Pharmacology Core Competency Exam

Front 1

3 ways to lower BP

However, kidney and adrenals + ___ system will fight attempts to lower BP unless it is disabled.

Back 1

dump fluid
dilate vessels
decrease HR and contractility.

RAS

Front 2

Essential HTN is due to ______ vasoconstriction

Despite vasocontriction induced increasing TPR in essential HTN, CO remains ___.

When LV wears out from too many years of HTN, CO ___, causing early ___.

Back 2

arteriolar/ "essential"

normal
drops
LVF

Front 3

Common drug that increases renal Na retention and thus interferes with effects of many anti hypertensives

Back 3

NSAIDs

Front 4

- For mild HTN, start with a ______
If HTN inadequately controlled by a thiazide, add a ______
- If HTN inadequately controlled by a beta blocker, add a _______

If HTN inadequately controlled by thiazide + beta blocker, add a _____

Back 4

thiazide
beta blocker
thiazide
vasodilator

Front 5

For antihypertensive drugs,

blacks response best to ___ and ___
Eldery to ___, ___, and ___
ACEs are most effective in?

Back 5

thiazides and CCBs
thiazides, CCBs, ACEIs
young whites

Front 6

_____ are the first choice when there are contraindications for thiazides or beta blockers for hypertension.

Back 6

ACEIs

Front 7

3 contraindications for beta blockers

Back 7

elderly
asthma
COPD

Front 8

3 contraindications for thiazides

Back 8

gout
sulfa allergy
Ccreat <50

Front 9

ACEs block production of angiotension II and cause what 2 3effects?

Back 9

vasodilation
decreased aldosterone
decreased circulating fluid volume

Front 10

____ are preferred for HTN in diabetics because they are ____ protective. They are ____ protective because they decrease glomerular pressure by dilating ___ arterioles.

Back 10

ACEs
renal
renal
efferent

Front 11

Dilating glomerular efferent arterioles in someone who has
bilateral renal artery stenosis (RAS), or RAS in a solitary kidney
may decrease glomerular filtration pressure to the point
where s/he develops

Back 11

ARF

Front 12

Angiotensin converting enzyme normally metabolizes _____. Part of its vasodilatory effects is due to increasing ______, but this can cause ___ ___, and potentially fatal ____ ____ and/or _____ as part of ANGIOEDEMA

Back 12

bradykinin
dry cough
laryngeal edema, hypotension

Front 13

ACEIs may cause first dose ____ (so give in office) and _____. Because they decrease aldosterone, dont give it with what drugs?

Back 13

syncope
hyperkalemia
K supplementation or K sparing drugs

Front 14

ARBs are very similar to ACEIs except decreased change of what? (So often switched to ARBS if that's a problem)

Back 14

angioedema and dry cough

Front 15

Any drug that causes vasodilation may cause edema somewhere. This is true of alpha blockers, ACE inhibitors, ARBs, and CCBs

Back 15

.

Front 16

nifedipine
amlodipine

Back 16

CCBs-dihydropyridines

Front 17

2 non dihydropyridine CCBs

Back 17

verapamil
diltiazem

Front 18

For CCBs, which drugs are more selective of the Ca channels of vascular smooth muscle?

As a result, used to treat what?

Back 18

IPINE drugs-nifedipine and amlodipine

HTN
peripheral vascular disease
raynauds

Front 19

When are CCBs indicated

Back 19

black hypertension
when thiazide or beta blocker control is inadequate

Front 20

___________ is a CCB that decreased HR and contractility more than it affects vasodilation.

_______ is a CCB that decreases HR and contractility and dilates coronaries and arterioles about equally.

Back 20

verapamil
diltiazem

Front 21

why can verapamil, diltiazem, nifedipine, and amlodipine be used for angina?

Back 21

They dilate coronary vessels

Front 22

_____ has marked negative chonotropic effect on the SA and AV nodes, so used to decrease HR in SVT.

Back 22

verapamil

Front 23

This HTN drug class can be used for migraine prophylaxis

Back 23

CCBs

Front 24

side effects (4) of CCBs?

(3 vasodilatory)
(1 calcium channel in smooth muscle effect)

Back 24

peripheral edema
flushing
headache

constipation

Front 25

Hypokalemia potentiates the toxicity of ______.

Back 25

digoxin

Front 26

4 classes of diuretics

Back 26

Thiazide diuretics - K-Sparing diuretics
- Loop “ - Osmotic

Front 27

Overall indications for diuretics

Back 27

EDEMATOUS states (heart failure, hepatic ascites, nephrotic syndrome)

NON EDEMATOUS states (HTN and DI)

Front 28

In HF, decreasing CO causes increasing renin, increasing antiogensin and aldoesterone, vasoconstrication, increased circ fluid volume, edema, high BP.

In hepatic ascites, cirrhosis increases portal BP. This causes fluid to exude from liver = ascietes. It also makes the liver produce fewer plasma proteins, so water leaks from the vessels.

Nephrotic syndrome--golmueruli damaged by diabetes, HTN, nephritis leak plasma proteins into the urine--decreases plasma osmolarity, increases aldosterone, = edema.

Back 28

.

Front 29

Polydipsia and polyuria of DI respond paradoxically to _____ because they decrease plasma volume, glomerular filtration, and the fluid to the distal tubule.

Back 29

thiazides

Front 30

Thiazide diuretics will dump fluid volume for HTN, but more important long term effect?

Back 30

arteriolar vasodilation

Front 31

_____ are called ceiling diuretics because they cause their maximal diuretic or anti-hypertensive effects at relatively low dose, with no extra effect at higher doses.

Back 31

thiazides

Front 32

2 most commonly used thiazides

Back 32

Hydrochlorothiazide & chlorthalidone

Front 33

thiazides decrease Na reabsorption in the ___ ____ tuble.

Not effective if pt really needs a loop because GFR < ___ ml/min or Ccreat < ___ ml /min

Back 33

distal convoluted
30
50

Front 34

Thiazides are a good first line choice for mild HTN, usually others are added to it.

Used to treat what because they increase renal reabsoprtion of calcium from urine?

Back 34

osteoporosis
prevent Ca stones

Front 35

Side effects of thiazides

Back 35

↑ K excretion…must monitor early in Tx for……………… Hypokalemia
- ↑ H+ excretion…..may cause……………………… Metabolic Alkalemia
- ↓ Uric acid secretion  hyperuricemia……………………… Gout

Front 36

to compensate for thiazide hypokalemia, add what?

Back 36

K sparing diuretic
K supplement
or bananas

Front 37

furosemide

Back 37

loop diuretic

Front 38

bumetanide

Back 38

loop diuretic

Front 39

____ diuretics will work in severe renal impairment. Also decrease renal vascular resistance and increase renal blood flow.

Back 39

loop

Front 40

______ are doc for pulmonary edema of heart failure.

They work fast, esp if IV, good for emergency.

Back 40

loop diuretics

Front 41

This antihypertensive class increases Ca and K excretion, so good to treat hypercalcemia and hyperkalemia

Back 41

loop diuretics (unlike Thiazides--where you reabsorb the Ca

Front 42

side effects of loop diuretics

Back 42

especially when given with an aminoglycoside Abx……………………………….. Ototoxicity
- severe rapid reduction in blood volume  hypovolemia  ………………………… Shock

Front 43

loop diuretic most likely to cause ototoxic deafness

Back 43

ethacyrynic acid

Front 44

3 K sparing diuretics

Back 44

TAS (for potassium)
Triamterene, Amiloride, Spironolactone

Front 45

K sparing diuretics are very mild. Any can be added to thiazides or loops to prevent or treat ________.
They may cause hyperkalemia. When given, you must monitor K levels!!! Also must stop any K supplementation!!!

Back 45

hypokalemia

Front 46

aldoesterone receptor antagonist

Back 46

spironolactone

Front 47

This duiretic is used when aldosterone is high (edematous states and hyperaldosteronism)

It has little or no effect when aldoesterone is not high, as in ____ ____

Back 47

spironolactone

addisons disease (primary adrenal insufficiency)

Front 48

Sprionolactone may cause what side effects?

Back 48

gynecomastia, menstrual abnormalities

Front 49

most common osmotic diuretic

Back 49

mannitol

Front 50

MoA for osmotic diuretics

Back 50

- Because it is freely filtered by the glomeruli into the tubular fluid
and is not reabsorbed, it ↑ fluid osmolarity and…………………... Holds water in the tubular fluid

↑ Urine

Front 51

Mannitol is no absorbed from GI tract, must be given how?

It does not increase Na excretion. It is used to increase what?

Back 51

mannitol
water excretion

Front 52

common uses for mannitol

Back 52

- Maintain tubular fluid flow after ingestion of toxic substance that may
clog the tubules and cause Acute Renal Failure

- Prevent Acute Renal Failure due to circulatory shock
- Treat ( lower ) Increased Intracranial Pressure

Front 53

On mannitol, to keep the tubules working and prevent dehydration, must do what?

Back 53

maintain po or IV fluid intake

Front 54

this occurs when myocardial O2 demand exceeds coronary O2 supply

Back 54

angina

Front 55

Some degree of atherosclerotic occlusion in
coronary vessel(s), so at some intensity of
exercise, O2-demand becomes greater than
O2-supply  pain

relieved by what?

Back 55

stable angina

rest or nitro

Front 56

unexplained temporary coronary vasopasm,
in women more than in men.

relieved by what?

Back 56

prinzmetal angina

nitro

Front 57

caused by 1) acute plaque change  partial thrombus, or..
2) atherosclerotic occlusion severe enough that
moment-to-moment sedentary changes in heart
activity can cause O2-demand to exceed O2-
supply

Not relieved by what?

Back 57

unstable angina

rest, nitro

Front 58

general treatment of angina

Back 58

Dilate coronary arteries
- Dilate systemic veins to ↓Preload
- Dilate systemic arterioles to ↓Afterload
- Decrease cardiac contractility

Front 59

to dilate coronary vessels for prompt relieve of stable or variant attack

Back 59

nitro:

nitrolingual spray or nitrostat sublingual tabs (decreases venous return, decreases preload, decreased cardiac work)

Front 60

To dilate coronaries and systemic veins long term to prevent anginal attacks, use?

Back 60

Nitroglycerin: - Patch ( Nitro-Dur )
- Ointment ( Nitro-BID )
- Long-acting tabs

Isosorbide mononitrate or dinitrate

Front 61

isosorbide mononitrate or dinatrate

Back 61

to prevent anginal attacks
long acting nitro tabs

Front 62

To prevent anginal attacks, can dilate coronaries and systemic arterioles with what?

Back 62

dihydropyridine class of Ca-channel blocker
Nifedipine ( Procardia XL )

Front 63

To decrease cardiac contractility long term to prvent angina

Back 63

beta blocker (propranolol, metoprolol)

or a NON DIHYDROPYRIDINE CCB (verapamil, diltiazem)

Front 64

this CCB is good to prevent variant angina

Back 64

diltiazem

Front 65

to help prevent angina,

____ mainly decreases HR and contractility. ____ decreases HR, contractility, dilates coronaries and arterioles

Back 65

verapamil
diltiazime

Front 66

side effects of nitroglycerin

Back 66

HA
postural hypotension

Front 67

Tolerance to long active nitrates develops rapidly, so should do what?

Back 67

remove patch or ointment at bedtime

Front 68

This HTN class can cause constipation

Back 68

CCBs

Front 69

Additional California Restrictions on Advertising

Back 69

Statutory Restrictions: A CA lawyer is prohibited by statute from making communications that contain:
(i) A GUARANTEE or WARRANTY of the outcome of a case;
(ii) Words or symbols (e.g. $$) that suggest quick cash or a quick settlement;
(iii) An IMPERSONATION of a lawyer or client, w/out disclosing that it is an impersonation
(iv) A DRAMATIZATION of an accident or other event w/out disclosing that it is a dramatization; and
(v) A contingent fee offer that does not explain how litigation costs will be handled. (R) atty fees

Front 70

Lifestyle change + meds can decrease the rate of progression of atherosclerotic plaque and even reduce pre existing plaque.

CAD is positively correlated with high ____ but more so with high ___.

