DIAMOX)
   • osmotic diuretics (MANNITOL)

Question 18

what does high ceiling diuretic mean?

Answer 18

it has a high theraputic index

ex: lasix does is 20 mg to 200 mg

Question 19

Diuretics: LOOP:
I. name 4 different loop diuretics:
II. how effecient are loop diuretics?
III. how do they work?

Answer 19

I. 1. lasix
	2. bumex
	3. torsemide
	4. ethacrynic acid
II. the most effecient diuretic
III. act at ascending loop of Henle to inhibit sodium, potassium and chloride reabsorption= more water loss.

Question 20

diuretics: loop:
1. Furosimide (aka)
2. how does it work

Answer 20

1. lasix
2. potent naturetic
   - -works in the ascending loop of henle to block reabsorption of Na+, K+, Cl-
   - -produces kaliuresis (excretion of K+ in urine as) by increasing sodium-potassium exchange (sodium is reabsorbed) in the late distal tubule and collecting duct
   - -also increases magnesium and calcium excretion.

Question 21

Loop diuretics: adverse effects

1. what lyte imbalance is seen? what are the side effects?
2. what organ toxicity is seen?
3. what is a side effect of its main purpose?
4. what does this side effect cause in the patient?

Answer 21

1. hypokalemia (d/t increased exchanged with sodium in late distal and collecting ducts) -causes dysrhythmias (irritablilty)
2. ototoxicity (reversible); tinnitus, ear pain, vertigo, balance issues, hearing impairment
3. dehydration -dry mouth, unusual thirst, decreased urine output
4. hypotension-dizziness and light headedness

Question 22

Usually sodium and potassium are exchanged for each other but what is different about the proportion of NA+ to K+ in the collecting duct (d/t exchange in the late DCT and early collecting ducts)?

Answer 22

NA+ & K+ are inversely proportional

Question 23

Diuretics: Lasix interactions:

1. what drug interacts with lasix with lyte imbalances are present? what is the reaction? what is the lyte?
2. what other drugs would cause the “organ toxicity” worsening the problem?
3. what drug is held on to due to the action of what lasix does?
4. what drug would counteract the effect of lasix and therefore should not be used with it?

Answer 23

1. Digoxin; hypokalemia potentiates dig toxicity; predisposes patient to ventricular arrhythmias
2. aminoglycosices (gent, tobra, strepto, neomycin, amikacin) all cause ototoxicity
3. lithium excretion is reduced; lithium is a salt and lasix increases salt/K+ exchange; pulls salt in and pushes K out
4. potassium sparing diuretics keep K+ in, so it would decrease action of lasix.

Question 24

what diuretics are considered low ceiling?

Answer 24

thiazide diuretics

Question 25

what does “thio-“ mean in chemistry?

Answer 25

sulfur

Question 26

diuretics: thiazide and related:
1. how often used?
2. how do they work?
3. what type of ceiling?
4. are they effective if your patient is in pulmonary edema?
5. what allergy should you use caution with this drug?

Answer 26

1. very frequently used diuretics
2. block reabsorption of sodium and chloride in the DCT therefore increasing renal excretion of sodium, chloride, water & potassium.
3. low ceiling, small theraputic index
4. not effective for immediate diuresis (slow acting)-considered a maintainance diuretic
5. caution with sulfa allergies (same as sulfites)

Question 27

diuretics: thiazide and related diuretics
1. how effective orally and how severe is naturetic effect?
2. how severe are side effects?
3. what patients may have undesirable side effects; what are these?

Answer 27

1. very effective orally with moderate naturetic effect
2. very few adverse side effects
3. diabetics (increased serum glucose); gout (increased levels of uric acid)

Question 28

diuretics: thiazide
1. action? where?
2. diuresis in comparison to lasix?
3. efficacy is dependent on what? what patient wont get thiazide?

Answer 28

1. blocks reabsorption of sodium and chloride in early segment of DCT
2. increased urine flow not as much as lasix
3. efficacy depends of kidney function ;do not give in renal failure (it won’t work??).

Question 29

diuretics: thiazide
1. what does diuresis do to perfusion?
2. what happens to the ECG?
3. what happens to catecholamine response? why?
4. how can this effect be counteracted?

