Pharm Test 3

Front 1

circulatory shock

Back 1

- acute life threatening condition ass. with insufficient blood delivery to tissues.

Front 2

types of circ. shock

Back 2

- hypovolemic - blood loss
- tx. - transfusions/fluid replacement and vasoconstrictors
- restore blood flow via vasoconstrictors while sustaining blood flow to key organs.
- alpha 1 receptor agonist with dopamine receptor and or beta 2 agonist effects

- distributive shock - intense vd due to infection (septic shock), allergic reaction (anaphylactic shock) or brain/spinal cord injury (neurogenic shock)

- cardiogenic shock - stopage of the heart.

Front 3

cardiogenic shock - acute heart failure

Back 3

- causes - acut mi, cardiac arrhythmias, valve issues, end stage chronic heart failure.

tx - positive ionotropic agents.

goal is to increase C.O.

- only (cardiogenic shock) Beta 1 receptor agonists
- beta 1 adrenergic receptor agonists - dobutamine
- phosphodiesterase inhibitors - milrinone (blocking this increases cAMP resultingin positive ionotropic effects)
- muscarinic rec. agonists - atropine (blocks effects of the parasympathetic n.s. on heart)

Front 4

chronic/ congestive heart failure

Back 4

- cardiac output is insufficient to meet the oxygen demands of the body

causes
- 1 = coronary artery disease/ MI
- 2 hypertension resulting in cardiac hypertrophy

others - valve disease/ dysfunction
- cardiomyopathy
- congenital defects
- endocarditis/ myocarditis

Front 5

left ventricular symptoms

Back 5

- pulmonary edema
- accumulation of blood in ventricles and enlarged heart

Front 6

right ventricular symptoms

Back 6

- back up of blood within the vnous circulation "pitting"edema of lower limbs.

Front 7

chronic heart failure

Back 7

- goal is to increase CO

- determinants of CO

Front 8

determinants of CO

Back 8

- contractility - force of contraction
- calcium dependent (involves ca dependent ca release)
- regulated by sns Beta 1 r's

2. heart rate - frequency of contraction
- regulated by sns beta 1
- increasing hr in hf is counterproductive because it just acc. the mismatch.

3. afterload - resistance against which the heart has to pump
- arterial smooth muscle
- regulated by sns (alpha 1 r's)
- regulated by the renin at system (angiotensin 2)

4. preload volume of blood in the heart prior to contraction
- return of blood to the heart via veins
- total blood volume - kidneys
- regulated by renin at sytem via at2.

Front 9

preload

Back 9

- volume of blood in the left ventriccle prior to contraction
determined by - venous return and blood volume if you decrease either of these you will decrease preload.

frank starling law says if you have too much or too little ventricular stretch you will get a fall in output due to faulty overlapping of the heart muscle contraction machinery.

Front 10

tx of chronic heart failure

Back 10

- heart failure = progressive condition with gradual decline in cardiac performance and acute epsodes of impaired function.

- general therapeutic goals - reducing symptoms and slowing disease progression during periods of stable (compensated) heart failure.
- managing episodes of acute (decompensated) failure.

- specific therapeutic goals
- improve Myocardial contractility without increasing heart rate
- reduce afterload
- reduce preload

increasing heart rate is not beneficial for CHF.

Front 11

tx of chronic heart failure

Back 11

- steps in the treatment of chronic heart failure
1. reduce the workload of the heart
2. reduce sodium
3. pharmacotherapy - involves multiple drugs

drugs
- ace inhibitors/ at receptor blockers
- diuretics
- cardiac glycosides
- beta blockers
- vasodilators (not calcium channel blockers)

Front 12

ace inhibitors

Back 12

- along with diuretics, are a first line drug class for managing chronic heart failure
- have replaced cardiac glycosides as a first line drug
- reduces symptoms and mortality
- captopril and enalopril

Front 13

therapeutic effects of ace inhibitors for CHF

Back 13

- via reduced at 2 receptor activation
1. relaxation of arterial smooth muscle
- reduced afterload
2. reduced aldosterone production/ release
- reduced sodium reabsorption and blood volume = reduced preload.

- via unknown mechanisms
- dilate veins - reduce preload
- reduce trophic changes in myocardium - prevent and reverse

ARBS - losartan - for unknown reasons, ace inhibitors are more effectivee than antiotensin receptor blockers; ARBS should only be used in patients who can't tolerate ACE inhibitors.

Front 14

diuretics

Back 14

- along with ace inhibitors are a first line drug class for managing chronic heart failure.

Review
- reduce Na+ reabsorption in the nephrons of the kidneys
- reduce blood volume and therefore preload
- drug classes
- thiazide diuretics - moderate efficacy; produce hypokalemia
- loop diuretics - high efficacy and produce hypokalemia
- potassium sparing diuretics - increase systemic potassium levels.