High LDL--decreased risk

Primary goal in Ch lowering is reduction of LDL

Back 70

high TC
high LDL

Front 71

Total Cholesterol = ____ + LDL + HDL

VLDL = _____/5

Back 71

VLDL

Trigs

Front 72

TC should be < ___
HDL < ___
HDL >___
Ratio should be ____

Back 72

200
130
60
as low as possible

Front 73

Statins are used to lower LDL

_____ and _______ decrease LDL 50%. Other statins decrease LDL less. All statins lower LDL by inhibiting the rate-limiting step in ____ synthesis.

Back 73

atorvastatin
rosuvastatin

cholesterol

Front 74

Statins decrease intracellular (hepatic) syn of cholesterol, which causes incd number of extracellular LDL receptors--increased cellular uptake of LDL, and decreased ___ LDL

Back 74

plasma

Front 75

side effects of statins

Back 75

myopathy and muscle pain
(test CPK MM often)

elevated liver enzymes (test AST and ALT often)

Front 76

This drug, for 1 penny a day, decreases the incidence of CVD events to the same degree as a statin ccosting 1-4 dollars a day

Back 76

aspirin

Front 77

_________ for very high trigylcerides

Back 77

fibrates

Front 78

fenofibrate

Back 78

fibrates

Front 79

gemfirozil

Back 79

fibrate

Front 80

This fibrate decreases TGs 50%_______

Back 80

fenofibrate

Front 81

Lifestyle change + meds can decrease the rate of progression of atherosclerotic plaque and even reduce pre existing plaque.

CAD is positively correlated with high ____ but more so with high ___.

High LDL--decreased risk

Primary goal in Ch lowering is reduction of LDL

Back 81

high TC
high LDL

Front 82

side effects of fibrates

Back 82

myopathy

Front 83

This class causes greatest (35%) increase in HDL

Back 83

niacin

Front 84

Total Cholesterol = ____ + LDL + HDL

VLDL = _____/5

Back 84

VLDL

Trigs

Front 85

single drug that causes largest changes in all 3 lipids

Back 85

Niacin

increases HDL, lowers LDL and TG

Front 86

TC should be < ___
HDL < ___
HDL >___
Ratio should be ____

Back 86

200
130
60
as low as possible

Front 87

Statins are used to lower LDL

_____ and _______ decrease LDL 50%. Other statins decrease LDL less. All statins lower LDL by inhibiting the rate-limiting step in ____ synthesis.

Back 87

atorvastatin
rosuvastatin

cholesterol

Front 88

side effects of niacin

Back 88

- may cause severe facial flushing
- prevent with Asa or NSAID
30 min before
- may cause Gout

Front 89

To lessen or prevent niacin flush, use what

Back 89

extended release niacin

Front 90

Statins decrease intracellular (hepatic) syn of cholesterol, which causes incd number of extracellular LDL receptors--increased cellular uptake of LDL, and decreased ___ LDL

Back 90

plasma

Front 91

these drugs can reduce LDL about 30%

Back 91

bile acid binding resins

Front 92

cholestyramine (Questran)

Back 92

bile acid binding resin

Front 93

colesevelam (welchol)

Back 93

bile acid binding resin

Front 94

colestipol (colestid)

Back 94

bile acid binding resin

Front 95

side effects of bile binding resins

Back 95

flatulence
bloating
abdominal pain
- May ↓ absorption of Vits ADEK
- May ↓ absorption of many drugs

Front 96

this drug decreases GI tract cholesterol absroption

Back 96

ezetimibe (Setia)

Front 97

- Statins
- Niacin
- Fibrates
- Bile Binding Resins
- Ezetimibe………………………………………………….………….………all ↓LDL and ↑HDL
to one degree or another

Back 97

f

Front 98

____ decrease LDL the most
____ increase HDL the most
________ decreases Trigs the most

Back 98

statins
niacin
fibrates

Front 99

Before statins, need to get what tests?
While on statins?

Back 99

Before you prescribe any one or especially any combination, remember to think of the possible need to get baseline liver function tests, and while on therapy, regular liver enzyme & CPK-MM levels for liver and muscle dysfunction

Front 100

An important drug combination
that significantly changes all cardiac lipids
in beneficial directions

Back 100

fenofibrate + statin

Front 101

other common lipid drug combos

Back 101

Fenofibrate + Niacin
- Statin + Niacin

Front 102

cardioprotective effects that is under utilized in clinical practice

Back 102

omega 3 fatty acids

Front 103

benefits of omega 3 fatty acids

Back 103

decrease Triglycerides

Front 104

Most common cause of HF

Back 104

Left systolic dysfunction due
coronary artery disease

Front 105

When ventricle is less able to eject blood, what kind of failure?

When ventricle is stiff, non compliant and cant fill properly?

Systolic or diastolic failure both cause

Back 105

systolic failure
diastolic failure
decreased CO

Front 106

What organ tries to assure its own function in HF
and in so doing most single-handedly makes HF worse

Back 106

kidney

Front 107

Three compensatory mechanisms that help
increase CO & maintain glomerular filtration
pressure in heart failure

Back 107

1) ↑Sympathetic tone  - ↑HR & contractility
- Vasoconstriction
- ↑Renin secretion

2) ↑Renin  Angiotensin  Vasoconstriction

Aldosterone  ↑renal Na & H2O reabsorp

3) Cardiac Hypertrophy  dilated & globular shape
( “remodeling” )

Front 108

Compensatory mechs that help increase CO cause what?

Back 108

Fluid overload
- ↑Cardiac filling pressures
- Hypertension
- ↑Preload, ↑Afterload
- ↑ Cardiac work
- Worse heart failure

Front 109

Classes of drugs used to treat HF

Back 109

ACEIs & ARBs
- Diuretics
- Beta & Alpha blockers
- Inotropic agents

Front 110

Several Causes of “decompensation”, or exacerbation,
or acute HF in the patient with Chronic HF

Back 110

- ↑Salt intake (hotdogs)
- ↑Exertion
- Illness, fever etc
- Emotion
- Not taking meds
- AMI

Front 111

Now the DOC for ALL
etc stages of heart failure because they
prevent or limit cardiac remodeling,
and ↓ morbidity & mortality

Back 111

ACEIs
captopril, lisinopril

Front 112

rare but serious side effects of ACEIs

Back 112

Pharyngeal Angioedema airway closure

- Acute Renal Failure in Pt with renal
artery stenosis…because the stenosis
chokes glomerular filtration pressure, for
which the glomerular efferent arterioles
compensate by constricting  pressure
OK.. then you add ACEI  arterioles
dilate  no filtration pressure  ARF

Front 113

The believed reason why ACEIs and ARBs decrease cardiac
remodeling (dilation / hypertrophy

Back 113

They block aldosterone
release  ↓ renal fluid retention 
↓cardiac filling pressures.

Front 114

A K+-sparing diuretic & direct aldosterone antagonist
used for the same reasons as ACEIs & ARBs, but in
advanced HF

Back 114

Spironolactone

Front 115

Diuretics used in mild heart failure
and/or mild edema

Back 115

thiazides

Front 116

Diuretics used in significant pulmonary or pedal
edema from HF, and/or in renal insufficiency…
i.e Creatinine clearance < 50 ml/min

Back 116

loops

Furosemide, Bumetanide

Front 117

Both thiazide and loop diuretics often cause

Back 117

hypokalemia

Front 118

Beta-blockers (negative inotropes ) which paradoxically
improve systolic function in HF and even ↓ cardiac
remodeling…because they ↓ renin which ↓aldosterone

Back 118

Metoprolol & Carvedilol

Front 119

is also an alpha-blocker, so it dilates
arterioles ( ↓BP & ↓cardiac work ) and
veins ( ↓preload & ↓ cardiac work )

Back 119

carvedilol

Front 120

________ have no role in HF

Back 120

CCBs

Front 121

The cardiac glycoside, ____ is a postiive inotropy (increases contractility) and is reserved for HF patient not responding
adequately to combination of
diuretic + ACEI + beta-blocker

Back 121

digoxin

Front 122

is for: - severe left systolic HF
- not diastolic HF
- not right sided HF

It has a very narrow therapeutic index

Back 122

digoxin

Front 123

dig toxicity from overdose:

Symptoms:

Back 123

severe potentially fatal dysrhythmias
- nausea & vomiting
- headache & confusion
- blurred vision, color distortion & halos

Front 124

Three electrolyte disturbances that predispose
to digoxin toxicity

Back 124

Hypokalemia
Hypomagnesemia
Hypercalemia

Front 125

if dix toxicity, stop the drug or give what?

Back 125

digiband

Front 126

Chemical inhibitors of platelet aggregation
synthesized by healthy endothelial cells

Back 126

Prostacyclin &
- Nitric oxide

Front 127

The platelet membrane has external receptors that………….….. can bind

Back 127

Exposed vascular collagen (injury)
- Thromboxane A2
- Thrombin
- ADP

Front 128

Binding of receptors activates platelets to release externally, thromboxane, thrombin, ADP, serotonin, PAF. This causes other platelet receptors to activate and release ______ internally. This activates ________ receptors and _____ to produce more _______

Back 128

calcium
GP IIB !!a
COx 1
thomboxane A2

Front 129

ACtivated GP IIb/!!a receptors bind ____ in the plasma, cross link 2 platelets, activate cross linking cascade, and produce what

Back 129

fibrinogen
platelet plus

Front 130

Vessel injury and platelet chemicals start the coag cascade, producing ____ and ____ -platelet plugs

Back 130

thrombin
fibrin

Front 131

The three main classes of
antiplatelet drugs

Back 131

Platelet COX-1 inhibitor
( Aspirin )

- Platelet ADP receptor blocker
Plavix ( clopidogrel )
Ticlid ( ticlopidine )

- Platelet GP llb/llla receptor blocker
ReoPro ( abciximab )
Aggrastat ( tirofiban )
Integrilin ( eptifibatide )

Front 132

clopidogrel (plavix)

Back 132

platelet ADP receptor blocker

Front 133

aspirin

Back 133

platelet COX 1 inhibitors

Front 134

Abciximab (reopro)

Back 134

platelet HP IIb/ IIIa receptor blocker

Front 135

Aggrastat ( tirofiban )

Back 135

platelet HP IIb/ IIIa receptor blocker

Front 136

___________acetylates and thereby inhibits COX-1
in platelets so that _________ a
key activator of platelets, is not produced.

Back 136

aspirin
thomboxane A2

Front 137

_______inhibit ADP-induced activation of
GP llb/llla receptors, so they do not
bind fibrinogen

Back 137

ADP receptor blockers

Front 138

_________block fibrinogen from binding
even activated GP llb/lllla receptors

Back 138

GP llb/llla receptor blockers

Front 139

Aspirin suppresses syn of thromboxane A2 irreversibly for how long?

Back 139

life of platelet (7-10 d)

Front 140

non acetylated salicylates have no ______ effect. COX-2 inhibitors….Celebrex ( celecoxib )…and APAP……………………….. also have no ______effect

Back 140

antiplatelet

Front 141

celecoxib

Back 141

COX 2 inhibitors

Front 142

disalcid

Back 142

non acetylated salicylate

Front 143

______ dont interfere with antiplatelet effects of aspirin, but when taken alone, they may cause
cardiovascular events by shifting the
balance of chemical mediators to produce
more __________ …for which
reason Vioxx ( rofecoxib ) was taken off
the market.

Back 143

COX 2 inhibitors
thromboxane A2

Front 144

__________ is used prophylactically against: - TIA/Stroke
- 1st & recurrent MI

Back 144

aspirin

Front 145

Evidence of PAD

Back 145

claudication, or
- visible arterial insufficiency, or
- ankle-brachial index < 0.

Front 146

Anyone known to have PAD,
as evidenced by: - claudication, or
- visible arterial insufficiency, or
- ankle-brachial index < 0.9
should be taking?

Back 146

ASA

Front 147

prolongs bleeding time
- increases risk of Hemorrhagic stroke
& G.I. bleed, esp. at high dose

Back 147

ASA

Front 148

Even in the absence of any
documented G.I. tract lesion ( ulcer )> ________ can cause Guaiac pos. stool

Back 148

aspirin

Front 149

are used - in Pts intolerant to aspirin
- for the same reasons as Asa
- also during stent insertion
for CAD.

Back 149

ADP receptor blockers
(plavix) clopidorgrel

Front 150

adverse effect of the ADP receptor blockers

Back 150

neutropenia-must monitor the blood

Front 151

The intrinsic & extrinsic pathways of
coagulation both eventually convert ______ to ______. Thrombin converts _____ to _________ forming a thomrbus.