Answer 29

1. excretion of water volume decreases cardiac output
2. decreased SVR with decreased sodium
3. low sodium blunts response to catecholamines (or vasopressors : epi, NE) d/t decreased ability to generate action potentials
4. effect counteracted by increased intake of dietary sodium

Question 30

diuretics: thiazides:
Hydrochlorothiazide: Clinical uses
1. number one use:
2. obvious but secondary use:
3. unconventional use:
4. safe to use for fluid overload in what condition?

Answer 30

1. used to treat essential hypertension by:
   
   • decreasing blood volume; immediate antihpertensive effect
   • reduces arterial resistance (develops over time and action is unknown - ??may have to do with sodium action potentials??)
2. treatment of edema in:
   
   • heart failure patients (mild to moderate)
   • mild renal or hapatic disease (remember, not for use in renal failure–will not work).
3. treatment of Diabetes Insipidus:
   
   • paradoxical effect, mechanism unknown
4. pregancy (category B)

Question 31

diuretics:
1. 2 main types of thyazide (A,B)
2. combinations of A?
3. combinations of B?

Answer 31

1. A.Hydrochlorothiazide (HCTZ)
   B. Chlorothiazide (diuril)
2. A. HCTZ can be used alone as (Apo-Hydro) or in combination:
   -HCTZ with propanolol=INDIRIL
   -HCTZ with ARB (olmesartan)= benicar; (losartan)=cozaar
3. B. Diuril can be used alone or in combination:
   -diuril (chlorothiazine) and reserpine=Diupres 20

Question 32

diuretics: thiazide LIKE diuretics:
1. thyazide-LIKE diuretic
2. what is it used for?
3. what condition is it contraindicated in?

Answer 32

1. Indapamide (Lozide)
2. used for long term management of heart failure, hypertension.
3. contraindicated in pregnancy (teratogenic effect).

Question 33

diuretics: hydrochlorothiazide:
contraindications:

Answer 33

contraindicated in sulfa allergy

Question 34

diuretics: hydrochlorothiazides
Adverse reactions:
1. ____e imbalance; which one? why? signs and symptoms?
2. increased __ A___levels? why?
3. altered serum L____ levels? which ones?
4. increased ____ G____ ? what is the cause?

Answer 34

1. electrolyte imbalance;
   
   • -potassium;
   • -d/t excessive loss especially with inadequate K+ intake
   • -s/s: dry mouth, thirst, irregular heart beat, mood and mental changes, muscle cramps, n/v, weak pulse
2. increased Uric acid levels
   
   • -d/t inhibited uric acid secretion from PCT (accumulates in joints)
3. increased Serum Lipid levels (hyperlipidemia)
   
   • -increased HDL, LDL
4. elevated blood glucose
   
   • -in part due to hypokalemia which REDUCES insulin secretion by pancreatic beta cells

Question 35

Potassium sparing diuretics:

1. action: where do they work? how?
2. what are these good for counteracting? what patient is it good for?
3. how effective is it?

Answer 35

1. act in DCT where sodium is usually reabsorbed and exchanged for potassium; blocks Na+ reabsorption (leaving more in the lumen) and therefore retains the K+, “sparing” the K+.
2. useful in counteracting postasium loss induced by thiazide and loop diuretics. Good for hypokalemic patients.
3. produces only modest increase in urine output, not potent as a stand alone drug.

Question 36

diuretics: potassium sparing:
 2 types;
1. A
2. B
3. what is the action of aldosterone?

Answer 36

1. A. epithelial sodium channel blockers (amiloride; triamterene)
2. B. aldosterone receptor antagonist (spironolactone (aldactone)), which blocks action of aldostorone.
3. aldosterone promotes sodium retention and potassium excretion; by blocking aldosterone, more sodium is excreted and potassium is spared.

Question 37

diuretics: potassium sparing
Aldactone: side effects:
1. electrolyte imbalance; which one?
2. endocrine effects; since it blocks aldosterone, what else will it block? how does it affect men and women differently?