- reduce edema in the lungs and venous system
- reduce blood volume and preload of the heart
- administered along with ace inhibitors
- thiazides used in mild failure
- loop diuretics - more severe cases
- hypokalemia offset by ace inhibitors, K+ supplements, potassium sparing agents
- aldosterone blocking potassium sparing agents. also used as first line agents.

Front 15

aldosterone antagonists+ ace inhibitors

Back 15

- spironolactone along with an ACE inhibitor reduces morbidity and mortality greater than an ACE inhibitor alone
- spironolactone, epleronone
- antagonists at aldosterone (MC receptors)
- prevents effects of aldosterone on sodium/ potassium exchange in the kidneys = weak diuretic.
- also prevents other non renal effects of aldosterone, possibly in the heart and the lungs.
- ACE inhibitors should have the same effects via reductions in aldosterone secretion; rationale for added benefit is unclear.
- side effects - aldosterone antagonists also tend to blocks receptor for sex hormones.
- note - both ACE inhibitors and spironolactone produce hyperkalemia; combination = increased risk.

Front 16

cardiac (digitalis) glycosides

Back 16

- until recently, first line tx for chronic heart failure (now ace inhibitors); now only used in specific patient populations
- can't switch from digitalis glycosides to ace inhibitors without deterioration of condition.

- drugs include digoxin and digitoxin.

beneficial effects - increase cardiac output by increasing myocardial contractility as a result of effects on calcium
- reduced congestive symptoms and improved exercise tolerance
- reduce lethality from progressive damage but increases sudden death
- margin of safety is very low; risk of cardiac arrhythmias
- treat overdose via administration of digitalis antibodies.

Front 17

mechanism of cardiac glycosides

Back 17

- inhibit the na/k atpase on cardica smooth muscle cell membranes by binding to the potassium site.
1. prevents transport of sodium into cell
2. increased intracellular socium = less transport of calcium out of cells in exchange for sodium

- more intracellular calcium = greater force of smooth muscle contraction
- hig

Front 18

potassium levles and digitalis glycoside effects

Back 18

potassium and digitalis glycosides compret for the same site on the na k atpase soooo...

- higher systemic potassium levles = less digitalis glycoside iffects
- so potassium sparing diuretics (spironolactone) decrease the efficacy of cardiac glycosides.

- lower potassium lavles equal more digitalis glycoside effects
- thiazide and loop diuretics

Front 19

beta blockers

Back 19

- reduce CO but they seem to improve survival in some patients.
- bisoprolol - carvedilol = metoprololothers are NOT effective

- often initiate with decompensated failure - combine with ACE inhibitors.
- reason for benefits may be reductions in heart rate which balances synchronized filling and contraction in heart. possibly reduced remodeling (cardiac hypertrophy)

- initiate slowly at low doses and cautiously increase.

bisoprolol and metoprolol - cardioselective beta blockers

- carvedilol - beta blocker with alpha one antagonist effects

Front 20

vasodilators

Back 20

- not a first line therapy in most patients
- administered to patients along with other agents according to their symptoms.
- venous dilators - nitrates decrease preload
- good for tx of people with PULMONARY edema as a primary symptom.

- arterial dilators - hydralazine - decreases afterload - good for treating patients with fatigue as a primary symptom.

DO NOT USE CCB"S as a tx for chf because it decreases co

Front 21

focal infection theory of disease

Back 21

- a localized or general infection caused by the dissemination of mo or toxic products from a focus of infection.

Front 22

resistance types

Back 22

- inherent (natural) resistance
- acquired resistance


- vertical evolution - mutation and selection

- horizontal evolution; exchange of genes between strains and species

Front 23

antibiotic susceptibilty testing

Back 23

- min inhib. conc. MIC - suppressed visible growth

- min bact. conc. (MBC)
- kills 99.9% of the original inoculum in a given time.

Front 24

superinfection

Back 24

- new infection arising from chemotherapy of the primary infection
- typically caused by removal of inhibitory influence of preexisting flora.

- more common with broad spectrum antibiotics and combination therapy.

Front 25

overview

Back 25

- inhibition of cell wall synthesis
- inhibition of DNA synthesis
- damage to existing DNA
- protein synthesis inhibitors.

Front 26

cell wall synthesis in hibitors types

Back 26

beta lactam

- glycopeptides

Front 27

beta lactam cell wall inhibitors

Back 27

penicillin, ampicillin, methicillin, piperacillin, cephalosporins, aztreonam, imipenem

Front 28

glycopeptide cell wall synthesis inhibitors

Back 28

- vancomycin, televancin, teicoplanin, dalbavancin.