Anticoagulants inhibit the action of _____ (Heparin and lepirudin) or the syn of thrombin (Warfarin)

Back 151

prothrombin to thrombin
fibrinogen to fibrin

thombus

thrombin

Front 152

bind anti-thrombin and activate it
to inhibit the action of thrombin

Back 152

heparins

Front 153

DVT & PE
- AMI
- Post-op Hip replacement
- in Dialysis machines

Back 153

heparin or LMWH

Front 154

the anticoagulants of choice in
pregnancy because they don’t
cross the placenta

Back 154

hep or LMWH

Front 155

Heparin is monitored usng the ____
keep at what levels?

Back 155

monitored by the aPTT
( 1.5 – 2.5 x normal )

Front 156

are replacing I.V. heparin because:
- given s.c…so outpatient use
- usually don’t need aPTT

Back 156

LMWHs: - enoxaparin ( Lovenox )
- dalteparin ( Fragmin )

Front 157

enoxaparin (lovenox)

Back 157

LMWH

Front 158

dalteparin (fragmin)

Back 158

LMWH

Front 159

main complication of heparin

Antidote?

Back 159

hemorrhage

lower dose
stop drug
protamine sulfate

Front 160

protamine doesnt work as well as an antidote for __

Back 160

LMWH

Front 161

contraindications for heparin or LMWH

Back 161

Bleeding disorders
- Recent Hemorrhagic Stroke
- GI ulcer
- Uncontrolled HTN
- Recent brain, spinal or eye surgery
- others

Front 162

non bleeding comps of heparin or LMWH

Back 162

Hypersensitivity Reactions
- Chills / Fever
- Urticaria
- Anaphylaxis
- Thrombocytopenia

Front 163

A rare but serious complication of Heparin

For thrombocytopenia plus thrombosis, must do what?

Back 163

Thrombocytopenia plus Thrombosis
(too complicated…just remember )



must DC Heparin
- may substitute lepirudin

Front 164

A direct thrombin antagonist that
binds thrombin and blocks its thrombogenic action

Back 164

is lepirudin ( Refludan )

Front 165

lepirudin ( Refludan )

Back 165

direct thrombin antagonist

Front 166

Warfarin ( coumadin )

Back 166

Vit. K antagonist”

Front 167

Several coagulation factors require ___ as a cofactor in hepatic synthesis

Coumadin deactivates ____ and prevents its reactivation.

Back 167

vit K

Vit K

Front 168

Monitor Coumadin how?

Back 168

monitored by the PT
( 1.5 – 2.5 x normal )

Front 169

Antidote for coumadin-induced bleeding

Back 169

oral vitamin K

Front 170

For severe coumadin-induced bleeding

Back 170

use I.V. Vit. K
or fresh frozen plasma

Front 171

Many drugs ↑ or ↓ the effect of warfarin

Back 171

so you must know what
else the patient is taking

Front 172

This antiplatelet should never be used in pregnancy

Back 172

warfarin

Front 173

alteplase (streptase)

Back 173

thrombolytic

Front 174

streptokinase (streptase)

Back 174

thrombolytics

Front 175

The thrombolytics bind and convert plasminogen to ________ to dissolve fibrin clots

Back 175

plasmin

Front 176

Alteplase has greater affinity for plasminogen
already bound to fibrin in a clot, therefore
it is _____ selective

Back 176

fibrin

Front 177

fibrin selective drug

Back 177

alteplase

Front 178

STK binds free plasminogen in plasma, so it induces a ___ ___ ___ and increases risk of hemorrhage

Back 178

systemic fibrinolytic state

Front 179

antidote for “fibrinolytic state” (caused by STK(

Back 179

Aminocaproic acid ( Amicar

Front 180

Thrombolytics are Contra-indicated

Back 180

- healing wounds
- pregnancy
- recent CVA
- metz CA

Front 181

used for acute thromboembolic disease
( AMI, Stroke, PE controversial )

What time frame is this?

Back 181

thrombolytics

2-6 hours

Front 182

For an AMI, intra-coronary delivery of a
thrombolytic is most successful, but may not be possible in __ to __ hrs, so often given ___

Back 182

2-6
IV

Front 183

given for Fe defic anemia

for how long

Back 183

ferrous sulfate

3-6 mos

Front 184

side effects of Fe

Back 184

constipation
black stools

Front 185

Parenteral Fe-therapy is reserved
for Pts

Back 185

who can’t tolerate or absorb oral Fe:
- inflammatory bowel dis.

Front 186

Parenteral Fe-therapy, i.m. or .i.v

Back 186

Iron Dextran ( DexFerrum )

Front 187

may be caused by: - ↑need, in pregnancy & lactation
- alcoholism  ↓folate absorp.
- folate-antagonist drugs:
- trimethoprim

Back 187

Folate-deficiency anemia ( megaloblastic )
may be

Front 188

given for folate def anemia

Back 188

generic folic acid

Front 189

folate antagonist drug

Back 189

trimethorpim

Front 190

caused by:
- Decreased Intrinsic Factor - pernicious anemia
- gastric resection etc
- Dietary deficiency-RARE

Back 190

Vit B12-deficiency anemia ( megaloblastic ) is

Front 191

For dietary B12-deficiency

Back 191

oral B12 ( cyanocobalamin )

Front 192

For pernicious anemia & other B12 malabsorption

Back 192

- i.m cyanocobalamin to normalize
- Nascobal nasal gel to maintain

Front 193

In B12-deficiency anemia, folic acid will correct the anemia per se, but the neurologic
effects of B12-deficiency will get worse:
- Paresthesias and/or tinnitus, decd vibration sense, balance problems

Back 193

.

Front 194

Unless the specific cause of megaloblastic anemia…
… B12 or Folate deficiency…is definitively determined

Back 194

megaloblastic anemia should
be treated with both B12 and Folic acid

Front 195

For severe anemia of: - End-stage renal
- HIV
- CA

Back 195

Erythropoietin ( Epogen )
( Procrit )
- plus Fe-supplement

Front 196

is now used to treat Sickle Cell disease.
- dilutes HbS by stimulating ↑production
of HbF
- also reduces painful crises by delaying
polymerization of HbS  ↓sickling.
- safety of longterm use not yet known.

Back 196

hydroxyurea

Front 197

drugs for A flutter

Back 197

propranolol
verapamil

Front 198

to treat A fib

Back 198

propranolol or amiodarone + anticoagulant (coumadin)

Front 199

Drugs for SVT--AV nodal re entry

Back 199

propranolol or verapamil

Front 200

Drugs for acute ventricular tachycardia (in AMI)

Back 200

lidocaine or amiodarone

Front 201

drugs for v fib not responding to electrical defibrillation

Back 201

amiodarone or lidocaine

Front 202

Out of propranolol, verapamil, lidocaine, and amiodarone, which act on atria and which act on ventricles

Back 202

P, V on atria
L and A on ventricles

Front 203

ASA and NSAIDs inhibit cox in all tissues and platelets. Thromboxane A2 is secreted by plateletes and causes platelet aggregation.

phospholipase A 2 converts to arachidonic acid, which goes to lipoxygenase and COX 1 and 2.

Back 203

.

Front 204

_______ permanently acetylates COX 1, thereby disabling COX-1
- thereby preventing TBX-2
- thereby preventing clots

Back 204

ASA

Front 205

____ has antiplatelet, antipyretic, and analgesic effects at low doses.

Its antiinflammatory effects really only occur at ____ doses

Back 205

ASA

high

Front 206

ibuprofen

Back 206

NSAID

Front 207

naproxen

Back 207

NSAID

Front 208

Most modern NSAIDs must be used in very high doses for true anti inflammatory effect

Some people have HS reactions to ASA, including what?

Back 208

. urticaria
bronchospasm (aspirin sensitive asthma)

Front 209

ASA has been associated with Reye's sybdrome in children, so should use APA for viral things in kids.

It is antipyretic and analgesic. Is it anti infllamatory or antiplatelet?

Back 209

No

Front 210

At high doses, APAP causes this?
Antidote is ____.

A moderate overdose of ASA causes ____, ____, ___. ____

Back 210

hepatic necrosis
NAC
salicysm (NV, tinnitus, hyperventilation, respiratory alkalosis)

Front 211

A toxic ovrdose of ASA causes?

Back 211

salicylate intoxication (convulstions, hypoventilation, resp and metabolic acidosis)

Front 212

indocin (indomethacin) is an ____ and is generally used for

Back 212

NSAID
gout

Front 213

ASA should not be used for gout. Why?

Back 213

because at low-dose it
↓ renal urate excretion

Front 214

a .powerful NSAID that:
- can be given I.M.
- is used in the ED
for migraine

Back 214

toradol (ketorolac)

Front 215

toradol (ketorolac)

Back 215

NSAID

Front 216

Certain prostaglandins produced by ____ protect ths gastric mucosa. ASA and NSAIDs inhibit Cox 1 and 2. Inhibiting Cox 1 causes ulcers. The Cox2 inhibitor (_____) leaves gastric mucosa protected. Cox 2 inhibitors have no ______ effect

Back 216

COX1
celecoxib
anti platelet effect

Front 217

celebrex (celexoib)

Back 217

COX 2 inhibitor

Front 218

good for musculoskeletal pain
- better than opioids for inflammation pain
- not good for visceral pain ( use opioid )

Back 218

ASA and NSAIDs

Front 219

monetlukast (singulair)

Back 219

leukotriene modifier

Front 220

MoA for leukotriene modifiers

Back 220

inhibit lipoxygense, or..
- Singulair ( montelukast ) - block leukotriene receptors

Front 221

These agents are anti-inflammatory because they
inhibit phospholipase A2, but also because they
inhibit lymphocytes (chronic inflammatory cells

Back 221

steroids (
glucocorticoids
- corticosteroids
- adrenocorticosteroids

Front 222

Good first choice for OA

Back 222

APAP

Front 223

modern NSAIDs and DMARDS are used for more serious forms of arthritis like

Most rheumatologists now use a combo of DMARDs

Back 223

Rheumatoid, lupus

Front 224

In most cases for RA, _____ is combined with another DMARD

Back 224

methotrexate (rehumatrex)

Front 225

TNF alpha antagonist

Back 225

enbrel (etanercept)

Front 226

…………………….……..approved for: - rheumatoid arthritis
- psoriatic arthritis
- skin psoriasis

Back 226

enbrel (etanercept)

Front 227

For rheumatoid or psoriatic arthritis,
many experts are now using

Back 227

Methotrexate plus Etanercept

Front 228

tx for acute gouty attack? (largely replaced colchicine)

Back 228

indocin (indomethacin)

Front 229

__________ is used for gout prophylaxis, esp after starting allopurinol therapy.

Back 229

colchicine

Front 230

_____-- inhibits xanthine oxidase, preventing the production of uric acid, and is used to lower serum uric.

Never give ____ during a gout attack-makes it worse.

Back 230

allopurinol (zyloprim)

Front 231

When cancer cells are killed in chemo, purines are processed into excess ___ ___. Thus, _____ is used for prophylaxis in chemo.

Back 231

uric acid
allopurinol

Front 232

Another way to lower serum uric acid (other than allopurinol)

Back 232

increase renal excretion

uricosuric drugs (probenecid, sulfinpyrozone)

Front 233

probenecid

Back 233

uricosuric drug

Front 234

- Sulfinpyrozone

Back 234

uricosuric drug

Front 235

usually for trauma pain, cancer or
other visceral pain, for which
NSAIDs are inadequate

Back 235

opioid

Front 236

morphine

Back 236

strong opioid

Front 237

methadone

Back 237

strong opioid

Front 238

fentanyl

Back 238

strong opioid

Front 239

meperidine

Back 239

strong opioid

Front 240

sufentanil

Back 240

strong opioid

Front 241

codeine

Back 241

medium potency opioid

Front 242

oxycodone

Back 242

medium opidoid

Front 243

hydromorphone

Back 243

medium opioid

Front 244

naloxone (naltrexone)

how fast does it work?

Back 244

opioid antagonist

within 60 sec

Front 245

THe analgesic effect of opioids is mediated by ___ receptors.

Back 245

mu

Front 246

how do opioids releive pain?