Answer 37

1. hyperkalemia (d/t potassium sparing)
2. blocks aldosterone (a steroid) and thus blocks sex steroids (men become more like women, women become more like men)
   
   • men: gynecomastia, impotence
   • women: menstrual irregularities, hirsuitism, deepening voice

Question 38

diuretics:potassium sparing
aldactone
uses: (4 things)

Answer 38

1. prevention and treatment of hypokalemia
2. treatment of primary aldosteronemia
3. anti-androgen effect for polycystic ovary disease (polycystic ov. disease usually occurs in obese)
4. treatment of hirsutism & seborrheaic acne

Question 39

diuretics: potassium sparing: Epithelial sodium channel blocker:
1. name 2 name brands?
2. brand names when mixed with HCTZ
2. adverse side effects:

Answer 39

1. Triamterene, Amiloride
2. maxzide, dyazide
3. hyperkalemia, n/v, diziness, peaked T wave, blood dyscrasias (rare).

Question 40

potassium sparing: triamterine/ amiloride
drug interactions:
1. what drugs should be avoided?
2. what supplements should be avoided?

Answer 40

1. drugs that increase potassium, ACE inhibitors

2. potassium supplements

Question 41

osmotic diuretics:

1. name 4 of them
2. how do they work?

Answer 41

1. mannitol, isosorbide, urea, glycol
2. no specific receptor or molecular target
   
   • freely filtered at glumerulus and undergo minimal absorption
   • increase osmotic pressure of tubular fluid, reducing bodies reabsorption of water
   • act via physiochemical properties

Question 42

osmotic diuretics: 
mannitol:
1. what is it?
2. how does it work?
3. clinical uses:

Answer 42

1. a sugar alcohol
2. given IV, it is filtered by glumerulus but NOT REABSORBED (passes thru), creating an osmotic gradient in the lumen of the nephrom causing water to move into lumen, sodium is also retained in the lumen.
3. used in:
   
   • oliguria
   • acute renal failure
   • promote excretion of toxic substances (administered with cisplatin to help secrete antineoplastic platinum compounds)
   • help alzheimers meds get to brain(shrinks endothelial cells increasing gap size in BBB)
   • increased ICP

Question 43

diuretics: carbonic anhydrase inhibitors:
1. what is it?
2. what does it do?

Answer 43

1. a naturally occuring enzyme present in :
   
   • nephron basolateral and luminal membranes
   • cytoplasm of epithelial cells
   • RBCs
2. Blocks sodium bicarbonate reabsorption causing sodium bicarb diuresis and a reduction in bicarbonate stores (increased secretion of HCO3-)

Question 44

diuretics: carbonic anhydrase inhibitor:
clinical uses (4 things)

Answer 44

1. treatment of glaucoma: Brizolamide or Dorzolamide reduces IOP
2. urine alkalynization: Acetazolamide increases urinary Ph which enhances excretion of uric acid and ASA
3. treatment of metabolic alkalosis: acetazolamide helps to excrete bicarb causing nomalization of Ph and increases carboxic drive
4. acute mountain sickness: acetazolamide: see next note:

Question 45

acute mountain sickness:

1. how does it occur?
2. what are symptoms (mild)?
3. what are severe symptoms?
4. what else will the patient be on?

Answer 45

1. occurs with rapid ascent above 10,000 feet (3000 meters)
2. mild symptoms include dizziness, insomnia, headache, nausea lasting days
3. serious cases cause rapidly progressing pulmonary or cerebral edema (this relieves hypoxia)
4. patient will also be on oxygen and steroids

Question 46

diuretics: clinical indications for anesthesia:
1. what factors caused by diuretics can cause problems with anesthesia?
2. hyperkalemia causes what affect that interferes with what anesthesia drug?
3. what does hypokalemia cause in anesthesia?
4. what does high dose lasix block and what does it cause? what anesthesia drug does it go against?
5. giving diuretics to ICH patients; what must they be monitored for?

Answer 46

1. hypotension and electrolyte imbalances
2. hyperkalemia produces metabolic acidosis that may affect duration of NMBs like nimbex
3. hypokalemia can cause decreased pancuronium levels
4. high dose lasix can inhibit phosphodiesterase which increases cAMP and increases muscle contraction which antagonizes NMBs.
5. must monitor patients with ICH for anuria and dehydration

Question 47

antihypertensives: ace inhibitors
1. uses:
2. where is renin stored?
3. what causes its release?

Answer 47

1. HTN, heart failure, post MI
2. stored in afferent and efferent vessels
3. released with adrenergic stimulation (beta 1 stimulation), reduction of wall tension in afferent receptors (low pressure), reduction in sodium levels at macula densa

Question 48

antihypertensives: ACE
angiotensin:
1. how many types of angiotensin
2. what does the release of AT cause (7 things)?