Back 246

1) raising the threshold for
pain neurotransmission in
the spinal cord & elsewhere

2) changing the brain’s
perception of pain..i.e. the
Affective component of pain



(pt says feel the pain, but dont care)

Front 247

MCC of death from opioid overdose

Back 247

respiratory depression

Front 248

_____ are strong GI anti motility agents, even short term use can cause major constipation.

Morphine and most opioids can cause ____ pupils. Most other drug overdoses cause pupillary ______.

Back 248

pinpoint (mniosis)
dilation (mydriasis)

Front 249

_______ synthetic opioid preferred for labor pain because of shorter action

Back 249

meperidine

Front 250

synthetic opioid whose transmucosal formulary is used for breakthrough pain in cancer

Back 250

fentanyl

Front 251

meperidine

Back 251

synthetic opioid

Front 252

_________ is a better anti tussive than morphine but with less analgesic/euphoric effects. In most OTC anti tussives, ____ replaces codeine

Back 252

codeine

dextromethorphan

Front 253

codeine + APAP (___) is PA prescibable for mild to mod pain

Back 253

tylenol # 3

Front 254

Extreme anxiety
- Vomiting
- Hyperventilation
- Hypethermia
- Diarrhea, Rhinorrhea &
Lacrimation

are withdrawal sn of?

Back 254

opioid addiction

Front 255

______ is used for detox of heroin and opioid addicts because more prolonged and milder withdrawal effects

Back 255

methadone

Front 256

______- can be used for opioid detox and can be given at ANY PRACTICE OFFICE because it has shorter and less severe withdrawal sn than methadone

Back 256

buprenorphine

Front 257

The term hyponotic also means ___.
Some anxiolytics and hypnotics are used specifically as sleep aids.

Currently, main class of drugs used as anxiolytics are _______.

Most end in what syllables?

Back 257

sedative
benzodiazepeines

zolam or sepam

Front 258

Benzodiazepines bind which receptors in the CNS?

Back 258

GABAA receptors
( γ-aminobutyric acid )

Front 259

The main inhibitory
neurotransmitter in the CNS

Back 259

GABA

Front 260

The physiologic changes driven by ↑sympathetic
activity during anxiety

Back 260

tachycardia
- palpitations -↑respiratory rate
- sweating
- trembling

Front 261

benzos act by binding to___________receptors
& opening membrane___
channels  hyperpolarizing
the membranes  fewer
“anxiety” action potentials

Back 261

GABA
Cl-

Front 262

GABA recptors--happens everywhere in the CNS, but part of the brain where it causes anxiolysis is the ____ ___, aka the emotional brain.

Benzos have nither _____ nor _____ activity, but they can be used for anxiety that accompanies ____ or _____

Back 262

limbic system

depression, schizophrenia

Front 263

Benzos vary greatly in their duration of action, but should NTO be used for a long time (weeks and moths), because they are _____.

Back 263

addictive

Front 264

diazepam (valium)

Back 264

benzodiazepine

long acting

Front 265

For chronic stress, use the long acting benzo ______.

For panic disorder, use the short acting ____.

Back 265

diazepam (valium)

alprozolam (xanax)

Front 266

alproxolam (xanax)

Back 266

short acting benzo

Front 267

To calm the unruly or delirious patient in
the emergency dept, use

Back 267

lorazepam ( Ativan )

Front 268

lorazepam ( Ativan )

Back 268

benzo

Front 269

A non-benzo that is as effective as benzos for
generalized anxiety..but has slow onset of action…days/weeks

Back 269

buspirone ( Buspar )

Front 270

A sedative H1 antihistamine with little potential for
abuse..used for anxiety in Pts with h/o drug abuse

Back 270

hydroxyzine ( Atarax )

Front 271

hydroxyzine ( Atarax )

Back 271

benzo

Front 272

buspirone ( Buspar )

Back 272

benzo

Front 273

The 3 benzos most commonly used for sleep

Back 273

1) long-acting flurazepam ( Dalmane )
( may cause daytime sedation )
2) intermediate-acting temazepam ( Restoril ) ( used when Pt has trouble staying asleep )
3) short-acting triazolam ( Halcion )
( used when Pt has trouble getting to sleep )

Front 274

flurazepam ( Dalmane )

Back 274

long acting benzo (may cause daytime sedation)

Front 275

temazepam ( Restoril )

Back 275

intermediate acting benzo (when pt has trouble staying asleep)

Front 276

triazolam ( Halcion )

Back 276

short acting benzo when pt has trouble getting to sleep

Front 277

good benzo for getting to sleep
good benzo for staying asleep
benzo that can cause daytime sedation

Back 277

triazolam (halcion)

temazepam (restoril)

flurazepam (dalmane(

Front 278

Benzos for sleep often cause
_____ insomnia or ____ sedation.

Back 278

rebound
daytime

Front 279

All Benzos should be used short-term and
if not, withdrawn slowly
why?

Back 279

because they - cause addiction
- cause withdrawal signs
- mix too well with ETOH

Front 280

GABA receptor antagonist and antidote for benzos

Back 280

flumazenil ( Romazicon )

Front 281

flumazenil ( Romazicon )

Back 281

GABA receptor antagonist

Front 282

zolpidem ( Ambien )

Back 282

non benzo hypnotic for sleep

Front 283

zaleplon ( Sonata )

Back 283

non benzo hyponotic for sleep

Front 284

Non benzo hyponotics for sleep like _____, ____, _____and ____ are replacing benzos for sleep

Back 284

eszopiclone ( Lunesta )
& ramelteon ( Rozerem
zolpidem ( Ambien )
zaleplon ( Sonata

Front 285

Why are non benzos replacing benzos for sleep

Back 285

- less disturbance of sleep architecture
- less next-day sedation
- less rebound insomnia

Front 286

eszopiclone ( Lunesta )

Back 286

non benzo sleep aid

Front 287

only sleepers that can be recommended for long term use (6 mos)

Both are good to decrease SLEEP LATENCY (help pts get to sleep)

Back 287

eszopiclone ( Lunesta )
& ramelteon ( Rozerem )

Front 288

rozerem (ramelteon)

Back 288

melatonin receptor antagonist

Front 289

All antidepressants potentiate.the effects of
________ and/or _____in the brain

Back 289

serotonin
NE

Front 290

SSRIs have largely replaced the TCAs and MAOIs why?

Back 290

- have fewer & less severe side effects
- are much safer in overdose

Front 291

side effects of TCAs

Back 291

orthostatic hypotension
- sedation
- dry mouth & blurred vision

Front 292

SSRIs have little effect at which receptors?

Back 292

muscarinic
- α-adrenergic
- or histamine receptors

Front 293

SSRIs usually take __ wks for improvement, ___wks for full effects

Back 293

2>12

Front 294

Pts who dont respond to one SSRI may respond to another.

They are also used for what conditions?

Back 294

GAD
- OCD
- PMDD
- Bulimia
- Panic disorder

Front 295

typical side effects of SSRIs

Back 295

- sexual dysfunction
- sleep disturbances

Front 296

For SSRI-induced sexual dysfunction,
i.e ED, loss of libido, anorgasmia etc
, do what?

Back 296

- decrease SSRI dose
- add Viagra
- or switch to…
bupropion ( Wellbutrin )
or mirtazapine ( Remeron )

Front 297

Wellbutrin ( bupropion can cause what?

Back 297

seizures
- ↓craving for nicotine

Front 298

_______ is a sedating SRRI and may help people sleep

Back 298

paxil (paroxetine)

Front 299

paxil (paroxetine)

Back 299

SSRI

Front 300

Prozac ( fluoxetine )

Back 300

SSRI

Front 301

____is an activating SSRI and - activating
- may help fight fatigue
- may cause anxiety

Back 301

prozac (fluoxetine)

Front 302

Any SSRI plus an MAOI can cause what?

Back 302

Serotonin Syndrome:
- hyperthermia
- myoclonus & rigidity
- ∆ mental status

Front 303

SSRIs are not effective against which type of pain?

Which are good for neuropathic pain?

Back 303

neuropathic pain

SNRIs or TCAs

Front 304

Effexor ( venlafaxine )

Back 304

SNRI

Front 305

Cymbalta ( duloxetine )

Back 305

SNRI

Front 306

______ or ______ may treat depression in the
patient for whom an SSRI fails

Back 306

Effexor ( venlafaxine ) or
Cymbalta ( duloxetine )

Front 307

____ or ____ are good for neuropathic pain.

Back 307

SNRIs
TCAs

Front 308

an atypical antidepressant that works
at a yet unidentified receptors:
- no sexual disturbances
- used for smoking cessation, as
Zyban ( wellbutrin )

Back 308

wellbutrin (bupropion)

Front 309

wellbutrin (bupropion)

Back 309

atypical antidepressant

Front 310

an atypical antidepressant that works
at serotonin and α2 receptors:
- no sexual disturbances
- very sedating, used for sleep

Back 310

Remeron ( mirtazapine )

Front 311

Remeron ( mirtazapine )

Back 311

atypical antidepressant

Front 312

________block serotonin & NE re-uptake
into neurons. They also block serotonin, a adrenergic, muscarinic, and histamine receptors.

Side effects?

Back 312

TCAs

- orthostatic hypotension
- glaucoma aggravation

Front 313

TCAs have a really narrow ther. index. Should be used with caution in what pts? Why?

Back 313

used with caution in bipolar disease
because they may unmask mania

Front 314

Good TCA for neuropathic pain

Back 314

Elavil (amitryiptyline)

Front 315

Elavil (Amitrriptyline)

Back 315

TCA

Front 316

The enzyme ___normally inactivates excess
NE, dopamine & serotonin
in the synaptic spaces. They thus function well as antidepressants.

Back 316

MAO

Front 317

Nardil ( phenelzine )

Back 317

MAOI

Front 318

Parnate ( tranylcypromine )

Back 318

MAOI

Front 319

Tyramine in foods like aged cheese, red wines, beer cause release of _____ from nerve terminals everywhere. So if an MAOI is on board, what sn?

Back 319

catecholamines


- headache
- tachycardia
- hypertensive crisis
- arrhythmias
- stroke

Front 320

Used to treat MAOI induced hypertensive crisis

Back 320

Minipress ( prazosin

Front 321

MAOIs are not used much anymore because of food interactions. Are indicated for what?

When When switching from an MAOI to any other
antidepressant , or visa versa, must do what?

Back 321

atypical depression

you must discontinue the first
drug for 2 to 6 weeks
before starting the other

Front 322

used prophylactically & acutely against mania in bipolar disorder.

Mechanism is unknonwn.

Back 322

lithium

Front 323

Lithium has very narrow TI. Side effects of overdose?

Back 323

ataxia
tremors

Front 324

____---- and ____ are often used in place of lithium for mania

Back 324

Tegretol ( carbamazepine ) or
Depakene ( valproic acid )

Front 325

Depakene ( valproic acid

Back 325

anticonsulvant

Front 326

Tegretol ( carbamazepine )

Back 326

anticonvulsant

Front 327

_____ are used for Schizophrenia
- Mania
- Delirium

Back 327

neuroleptics

Front 328

In schizophrenia, neuroleptics do not eliminate the
fundamental thought disorders, but do what?

Back 328

but they ↓hallucinations & ↓delusions

Front 329

_________are divided into 3 categories--low potency typicals, high potency typicals, and atypicals.

Back 329

neuroleptics

Front 330

Thorazine ( chlorpromazine )

Back 330

low potency typical neuroleptic

Front 331

Haldol ( haloperidol )

Back 331

high potency typical neuroleptic

Front 332

Typical neuroleptics cause antipsychotic effects primarily by?

Back 332

blocking dopamine D2 receptors
in the mesolimbic system

also block D2 receptors in the
nigrostriatal pathway

Parkinson’s-like EPS

Front 333

Other EPS?

Back 333

Dystonia
- akathisia
- tardive dyskinesia

Front 334

Blocking D2 receptors with a ______………………………………... is similar to the death of dopaminergic
neurons in the Parkinson’s

which leaves cholinergic overbalance
in the Extrapyramidal system
which causes EPS

Back 334

neuroleptic

Front 335

As with Parkinson’s, one way to treat the
cholinergic overbalance & EPS

Back 335

is with a pure anticholinergic
- Cogentin ( benztropine )
or a very anticholinergic antihistamine
- Benadryl ( diphenhydramine )

Front 336

cogentin (benztropine)

Back 336

anticholinergic

Front 337

benadryl (diphenhydramine)

Back 337

anticholinergic antihistamine

Front 338

Typical neuroleptics usually get ride of what schizophrenia sn? Not as good with?

Back 338

positive sn (hallucinations, delusions)

negative sn (blunted affect, apathy, impaired attention)

Front 339

clozaril (clozapine)

Back 339

atypical neuroleptic

Front 340

risperdal (risperidone)

Back 340

atypical neuroleptic

Front 341

Adv of atypical neuroleptics?

Back 341

mixed blocking effects on dopamine and serotonin receptors, so little or no EPS

AND improve both positive and negative sn

Front 342

side effect of clozaril (clozapine)

so thus is reserved for whom?

Back 342

can cause fatal agranulocytosis
( must monitor WBC )


is reserved for severe schizophrenia
refractory to other drugs

Front 343

All neuroleptics take several weeks to work. They can cause what?

Back 343

Neuroleptic malignant syndrome--potentially fatal muscle rigidity and fever

Front 344

tx for Neuroleptic malignant syndrome

Back 344

stop the neuroleptic and..
- give the muscle relaxant, dantrolene

Front 345

Location of alpha 1A receptor

antagonism causes?

prototype antagonist?

Back 345

prostate smooth muscle
increased urinary stream

tamsulosin (flomax)

Front 346

tamsulosin (flomax)

Back 346

alpha 1 A blocker

Front 347

Location of alpha 1B receptor?

antagonism causes?
ex?
agonism causes?
ex?

Back 347

vasodilation
(doxasozin-cardura)

vasoconsriction--EPI/NE

Front 348

doxazosin (cardura)

Back 348

alpha 1B blocker

Front 349

receptor location of alpha 2 receptrs? agonism causes?
ex?

Back 349

medullary vasomotor center

↓ Sympathetic clonidine
Vasomotor Tone ( Catapres )
Center
↓ HR
↑ Vasodilation

Front 350

clonidine (catapres)

Back 350

alpha 2 blocker

Front 351

beta 1 receptor location

antagonism causes?
ex?
agonism causes?
ex?

Back 351

heart, kidney
decd HR, contractility, decd renin, decd BP
propranolol (inderal)
Incd HR, incd contractility, incd renin, EpiNE,

Front 352

beta 2 receptor location?

agonism causes?
prototype agonist?

Back 352

airways
arterioles

bronchodilation, increased vasodilation

albuterol, EPi, NE

Front 353

cross effect of alpha 1A blockers?

Back 353

- Flomax also blocks alpha 1B to some extent, so possible……………  Postural Hypotenison

Front 354

cross effects of alpha 1B blockers

Back 354

- Doxazosin also blocks alpha 1A pretty well, so …………………….  ↑ Urinary stream in BPH
Blockers - Doxazosin blocks arteriolar alpha 1B, so …………………………..  Postural Hypotension
- Doxazosin also blocks arteriolar alpha 1B in the NOSE, so possible  Nasal Congestion

Front 355

decongestants like pseudoephedrine, phenylephrine, are sympathomimetics. They agonize arteriolar alpha ___ everywhere, so vasoconstriction causes what?
also agonize beta 1 in heart, so possible what?

Back 355

alpha 1B

nasal decongestion
increased BP

palpitations

Front 356

Beta 2 agonists like albuterol can also agonize beta 1 in heart, causing possible

Back 356

palpitations

Front 357

Doxasozin and other azosin drugs are ___ blockers. They decrease TPR and BP by binding alpha 1b receptors--causing arteriolar dilation. They also blocke alpha 1b in the veins, causing venodilation and decreasing venous return.

May cause what sn?

Thus should be taken what time of day?

NOT FIRST LINE for htn

Back 357

alpha

reflex tachycardia
postural hypotension and syncope
should be taken at bedtime

Front 358

alpha agonists are not antagonists per se. Because they decrease sympathetic tone form the spinal cord to the heart and blood vessels, they are sympathoplegic.

Back 358

j

Front 359

clonidine

Back 359

alpha agonist

Front 360

methyldopa

Back 360

alpha agonist

Front 361

alpha agonists pharmacologically imitate what the carotid sinus reflex (aka baroreceptor reflex) does when blood pressure is too BP. They intercede in the reflex at the level of the vasomotor center in the medulla by binding and agonizing alpha 2 receptors there. The result is new output from the vasomotor center down the reticulospinal tract in the spinal cord. The reticulospinal tract axons make inhibitory synaptic contact with preganglionic sympathetic cell bodies in the intermediolateral cell column at various levels of the spinal cord. This decreases the sympathetic output, or tone, to the heart and blood vessels, causing what?

They do NOT cause what?

Back 361

decd heart rate
incd vasodilation
decreased BP

postural hypothension

Front 362

3 types of beta blockers

Back 362

non selective )block beta 1 in heart and beta 2 in airways)
selective (block beta 1 more than beta 2)
combined alpha 1 block and non selective beta block

Front 363

propranolol

Back 363

non selective beta blocker

Front 364

atenolol

Back 364

selective beta blocker

Front 365

metoprolol

Back 365

selective beta blocker

Front 366

labetalol

Back 366

combined alpha 1 block and non selective beta block

Front 367

carvedilol

Back 367

combined alpha 1 block and non selective beta block

Front 368

common uses for selective or non selective beta blockers

Back 368

Chronic Angina
- Status post-MI
- Migraine prophylaxis
- Hyperthyroid Sx

Front 369

timolol

Back 369

beta blocker

Front 370

open angle glaucoma tx, to decrease aqueous humor secretion

Back 370

timolol

Front 371

The reason beta blockers may be a good choice
for Hypertension

Back 371

They also block the beta receptors
in the juxtaglomerular apparatus,
so  ↓ Renin  ↓ Angiotensin II
↓ Aldosterone

Front 372

dont give non selective beta blockers to?

dont give to diabetics why?

Back 372

astma or emphysema pt

It may mask the sympathetic warning
signs…tremor & tachycardia…of
hypoglycemia

Front 373

Never stop a beta blocker abruptly, may cause _____.

Adverse effects of beta blockers?

Back 373

dysrhytmias

- ↑Triglycerides & ↓HDL
- Erectile dysfunction
- Exercise intolerance

Front 374

These HTN drugs are bad for raynauds pt becuase may also block arteriolar beta 2--peripheral vaoconstriction-cold hands and feet

Back 374

non selective beta blockers

Front 375

labetolol

Back 375

combined alpha and beta blocker

Front 376

carvedilol

Back 376

combined alpha and beta blocker

Front 377

_________ may be used instead of hydralazine for HTN of pregnancy

Back 377

labetolol

Front 378

Labetolol and carvedilol are sometimes used in heart failure. Because ____ works fast, it can be used in hypertensive emergencies.

Side effects of the alpha blockade?

Back 378

labetolol

postural hypotension (dizziness)

Front 379

vancomycin (glycopeptides)

Back 379

cell wall synthesis inhibitor

Front 380

beta lactams:
Penicillins
- Cephalosporins
- Carbapenems

Back 380

cell wall synthesis inhibitors

Front 381

- Macrolides
- Aminoglycosides
- Streptogramins
- Tetracylines

Back 381

protein synthesis inhibitors

Front 382

fluoroquinolones

Back 382

DNA replication inhibitors

Front 383

sulfamethoaxazole
trimethoprim

Back 383

folate antagonist

Front 384

UTI anti septic abx

Back 384

nitrofurantoin

Front 385

often need empiric treatment with
broad-spectrum Abx before you get
the culture & sensitivity results

Use a broad spectrum abx when the infx is likely polymicrobial


abx should be bactericidal, not static for critically ill pts.

The BBB prevents penetration of non lipid-soluble
drugs into the CNS, except when there is
CNS inflammation (capillary leakiness )


Most drugs are metabolized by the liver or secreted/excreted by the kidneys.

Before prescribing any drug, Ask yourself if the patient…
- is pregnant
- might be pregnant
- has drug allergies
- is old
- has ↓ kidney/ liver function

Back 385

l

Front 386

Uses for prophylactic abx or antivirals

Back 386

before bowel surgery, joint replacement etc
or ANTIVIRALS - before dental procedure in Pt with artificial
heart valve.
- against TB and meningitis in those exposed
- zidovudine before HIV-pos mother gives birth

Front 387

Broad-spectrum Abx, or combinations of Abx - can cause superinfections ( overgrowth ) of
one unaffected organism, typically in the
upper respiratory, G.I. or G.U. tracts

Ex of antibiotic that often causes it?
Ex of superinfection?

Back 387

clindamycin

c diff colitis
candida albicans or fungi

Front 388

Cat _ = safe in human studies, at least in first trimester.

For category B. C, D, sometimes potential drug benefit outweighs the risk.

Cat __ = known fetal risk
Cat __ = no good, known risk outweighs benefit

Back 388

A

D
X

Front 389

abx for susceptible streptococcal infx
- all stages of syphilis ( T. pallidum )

Back 389

Penicillin G (IV)
VK (oral)

Front 390

These are penicillinase resistant
Methicillin is not used because it's too toxic

Back 390

Cloxacillin, Dicloxacillin, Nafcillin, Methicillin

Front 391

cloxacillin

Back 391

anti staph penicillin

Front 392

dicloxacillin

Back 392

anti staph penicillin

Front 393

methicillin

Back 393

anti staph peniccilin

Front 394

nafcillin

Back 394

anti staph peniccilin

Front 395

Main Uses: - Susceptible Staph infx:
- Cellulitis - Endocarditis

Back 395

anti staph penicillins
Cloxacillin, Dicloxacillin, Nafcillin, Methicillin

Front 396

amoxicillin

Back 396

aminopenicillin

Front 397

ampicillin

Back 397

aminopenicillin

Front 398

_____ is an abx that is famous for a bad rash

Back 398

ampicillin

Front 399

abx for Main uses: - URIs
- UTIs
- PUD ( H. pylori )

Back 399

aminopenicillins (amoxicillin, ampicillin)

Front 400

piperacillin

Back 400

anti pseudomonal PCN

Front 401

carbenicillin

Back 401

anti pseudomonal PCN

Front 402

ticarcillin

Back 402

anti pseudonomal PCN

Front 403

of the anti pseudomonal PCNs, which is PO?

Susceptible to what?

Back 403

carbenicillin
beta lactamases

Front 404

abx: - Main uses: - Pseudomonas
- HAP & other nosocomial

Back 404

anti pseudomonal PCNs

Piperacillin, Carbenicillin, Ticarcillin, others

Front 405

BETA-LACTAM + BETA-LACTAMASE-
INHIBITOR COMBINATIONS

Back 405

zosyn = Piperacillin tazo
unasyn = ampicillin + sulbactam
augmentin = amox clavulanate

Front 406

Main uses: - GI infx
- Abscesses
- HAP & other nosocomial
- Diabetic wounds

good empiric coverage of nosocomial infections

Which are NOT anti pseudomonal

Back 406

beta lactam + beta lactamase inhibitor combos

zosyn = piperacillin tazo
augmentin = amox clav
unasyn = ampicillin + sulbactam

augmentin and unasyn

Front 407

The ________ are less beta lactamase susceptible than other PCNs

Back 407

cephalosporins

Front 408

cephalexin

Back 408

1st gen cephalosporin

Front 409

abx for cellulitis and surgical prophylaxis

Back 409

1st gen cephalosporin

cephalexin

Front 410

cefaclor

Back 410

2nd gen cephalosporin

Front 411

Better Gram neg coverage than 1st Gen
- Main Uses: - Gonorrhea
- Surgical prophylaxis

Back 411

2nd gen cephalosporin

cefaclor

Front 412

cefixime

Back 412

3rd gen cephalosporin

Front 413

ceftriazone

Back 413

3rd gen cephalosporin

Front 414

- Better Gram neg coverage than 2nd Gen
- Main Uses: - Meningitis
others - HAP
- Lyme dis
- Febrile neutropenia

Back 414

3rd gen cephalosporins

cefixime
ceftriazone

Front 415

cefepime

Back 415

4th gen cephalosporin

Front 416

- Main Uses: - Anti-pseudomonal
- HAP / nosocomial
- Febrile neutropenia

Back 416

Cefepime ( Maxipime )