Answer 48

1. 3 types (but only 2 have actions): AT1, AT2 (AT3 no known axn)
2. -increase in inositol phosphate (IP3) which causes increased intercellular calcium
   
   • increase in arachidonic acid metabolites
   • decrease in cAMP
   • adrenal cortex activation increases release of aldosterone
     - causes vasocostriction of arterioles (local and systemic)
   • causes release of aldostorone
   • alteration of cardiac and vascular structures (causes remodeling of heart)

Question 49

1. remodeling of the heart means what?

2. what medication prevents this?

Answer 49

1. increased thickness of the heart and blood vessel walls after damage (post MI)
2. ACE inhibitors

Question 50

1. what are ‘ prils’ used for?

2. what vessels does it work on?

Answer 50

1. hypertension, cardiac failure, diabetic nephropathy, post MI
2. works mainly on arterioles (less on veins) so less chance of postural hypotension, but decreases both preload and afterload

Question 51

anesthetic aspects of “prils”

1. blood pressure effects with diuretics
2. nsaid interaction (after how many days)
3. blood pressure with anesthesia is…
4. lisinopril increases action what MRs?
5. what do antacids do to what___ pril?

Answer 51

1. hypotension increased when on pril + diuretic
2. nsaids used more than 7 days decrease antihypertensive effect
3. hard to control hypotension with anesthesia from ACEs
4. lisinopril increases of “curarie like” MRs
5. antacids block captoril d/t chelating (binding) action of the calcium carbonate

Question 52

name some “prils” (5)

Answer 52

lisinopril, captoril, enalapril, fosinopril, ramipril

Question 53

drug interactions of prils:

what medications should be used with caution (4) and reasons?

Answer 53

1. loop and thiazide diuretics (increase hypotension and renal insuffeciency)— but good for CHF patients
2. some antihypertensives (too strong)
3. drugs that increase K+ levels
4. lithium drugs (levels will increase).

Question 54

ACE inhibitor s/e

1. how do prils cause cough? whats the chance (%)?
2. what cutaneous side effect is common?
3. what patient is it contraindicated with?

Answer 54

1. comes from bradykinin release; chance: 5%
2. rash: 5-10% risk
3. –pregnancy (teratogen)
   
   • -renal failure: this patient is dependent on angiotensin II to maintain renal blood flow and glumerular filtratin

Question 55

ARBS:

1. How do they work?
2. what was the first ARB?
3. if combined with HCTZ, what is name?

Answer 55

1. competatively prevent angiotensin II from attaching to ARB receptors to prevent hypertension
2. Losartan (cozaar) was 1st;
3. combined with HCTZ is Hyzaar

Question 56

1. what sites do ARBS work at?

2. side effects

Answer 56

1. vascular smooth muscle, adrenal glands (decrease aldosterone secretion-which increases water and salt excretion),
2. no MAJOR adverse side effects (no effect on calcium, , no effect on arachadonic acid so no cough, no effect on K+,
   
   • headache
   • flushing
   • dizziness
   • cough
   • sinusitis
   • fatigue
   • chest pain
   • benign ST changes on ECG
   • muscle cramps/ arthalgia

Question 57

ARBS

1. contraindications:
2. anesthesia implications:

Answer 57

1. pregnancy (2nd and 3rd trimester, renal artery stenosis (needs angiotensin II to maintain perfusion).
2. marked hypotension with anesthesia, increased NM action with curarae like MRs.

Question 58

BETA BLOCKERS:

1. uses:
2. side effects:

Answer 58

1. -inexpensive, can be beta 1&2 or just beta 1
   - decrease pulse and oxygen demand
   - block inotropic, dromotropic and chronotropic effects
2. -blocks glycogenolysis that occurs with catecholamines, -blocks symptoms of hypoglycemia and recovery may be delayed
   
   • may cause life threatening bronchospasm

Question 59

beta blockers:

1. timolol:
2. pindolol:
3. nadolol:
4. propanolol:

Answer 59

1. timolol blocks beta receptors on cilliary blood vessels (decreases aqueous humor in glaucoma)
2. pindolol-has intrinsic beta activity; used for chronic hypertension
3. nadolol is non selective-may cause bronchospasm
4. propanolol (inderal): good for angina, migraines, SVT, tremors, social phobia, general anxiety disorder, hypertension