4th gen cephalosporin

Front 417

imipenem/cilastratin

Back 417

carbapenem

Front 418

meropenem

Back 418

carbapenem

Front 419

ertapenem

Back 419

carbapenem

Front 420

Not first-line agents
- Broadest-spectrum Abx available
- Stable to most beta-lactamases
- Main Uses:
- Mixed aerobic/anaerobic infx
- Nosocomial
- Febrile neutropenia

Back 420

carbapenems
Imipenem/cilastatin, Meropenem, Ertapenem

Front 421

___ is a cabapenem that can cause seizures in high doses

Back 421

impinem

Front 422

vancomycin

Back 422

glycopeptide

Front 423

dalbavancin

Back 423

glycopeptide

Front 424

- Poor bioavailability po - May cause Red Man syndrome
- Main Uses:
- I.V. DOC for MRSA
- C. diff colitis , po, only if
metronidazole fails

Back 424

Vancomycin, Dalbavancin

glycopeptides

Front 425

gentamicin

Back 425

aminoglycosides

Front 426

streptomycin

Back 426

aminoglycosides

Front 427

neomycin

Back 427

aminoglycosides

Front 428

tobramycin

Back 428

aminoglycoside

Front 429

Protein synthesis inhibitors
- Synergize well with beta-lactams ( wall inhibitors )
- Cause nephro~ and ototoxicity ( monitor! )
- Main Uses: - Aerobic Gram neg bacilli ( Pseudomonas )
- Enterococci
- Neomycin only topical… too toxic

Back 429

aminoglycosides

gentamicin, streptomycin, neomycin, tobramycin

Front 430

clindamycin

Back 430

LINCOSAMIDES

Front 431

lincomycin

Back 431

LINCOSAMIDES

Front 432

often cause c diff
main uses:

acne
aspiration pneumonia

Back 432

lincosamides

clindamycin
lincomycin

Front 433

erythromycin

Back 433

macrolide

Front 434

clairthromycin

Back 434

macrolide

Front 435

azithromycin

Back 435

macrolide

Front 436

excellent lung penetration
often cause NVD
Main Uses:
- Strep CAP & URIs
- Atypicals: Mycoplasma & Chlamydia
- PUD…Clarithromycin
- Mycobacterium Avium Intracell. in AIDS

Back 436

macrolides
Erythromycin, Clarithromycin, Azithromycin

Front 437

telithromycin

Back 437

ketolides

Front 438

macrolide analogue

main uses--macrolide resistant strep pneumo

Back 438

telithromycin (ketolide)

Front 439

tetracycline

Back 439

tetracycline

Front 440

doxycycline

Back 440

tetracycline

Front 441

main uses:
mycoplasma and chlyamidia
tick borne diseases

Back 441

tetracycline (doxy and tetracycline)

Front 442

side effects of tetracyclines

Back 442

cause tooth discoloration < 12
cause photosensitivity

Front 443

good CNS penetration
may cause gray baby syndrome

Back 443

chlroamphenicol

Front 444

quinupristin

Back 444

streptogramin

Front 445

dalfopristin

Back 445

streptogramin

Front 446

synercid

Back 446

streptogramin

Front 447

synercid (quinupristin/dalfopristin)

Back 447

streptogramin

Front 448

kills VRE faecium, not faecalis

- Main Uses:
- VRE
- MRSA when can’t take other Abx

Back 448

streptogramins
(Quinupristin / Dalfopristin ( Synercid )

Front 449

linezolid

Back 449

oxazolidinones

Front 450

main uses:
MRSA
VRE

Back 450

linezolid (oxazolidinones)

Front 451

Cause disulfiram reaction with ETOH
- Main Uses: - C. diff colitis
- PID
- Protozoa…Giardia lamblia

Back 451

metronidazole (nitromidazoles)

Front 452

metronidazole

Back 452

nitromidazole

Front 453

ciprofloxacin

Back 453

fluoroquinolone

Front 454

levofloxazin

Back 454

fluoroquinolone

Front 455

gatifloxacin

Back 455

fluoroquinolones

Front 456

Main Uses: - CAP… Strep. pneum
- Anthrax ..Cipro
- Traveler’s diarrhea…Cipro
- STDs & prostatitis, not syphilis

Back 456

fluoroquinolones

(cipro, levo, gati)

Front 457

Bactrim/Septra is what?

Back 457

trimpethoprim/sulfamethoxazole

Front 458

Main Uses:
- UTIs
- Opportunistic infx ..pneumocystis
- Toxoplasma gondii

Back 458

bactrim/septra
(TMP/SMX)

Front 459

macrodantin

Back 459

nitrofurantoin

Front 460

main use: UTIs

Back 460

macrodantin (nitrofurantoin)

Front 461

_____--- agents block transmission between the parasympathetic postganglionic
fiber and the target organ, i.e. salivary glands, heart, G.I. tract etc

Back 461

antimuscarinic

Front 462

_______ is the prototype antimuscarinic. It causes atropine causes reversible, competitive blockade of muscarinic receptors, which can be overcome by a
greater concentration of acetylcholine (Ach) itself or equivalent muscarinic agonist.
- atropine has little effect on the nicotinic cholinergic receptors (NN) of the autonomic ganglia.
- atropine does not distinguish among the M1, M2 or M3 muscarinic receptor subtypes

Back 462

atropine

Front 463

dicyclomine (bentyl)

Back 463

atropine analogue-antimuscarinic

Front 464

tropicamide (mydriacil)

Back 464

atropine analogue-antimuscarinic

Front 465

3 main categories of drugs that are not anticholinergics but have anticholinergic effects

Back 465

antihistamines
TCAs
antipsychotics

Front 466

dimenhydrinate (dramamine)

Back 466

antihistamine

Front 467

diphenhydramine (benadryl)

Back 467

antihistamine

Front 468

amitriptyline (elavil)

Back 468

TCA

Front 469

haloperidol (Haldol)

Back 469

antipsychotic

Front 470

tropicamide (mydriacil)

Back 470

antimuscarinic for pupillary dilation

Front 471

cyclopentolate (cyclogil)

Back 471

antimuscarinic for pupillary dilation

Front 472

before the advent of histamine H2
receptor blockers and acid (proton) pump inhibitors, antimuscarinic drugs were used mainly to treat
peptic ulcer disease because they reduce vagal-muscarinically-induced gastric acid secretion. They are
still used as adjuncts in such treatment if the H2 blocker is not fully effective or is not well tolerated.
Quaternary (4O ) compounds are preferred in order to avoid CNS side effects (they don’t cross the
blood-brain barrier), but peripheral side effects such as blurred vision, dry mouth, constipation and
urinary retention will still occur.

Back 472

l

Front 473

dicylomine (bentyl)

Back 473

antimuscarinic for IBS and peptic ulcer

Front 474

hyoscyamine (levsin)

Back 474

antimuscarinic for IBS and peptic ulcer

Front 475

Gastroesophageal reflux disease (GERD) and peptic ulcer disease are related. In GERD, gastric acid, either normally or excessively secreted, refluxes past a faulty lower esophageal sphincter into the lower esophagus (or upper esophagus if one is recumbent) and causes burning pain commonly known as heartburn. In peptic ulcer disease, the gastric mucosal barrier is faulty and even normal levels of acid may erode the gastric musculature. In either case, acid is the injurious agent and its secretion is wonderfully blocked in most patients by either an H2 blocker or a proton pump inhibitor…which are NOT classified as anticholinergics.

Back 475

,

Front 476

atropine _ diphenoxylate (lomotil)

Back 476

anti muscarinic for traveler's diarrhea

Front 477

loperamide (imodium AD)--contains no antimuscarinic, only the opioid

Back 477

for traveler's diarrhea and mild GI tract hypermotility

Front 478

tolterodine (Detrol)

Back 478

antimuscarinic for overactive bladder and urge incontinence

Front 479

FOR ASTHMA & CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD): Since parasympathetic
muscarinic activity in the bronchial tree causes bronchoconstriction, an inhaled antimuscarinic such as ipratropium will permit bronchdilation and facilitate breathing. The localized delivery of these bronchodilators as inhalants helps limit systemic antimuscarinic side effects. The same applies to the inhalant formularies of other bronchodilators (see further below)

Back 479

;

Front 480

ipratropium (atrovent)

Back 480

antimuscarinic for astma and COPD

Front 481

tiotropium (spiriva)

Back 481

antimuscarinic for asthma and COPD

Front 482

FOR PARKINSON’S DISEASE: Antimuscarinics were used especially before the development of levodopa,
which is the drug of choice today. However, antimuscarinics are still used as adjunctive
therapy since no single drug, levodopa or other, is fully effective over the typically prolonged

course of the disease.This problem is an overbalance of cholinergic muscarinic activity

Back 482

;

Front 483

benztropine (cogentin)

Back 483

antimuscarinic for parkinsons

Front 484

diphenhydramine (benadryl)

Back 484

antimuscarinic for parkinsons

Front 485

scopalomine (transderm scop)

Back 485

antimuscarinic for motion sickness

Front 486

diphenhydrinate (dramamine)

Back 486

antimuscarinic for motion sickness

Front 487

meclizine (antivert)

Back 487

antimuscarinic (antihistamine) for motion sickness

Front 488

Severe cholinergic excess tends to occur in rural communities where insecticides are used, or where wild poisonous mushrooms are mistakenly picked and eaten (Amanita muscaria etc). The result of either is a medical emergency. Because therapy must treat effects in both the peripheral and central nervous systems, a tertiary amine (not quaternary) must be used for its ability to penetrate the blood brain barrier. Atropine is usually the drug of choice, but large repeated doses over 24 to 48 hours may be required.

Back 488

l

Front 489

trimethaphan (arfonad)

Back 489

ganglionic blocking drug (for poisoning caused by a cholinomimetic agent)

Front 490

initial DOC for simple partial seizure

Back 490

phenytoin

Front 491

abnormal activity in one
limb or muscle group
- no LOC

Back 491

simple partial seizure

Front 492

LOC, but Pt does not fall
- bizarre behavior or mouth
movements instead
- sensory hallucinations

Back 492

complex partial seizure

Front 493

initial DOC for complex partial seizure?

tonic clonic (grand mal siezure)

Back 493

phenytoin

Front 494

type of generalized seizure
- LOC, falling, motor convulsion
- followed by “postictal
depression” (confusion )

Back 494

tonic clonic seizure

Front 495

a type of generalized seizure
- kids 3 to 5 yo, lasts until puberty

Back 495

absence seizure

Front 496

DOC for absence seizure

Back 496

ethosuximide

Front 497

type of generalized seizure
- kids 3 mos to 5yr with a
high-fever illness
- tonic clonic
- no medication needed


tx?

Back 497

febrile seizure

no tx needed

Front 498

DOC for seizures during pregnancy

Back 498

phenobarbital

Front 499

DOC for seizures of eclampsia

Back 499

mag sulfate or diazepam (valium)

Front 500

DOC for status epilepticus

which lasts longer?

Back 500

I.V. diazepam (Valium ) or
I.V. lorazepam ( Ativan )


lorazepam

IV drip of phosphenytoin is also started for long term control

Front 501

side effects of phenytoin, esp in children

Back 501

gingival hyperplasia
coarsening of facial features

Front 502

Other uses for the anticonvulsant, carbamazepine ( Tegretol )………………………..-

Back 502

in trigeminal neuralgia
- in bipolar disease

Front 503

In type ___ HS reactions, prior exposure to allergen/antigen causes mast cell growth and IGE production by B lymphocytes.

Mast cell degranulation causes release of preformed histamine, which binds histamine H receptors, esp on blood vessels and airway mucosa, causing

arteriolar dilation, capillary and venule leakiness, mucus production, smooth muscle contraction, bronchoconstriction.

If allergen was ingested, can also get intestinal smooth muscle contraction, abdominal cramps and diarrhea, urticaria (itchy red wheals)

Once the process gets going, a Late Phase response 2 to 8 hours later sustains it and/or makes it worse and is caused by chemical junk-induced recruitment of various inflammatory cells, most characteristically eosinophils. In fact, a high eosinophil count (eosinophilia) is a diagnostic marker of atopy, i.e. increased tendency for IgE-mediated (or Type I ) allergic reactions.

Back 503

1

Front 504

However it is caused, whether by inhalation or ingestion of the allergen, the components of the Early Phase response
can cause severe dyspnea (allergic asthma or drug reaction). The more localized allergic response in allergic rhinitis & conjunctivitis is famous for causing itchy eyes and nose. Other symptoms are, of course, sneezing, nasal congestion, rhinorrhea, red watery eyes. How else do you decide that this patient has an allergy?

Back 504

pale nasal mucosa
- clear discharge
- no fever

Front 505

ANTIHISTAMINES: - competitively antagonize histamine H1 receptors, with no effect on H2 receptors
- are divided into 1st generation and 2nd generation agents.

___ ___ agents have sedative effects because they cross the blood-brain barrier and enter the
CNS  Central anticholinergic effects  fatigue & sleepiness.
- have peripheral anticholinergic effects  - dry mouth & eyes, blurred vision
- urinary retention &constipation
- may have anti-emetic activity
- help relieve the itch, plus they attenuate all the above responses


prototype

Back 505

first gen

diphenhydramine (benadryl)

Front 506

hydoxyzine

Back 506

sedative first gen antihistamine

Front 507

promethazine (phergan)

Back 507

sedative first gen antihistamine

Front 508

promethazine

Back 508

anti emetic first gen antihistamine

Front 509

meclizine (antivert)

Back 509

anti emetic and anti vertigo first gen antihistamine

Front 510

___ is incontrollable restlessness
___ is spastic torticollis
____-- is incessant mouth, tongue, jaw movement

Back 510

akathisia
acute dystonic reactions
tardive dyskinesia

Front 511

benztropine (cogentin)

Back 511

anticholinergic (muscarinic receptor blocker)

Front 512

antihistamines are rarely used to treat EPS caused by parkinsons.
ex?

Back 512

benadryl

Front 513

dimenhydrinate (dramamine)

Back 513

OTC antihistamine

Front 514

scopalamine (transderm scop)

Back 514

antimuscarinic for treatment of motion sickness and vertigo

Front 515

The combination of a sedative antihistamine and any other CNS-depressing drug ( ETOH,
benzodiazepines, barbiturates, opiods ) can be devastatingly additive…i.e. fall asleep in the shower.

Back 515

f

Front 516

The patient with known Narrow Angle Glaucoma: If the pupils of a person with a narrow anterior
chamber (angle) are caused to dilate significantly for too long, it will close the angle even more and
decrease drainage

or…anything that
inhibits contraction of the cholinergically activated papillary constrictor muscle…such as the anticholinergic
effect of a 1st generation antihistamine.

Back 516

,

Front 517

However, for the average child with a nasty, itchy reaction to something (poison ivy etc) who can’t sleep because of it, OTC Benadryl is a good choice because its sedative effect will put her/him to sleep as it slakes the itch.

Back 517

f

Front 518

3 major categories of anti emetics

Back 518

antihistamines / anticholinergics
- dopamine antagonists
- serotonin antagonists ( 5-HT3 receptor blockers )

Front 519

______ are used mostly for motion sickness and vertigo

Back 519

anti emetic antihistamines/anticholinergic

Front 520

3 ex of anti emetic antihistamines/anticholinergics

Back 520

meclizine ( Antivert )
- dimehydrinate ( Dramamine )
- scopolamine ( Transderm Scop )

Front 521

These aused primarily for nausea due to: - chemo~ or radiation therapy
- surgery

Back 521

anti emetic dopamine antagonists

or anti emetic 5HT3 antagonists

Front 522

promethazine (phenergan)

Back 522

antihistamine/anti emetic dopamine antagonist

Front 523

prochlorperazine (compazine)

Back 523

anti emetic dopamine antagonist

Front 524

dolasetron (anzemet)

Back 524

anti emetic 5HT3 angatonist

Front 525

best anti emesis against chemo

Back 525

5-HT3 antagonist + a corticosteroid…- methylprednisolone, or..
- dexamethasone

Front 526

best drug for anticipatory nausea

Back 526

lorazepam (ativan)

Front 527

2nd gen antihistamines do not have do not have peripheral anticholinergic effects
- do not have sedative or anti-emetic effects (don’t cross the blood brain barrier)

Back 527

.

Front 528

desloratadine (clarinex)

Back 528

2nd gen antihistamine

Front 529

cetirizine (zyrtec)

Back 529

2nd gen antihitamine

Front 530

For pruritis due to atopic dermatitits

Back 530

zonalon (doxepin) cream

Front 531

For ocular itch of allergic conjunctivitis

Back 531

Acular ( ketorolac ) oph. soln. = NSAID

Front 532

A nasal spray for the nose itch of allergic rhinitis

Back 532

Astelin (azelastine) = 1st Gen.antihistamine nasal spray

Front 533

decongestants - are all alpha-1 adrenergic agonists which cause vasoconstriction (of arterioles ) in the nose if taken by nasal spray… and vasoconstriction everywhere if taken orally ...see below. Constriction of arterioles in the nasal mucosa decreases both blood pressure and flow in the capillaries and venules…this decreases mucosal edema (congestion) by limiting further fluid leakage into the tissue, while at the same time permitting the fluid which has already leaked into the tissue to be reabsorbed and carried away by the same capillaries and venules.

- if taken orally, these alpha-1 agonists are delivered everywhere and:

agonize the alpha 1 receptors on systemic arterioles, causing ____
affect beta 1 receptors in hte heart, causing _____

best way to prevent this?

Back 533

increased BP
increased HR and palpitations

nasal spray

Front 534

Remember that giving an antihistamine to someone with sinusitis is not a good idea. Mucus production
is stimulated by both cholinergic parasympathetic fibers and local histamine, so the antihistamine and its
anticholinergic effect will tend to dry up ( inspissate ) the mucus, leaving infected “mucus bricks” in the
sinuses.

- Give an antitussive only to the person with a non-productive cough. Do not give it to the person with a
productive cough; inhibiting this cough will only increase the chance that the bronchitis will become
pneumonia.

- Do not give a systemic decongestant ( sympathomimetic ) to a person who has hypertension or a
dysrhythmia.

Back 534

k

Front 535

fluticasone (flonase)

Back 535

nasal steroid

Front 536

nasonex (mometasone)

Back 536

nasal steroid

Front 537

Compared to: - Antihistamines ….._____________ are most effective against all symptoms of allergic rhinitis, including:
- Decongestants - rhinorrhea
- Mast celll stabilizers - itch
- Anticholinergics - congestion
- Leukotriene blockers - sneezing

They may cause local irritation, rarely bloodly dishcarge, candida overgrowth, systemic side effects only with very high doses

Back 537

nasal steroids

Front 538

sedative antihistamine ex

Back 538

Benadryl Allergy
( diphenhydramine )

Front 539

non sedative antihistamine

OTC and prescription ex?

Back 539

Alavert Zyrtec
( loratadine ) ( cetirizine )

Front 540

prescription nasal antihistamine

Back 540

Astelin
( azelastine )

Front 541

OTC nasal decongestant ex

Back 541

Neosynephrine 12 HR Spray
( phenylephrine )

Front 542

OTC and prescription oral decongestant ex

Back 542

Sudafed Entex PSE
( pseudoephedrine ) ( pseudoephedrine

Front 543

oral decongestant + antihistamine OTC and prescription ex

Back 543

ActiFed Cold & Allergy Zyrtec-D
(phenylephrine + chlorpheniramine ) (cetirizine + pseudoephedrine)

Front 544

nasal steroid prescription ex

Back 544

flonase (fluticasone)

Front 545

nasal mast cell stabilizer

Back 545

nasalcrom (cromolyn sodium)

Front 546

antitussive OTC and prescription ex

Back 546

Delsym 12 HR Tessalon
( dextromethorphan ) ( benzonatate )

Front 547

sinusitis is often viral, hard to dtx from bacterial. Dx is bacterial sinusitis when?

most common pathogens?

Back 547

- at least 7 days of symptoms, including:
- maxillary pain or tenderness in the face or upper molars (especially unilateral )
- purulent nasal discharge
- most common pathogens = Strep. pneum and H. flu

Front 548

best starting abx for sinusitis?

also good?

Back 548

amoxicillin (probably high dose), with or without clav or TMP-SMX

or zithromax, biaxin

Front 549

slender rod-shaped bacteria that are
acid-fast, because they take stain well
but do not decolorize with acid solvents

cause what infections?

Back 549

mycobacteria

TB, leprosy

Front 550

5 first line drugs for TB

2nd line are less effective or more toxic

2 important 2nd line?

Back 550

Rifampin
Isoniazid
Pyrizinamide
Ethambutol
Streptomycin

fluroquinolones (ciprofloxacin) or macrolides (azithromycin)

Front 551

____is the most potent anti Tb drug?

_____ is the most potent anti leprosy drug?

because of drug resistance, TB is always treated with multiple drugs.

Back 551

izoniazid

rifampin

Front 552

traditional short course TB tx?

Back 552

IRP = Isoniazid + Rifampin + Pyrazinamide x 2 mos…then
Isoniazid + Rifampin………………. .x 4 mos

Front 553

isoniazid often causes ____ deficiency, which causes peripheral neuritis (paresthesias) and is treated with ____.

Back 553

pyridoxine

pyridoxine (vitamin B6)

Front 554

side effect of ethambutol?

Back 554

optic neuritis
monitor visual acuity

Front 555

triple drug regimen for leprosyg

Back 555

Rifampin + Dapsone + Clofazimine

Front 556

fungal infections are often chronic.
systemic mycoses are often life threatening. What is the 4th MCC of septicemia?

Tx for life threatening systemic mycoses?

Back 556

candidemia

amphotericin B

Front 557

drug options for systemic mycoses

Back 557

amphotericin B
ketoconazole ( Nystatin )
- itraconazole ( Sporonox )
- fluconazole ( Diflucan

Front 558

____-- has largely replace ketoconazole (nystatin)

Back 558

itraconazole (sporonox)

Front 559

The Trichophyton species are fungi that
cause the various superficial skin infections
called Tineas. These fungi are ………………………………………………….… also called Dermatophytes

Back 559

,

Front 560

protozoal infections are most common in underdeveloped tropical countries.

They are eukaryotes, with metabolic processes closer to humans, so difficult to treat.

Back 560

.

Front 561

2 most iportant GI tract protozoa

both are treated with?

Back 561

Giardia lamblia
- Entamoeba histolytica, aka
- Amebic dysentery
- Amebiasis


metronidazole (flagyl)

Front 562

a protozoa that commonly infects humans is?

found in what?

treated with?

Back 562

toxoplasma gondii

cat poop, infected meat

pyrimethamine

Front 563

____ both infects RBC (ertythrocytic stage) and liver (exoerythrocytic stage)

Back 563

p falciparym

Front 564

________ (DOC) or _____- for erythrocytic stage of malaria

________ for exo ertyrhocytic stage
_______ for resistant p falciparum

Back 564

chloroquine, duinine

promaquine

quinine

Front 565

worms are either nematodes, trematodes, or cestodes. Worms with a complete GI tract are the ______. _____ is used to treat them.

Back 565

nematodes
mebendazole (vermox)

Front 566

mebendazole (vermox)

Back 566

anti helminthics

Front 567

treat nematode that causes visceral larva migrans with?

Back 567

thiabendazole (mintezole)

Front 568

____ are worms that look like a leaf. Most important one is?

Treated with?

Back 568

trematodes

schistosoma-schistosomaiasis

praziquantel

Front 569

praziquantel

Back 569

anti helminthic

Front 570

4 classes of viral diseases for which anti viral drug treatment is available

Back 570

Respiratory infections
- Influenza A & B
- Respiratory Syncytial virus
2) Hepatitis B & C
3) Herpes
- Herpes 1 & 2
- Herpes zoster
- Cytomegalovirus
4) AIDS

Front 571

used for prevention and treatment of flu A only

Back 571

symmetrel (amantadine)

flumadine (rimantadine)

Front 572

vaccination against flu A is preferred, but amantadine and rimantadine are used when?

Back 572

those at high risk
have not been vaccinated
or during epidemics

Front 573

___________- is a viral neuramidase inhibitor used for prevnetion or treatment of both Flu A and B

MUST be given 48 hours in ADVANCE

Back 573

tamiflu (oseltamavir)

Front 574

_- is used for RSV in infants, children, and adults with hep C

Back 574

rebetol (ribavirin)

Front 575

most common causes of chr hepatitis?

Back 575

hep b and c

Front 576

chr hep b is treated with?

chr hep C?