Question 60

propanolol:

1. uses:
2. how does it work?
3. contraindicated in…

Answer 60

1. mild to moderate HTN; used with vasodilators for severe HTN, arrhythmias
2. blocks B1 & B2, inhibits stimulation of Renin production
3. contraindicated in 1st degree heart block, CHF, cardiogenic shock, COPD & asthma

Question 61

METOPROLOL:(lopressor/toprol)

1. Action:
2. good for what patients?
3. uses:
4. anesthesia side effects:

Answer 61

1. cardioselective: blocks B1 (spares B2), blocks Renin production
2. can be used on asthmatics, diabetics and pvd patients
3. used for HTN, angina, MI, CHF
4. enhances CNS depression with benzos, causes marked bradycardia when used with Neostigmine reversal, masks signs of hypoglycemia and hyperthyroidism

Question 62

LABETOLOL (trandate/normodyne)

1. action (receptors and effects)
2. uses (intra op, post op etc.)

Answer 62

1. alpha 1, beta 1 beta 2 blocker (directly blocks SA node impulse generation, vasodilates
2. used intra op on cardiac, vascular, general and intracranial surgeries; used to treat pheocrhromcytoma and clonidie withdrawl, attenuates post op HTN and tachycardia

Question 63

beta blocker anesthetic considerations:

6 things:

Answer 63

• should not be stopped abruptly d/t rebound HTN and tachy
• discontinuing pre-op increases chance for post op MI
• anesthetic agents increase cardiac depression effects
• hypoglycemia and hyperthyroid symptoms masked (harder to dx)
• tachycardia d/t intra op bleeding is blunted (harder to dx)
• reversal agents will cause marked bradycardia with BBs

Question 64

calcium channel blockers:

1. ACTION:
2. clevidipine is used for…
3. verapamil does what? what part of heart?

Answer 64

1. blocks calcium entry into cells decreasing contraction; causes vasodilation of arterioles and is negative inotropic and chronotropic to heart
2. used for periopertive HTN
3. slows SA and AV conduction TRANSMURALLY

Question 65

CALCIUM CHANNEL BLOCKERS:

1. name 4 major ccbs:
2. potency:
3. action
4. Adalat (aka) used when?

Answer 65

1. amlodipine, nifedipine, diltiazem, verapamil
2. very potent
3. directly act on smooth muscle of arterioles to cause relaxation; also decreases heart rate and force of contraction (minimally)
4. aka nifedipine; used in acute situations

Question 66

1. what Calcium channel blocker group causes a strange oral disorder?
2. what is the disorder?
3. what is the other CCB group (class)

Answer 66

1. Dihydropyradines (amlodipine, nifedipine)
2. gingival hypertrophy
3. non-dihydroperidine (diltiazem)

Question 67

anesthetic considerations of CCBs:

1. CCBs interact how with anesthesia
2. what decreases these effects? who is most at risk?
3. what defeciency will have prolonged recovery with (what?) CCB?
4. what CCB has increased sedation with ____?
5. increased risk of ___ and ___ if used with what other antihypertensive

Answer 67

1. CCBs increase hypotensive and cardiodepressive effects of anesthesia
2. adequate hydration; elderly persons
3. patients with pseudocholinesterase deficiency have reduced clearance and prolonged recovery with Clevidipine
4. Diltiazem increases sedative effects of benzos
5. if used with beta blockers, increased chance of hypotension and bradyarrhythmias

Question 68

what drugs are used for heart failure (5)?

Answer 68

1. cardiac glycosides (dig)
2. prils
3. diuretics
4. beta blockers
5. ace inhibitors

Question 69

1. what is a good drug therapy combination for CHF?
2. why?
3. what group is it bad for?
4. why?

Answer 69

1. ace inhibitors mixed with diuretics
2. decreases mortality rates
3. renal failure patients
4. they need angiotensin II to maintain GFR and renal artery blood flow

Question 70

cardiac glycosides:

1. brand name?
2. theraputic window?
3. action:

Answer 70

1. digoxin, digitek
2. small (1.5-2)
3. positive inotrope with negative chronotropic action
4. inhibits Na+/K+-ATPase enzyme (this enzyme decreases movement of calcium into cell and sodium out)which allows for more calcium to stay in the cell increasing strength of contraction and decreasing rate.

Question 71

dig toxicity:

s/s

Answer 71

1/ s/s:

• fatigue
• confusion
• delirium
• psychosis
• gi distress
• halos /photophobia
• color disturbances
• arrhythmias

Question 72

how does dig cause color disturbances, photophobia and halos in eyes?

Answer 72

dig is rapidly taken into rods and cones of eyes

Question 73

dig: caution in surgery:

what can happen intra-op?

Answer 73

• electrolyte imbalances
• hypokalemia
• v-fib
• AV block
• sinus brady

Question 74

1. what skin side effect can dig cause?

2. what patients is dig reserved for?

Answer 74

1. digitalis purpura

2. systolic dysfunction (increases contractile force)

Question 75

cardiostimulatory drugs:

1. what are they?
2. how do they work?
3. what are they (3 of them) and what do they do?

Answer 75

1. drugs that have inotropic, chronotropic and dromotropic effects
2. may reduce afterload or enhance myocardial contractions
3. -dobutamine: synthetic beta agonist; causes mild vasodilation and decreases pre and after load while increasing contractility
   
   • nitrates: vasodilator acts on venous capitance vessels decreasing preload to failing heart while vasodilating arteries to decrease afterload
   • dopamine: natural catecholamine which increases cAMP production in myocardium to increase contractility at moderate dose (vasodilates renal at low dose, vasoconstricts vessels at high dose).

Question 76

Endothelin Receptor Antagonist:

1. what is it?
2. how does it work?
3. uses:
4. chemical and brand name:
5. contraindications:
6. side effects:

Answer 76

1. competetive antagonist of Endothelin 1 which is produced excessively in CHF (endothelin 1 causes pulmonary vasoconstriction (increases pulm vasc resistance)).
2. inhibits Endothelin 1 causing vasodilation
3. pulmonary artery hypertension
4. Bosentan (Tracleer)
5. contraindicated in pregnancy (teratogen)
6. liver damage

Question 77

angina:

1. cause:
2. symptoms:
3. at what point of blockage will a patient have angina symptoms?
4. management of angina:

Answer 77

1. narrowing of coronary vessels d/t plaque, vasospasm, increased cardiac workload (or combination of these).
2. can be symptom free (especially diabetics), n/v, feelings of impending doom, dizziness, shoulder pain radiating down top of arm, women may have jaw pain; men have classic substernal crushing pain.
3. 90% occlusion
4. nitrates, CCBs, BBs, control weight, stop smoking, reduce blood pressure, exercise, surgical revascularization, stents or laser therapy.

Question 78

Nitrates:

1. what can increase effects of nitrates?
2. what is the sub lingual version called?
3. what is the onset and duration
4. what is the time released (prophylactic) version called? what is it made from?

Answer 78

1. alcohol
2. isorbide di-nitrate
3. 2 min onset/ 3 hour duration
4. Isorbide mono-nitrate (imdur); a metabolite of isorbide di-nitrate

Question 79

Heart failure: 10 causes:

Answer 79

1. dilated cardiomyopathy=5-10%
2. CAD & HTN=5-10%
3. alcoholic, viral or hypertrophic cardiomyopathy
4. IHD (ischemic heart disease)
5. mitral valve regurg
6. septicemia
7. alcohol intoxication
8. cocaine
9. drug induced (cyclophosphamide chemotherapy)
10. excess thyroxin ingestion

Question 80

heart failure:

s/s

Answer 80

1. cough
2. change in breathing
3. dyspnea
4. palpitations
5. swelling/ ankle edema
6. abdominal swelling
7. anorexia and bloating
8. fatigue/ weakness
9. excercise intolerance

Question 81

goals of managing heart failure:

8 things

Answer 81

1. NUMBER 1: delay onset of symptoms
2. improve quality of life
3. reduce hospitalizations
4. treat underlying diseases
5. decrease sodium to 1-2 g/day
6. reduce fluids to <2L/day
7. walk 20-30 min/day
8. lifestyle changes (low fat, smoking cessation, decrease stress).

Question 82

antiarrhythmics:
Lidocaine:
1.class
2. s/s toxicity

Answer 82

1. class 1B
2. s/s of toxicity:
   
   • tinnitus
   • metalic taste
   • slurred speech
   • paresthesias
   • tremors
   • seizures to coma
3. patients with liver impairments