Back 576

intron A (interferon A)
interferon a plus ribavirin

Front 577

doc for herpes encephalitis

Back 577

zoviraz (acyvclovir)

Front 578

2 drugs for acute herpes (genital, labial, zoster) or to suppress herpes (genital, labial)

which is more potent with a greater oral bioavailability?

Back 578

zovirax (acyclovir)
valtrex (valacyclovir)

valtrex (valacyclovir)

Front 579

__________ is approved only for CMV (CMV retinitis)

Back 579

Cytovene ( ganciclovir

Front 580

Cytovene ( ganciclovir

Back 580

antiviral

Front 581

zidovudine ( AZT )
- didanosine ( ddl )
- zalcitabine ( ddC )
- stavudine ( d4T )
- saquinavir
- ritonavir

Back 581

anti HIV drugs

Front 582

Cholinomimetics agonize the muscarinic cholinergic (M2 or M3) receptors on the parasympathetic target organ.

Cholinomimetic drugs which agonize cholinergic receptors themselves are categorized as direct acting cholinomimetics.

A srug which antagonizes acetylcholinesterase is an indirect acting cholinomimetic.

Direct acting cholinomimetics?

Back 582

bethanechol (urecholine)
carbachol (miostat)
pilocarpine (pilocar)

Front 583

behanecol (urecholine)

Back 583

direct cholinomimetic

Front 584

carbachol (miostat)

Back 584

direct cholinomimetic

Front 585

pilocarpine

Back 585

direct cholinomimetic

Front 586

reversible indirect acting cholinomimetic

Back 586

neostigmine
physostigmine
donepzel
galantamine

Front 587

irreversible indirect acting cholinomimetic

Back 587

organophosphates

Front 588

donepezil

Back 588

indirect cholinomimetic

Front 589

glantamine

Back 589

indirect cholinomimetic

Front 590

edrophonium (tensilon)

Back 590

reversible cholinomimentic

Front 591

neostigmine

Back 591

indirect cholinomimetic

Front 592

physostigmine

Back 592

indirect cholinomimetic

Front 593

2 drugs for AD (indirect cholinomimetics)

Back 593

donepezil
glantamine

Front 594

The ciliary body lies behind the peripheral edge of the iris and it produces aqueous humor at a
steady rate. This fluid flows medially (toward the pupil) in the space between the back of the
iris and the front of the lens (the posterior chamber). It then flows forward through the pupil
itself and into the space between the front of the iris and the back of the cornea (the anterior
chamber). Since it is produced at a steady rate in order to nourish the lens and cornea, it must
exit the anterior chamber somehow or fluid pressure will build up. To exit, it is absorbed by a
network of trabeculae at the angle formed where the back of the cornea meets the front–
peripheral edge of the iris. The trabeculae lead to a conjunctival vein called the canal of
Schlemm (aka sinus venosus sclerae) which drains it into the conjunctival venous blood.

- Most irises are rather flat and permit the above angle in the anterior chamber to be rather wide
or "open", as seen below, bottom-left.

- However, an anatomic variant is the iris that bulges forward and creates a “narrow angle” as
seen below, bottom-right This narrow angle variant can be detected by shining a penlight
from the lateral side of the eye across the front. Below, top-right, a light has been shined from
the lateral side of the right eye; the bulging iris casts a shadow on the medial side, from which
one concludes that this eye has a narrow angle

A narrow angle puts one at risk for rapid build-up of fluid pressure if the pupil becomes
significantly dilated for several hours…because as the iris contracts radially it becomes
fatter. This can acutely compress the already narrow angle, causing acute obstruction of fluid
outflow and rapid increase in intra-ocular pressure within 1 to 5 hours.

Back 594

k

Front 595

Eye exam  dilated eyes (mydriasis) from mydriatic drugs..Mydriacyl (tropicamide)
or Cyclogyl (cyclopentolate)
- Pre-op atropine (anticholinergic)
- Antidepressants…which, as a class, also have anticholinergic effects
- Nebulized bronchodilators (beta 2 agonists)  cross react with alpha 1 receptors of
radial muscles of iris

- Several hours of the above dilation causes: - acute eye pain
- blurred vision…see halos around lights
- nausea & even abdominal pain


conjunctivitis, steamy cornea, pupil dilated &
unreactive to light
- permanent vision loss within 2 –5 days

Back 595

kj

Front 596

Acute narrow angle glaucoma is a medical emergency. Must
first decrease pressure by re-constricting the pupil and re-opening
the angle with:

Back 596

muscarinic agonist : - pilocarpine (Pilopine) drops, or
-carbachol (Isopto-carbachol) drops
plus

- anticholinesterase: - physostigmine ophth. Ointment, or

both cause ciliary contraction, which stretches the trabeculae and further enhances drainage.

A carbonic anhydrase inhibitor is also used in order to decrease fluid production.

Front 597

In chronic open angle glaucoma, aka Simple glaucoma, Wide angle glaucoma

- No angle problem here. Inc’d intra-ocular pressure is due to inadequate trabecular drainage of
unknown etiology: - the glaucoma is more typically bilateral
- Idiopathic…familial or related to diabetes


Long term drug treatment is required. Main players?

Back 597

he main players are
in fact alpha-agonists and beta-blockers (subjects of the next handouts) and carbonic
anhydrase inhibitors and prostaglandins,

Front 598

These _
enhance drainage by causing ciliary muscle contraction and thereby
stretching the trabeculae.
- Muscarinic agonists: pilocarpine & carbachol
- Anticholinesterase: physostigmine

Back 598

cholinomimetics

Front 599

_______ decrease aqueous humor production because it has high HCO3.

Back 599

carbonic anhydrase inhibitors

Front 600

acetazolamide (Diamox)

Back 600

carbonid anhydrase inhibitor

Front 601

brinzolamide (Azopt )

Back 601

carbonic anhydrase inhibitor

Front 602

prostaglandins increase drainage of the eye. Ex?

Back 602

bimatoprost (lumigan)

Front 603

bimatoprost (lumigan)

Back 603

prostaglandin

Front 604

non selective alpha agonists increase eye ___---
alpha 2 agonists decrease ____ production

beta blockers decrease ___ production.

Back 604

drainage
humor
humor

Front 605

dipivefrin (propine)

Back 605

alpha agonist (nonselective)

Front 606

- aproclonidine ( Iopidine

Back 606

alpha 2 agonist

Front 607

brimonidine ( Alphagan )

Back 607

alpha 2 agonist

Front 608

this beta blocker can be used to decrease humor production

Back 608

betaxolol (betoptic)

Front 609

For conditions in which the G.I. tract or U.T smooth muscle activity is
depressed in the absence of obstruction:
- Post-Op Ileus: =atony or paralysis of stomach or bowel. This occurs
after a surgeon has his or her fat mitts in your
abdomen …the viscera say What was that!? Let’s
be still for a while.

- Urinary Retention, occurs: - post-op
- postpartum
- after spinal cord injury or disease,
i.e neurogenic bladder

- Reflux esophagitis: - inadequate lower esophageal sphincter tone
(GERD)

Back 609

m

Front 610

For post op ileus, urinary retention, reflux esophagitis, which drugs should be used?

Back 610

- muscarinic agonist: -bethanechol (Urecholine )
- anitcholinesterase: - neostigmine (Prostigmin )

Front 611

tx for sjogrens

Back 611

muscarinic agonist

Front 612

Ab-mediated reduction in the number of functional nicotinic NM receptors
( MG ) in neuromuscular junction.
- anticholinesterases are very useful, but not direct-acting cholinomimetics

Back 612

MG

Front 613

_____ is used to dx MG. (Will see improvement within 5 min)

Back 613

tensilon

Front 614

longterm treatment for MG

Back 614

pyridostigmine ( Mestinon ) or..
anticholinesterases - neostigmine (Prostigmin ) or

Front 615

neostigmine (prostigmin)

Back 615

anticholinesterase

Front 616

pyridostigmine ( Mestinon )

Back 616

anticholinesterase

Front 617

donepezil (aricept)

Back 617

anticholinesterase for AD

Front 618

galantamine (reminyl)

Back 618

anticholinegesterase for AD

Front 619

REVERSAL OF SURGICAL NEUROMUSCULAR BLOCKADE: Pharmacologically-induced skeletal
muscle relaxation is needed for most surgeries that take place under general anesthesia. This is achieved
by neuromuscular blockade, that is, imposed dysfunction of the motor endplate. It causes skeletal
muscle paralysis that is due not to upper or lower motor neuron dysfunction, but due to transmitter
dysfunction at the neuromuscular junction.
After the surgery, it is desirable to remove this blockade. The blockade is reversed by injecting an anticholinesterase that will increase the amount Ach and its half-life at the motor endplate. The anticholinesterases typically used to reverse blockade are

Back 619

neostigmine (Prostigmin)
- pyridostigmine (Mestinon)

Front 620

Insecticide anticholinesterases are found in bug bombs, spray cans, flea collars, crops sprays etc.
Since they are cholinomimetics, human exposure causes excessive parasympathetic vegetative
manifestations,…i.e miosis, salivation, hyperactive bowel sounds, lethargy, and either bradycardia
(muscarinic effect) or tachycardia (nicotinic effect). A mnemonic that captures most of the effects
is DUMBELS:

antidote?

Back 620

- Diarrrhea, Urination, Miosis, Bronchorrhea, Bronchospasm, Bradycardia, Excitation: anxiety,
fasciculations, seizures, Lacrimation, Salivation

atropine-competitively blocks all muscarinic receptors, M1, M 2, M 3 etc. It
has little effect on nicotinic receptors. Will give symptomatic relieve, but
may need repetitive doses.

Front 621

tx for tinea corporis, cruris, pedis, versicolor

Back 621

spectazole (econazole)

Front 622

tinea capitis

Back 622

nizoral shampoo (ketoconazole)

Front 623

tinea unquiiun (onychomycosis)

Back 623

sporonox (itraconazole)
lamisil (terbinafine)

Front 624

oral candidiasis

Back 624

diflucan (fluconazole)

Front 625

cutaneous candidiasis

Back 625

spectazole (econazole)

Front 626

vulvar candidiasis

Back 626

gyne lotrimim (clotrimazole)
diflucan (fluconazole)

Front 627

vaginal candidiasis

Back 627

gyne lotrimim (clotrimazole)
diflucan (fluconazole)

Front 628

pruritis

Back 628

Benadryl (diphenhydramine) tabs, liq. OTC
- Zonalon (doxepin

Front 629

dry skin tx

Back 629

aveeno

lac hydrin

Front 630

tx for atopic dermatitis (eczema)

Back 630

steroids-aclovate (alclometasone)

elidel (pimecrolimus)

Front 631

acne vulgaris tx

Back 631

clindagel (clindamycin)

Front 632

acne rosacea tx

Back 632

metrogel (metronidazole)
clindagel (clindamycin)

Front 633

impetigo tx

Back 633

bactroban (mupricin)

Front 634

allergic condtact derm tx

Back 634

calamine lotion
lidex (flucinonide)

Front 635

for bad poison ivy

Back 635

Oral Prednisone * (see page bottom)

If someone has a large patch on even one limb, covering
say, 20% of an arm, it is going to drive her crazy for
weeks. Use oral prednisone. Even 20 mg a day for just
a week will work wonders, far beyond any topical
treatment. Within hours of the first dose, the patient will
see the poison ivy begin to recede.

Front 636

urticaria/angioedema

Back 636

Atarax (hydroxyzine) tabs, syrup, Rx
- Zyrtec (ceterizine) tabs, syrup

Front 637

warts

Back 637

freezing with liquid nitrogen
- Aldara (imiquimod) cm, Rx
- Duofilm (salicylic acid), OTC

Front 638

scabies tx

Back 638

elimite (permethrin)

Front 639

pediculosis tx

Back 639

nix (permethrin)

Front 640

psoriasis tx

Back 640

limited:
- Enbrel (etanercept), inj., Rx
- Dovonex (calcipotriene)

generalized:

Soriatane (acitretin), Rx
- Rheumatrex ( methotrexate), Rx

Front 641

varicella tx

Back 641

For pruritis: - Benadryl (diphenhydramine), tabs or liq.,OTC
- Calamine lotion, OTC
Antipyresis: - acetaminophen

Front 642

herpes tx

Back 642

Fever sore & Facial: - Abreva (docosanol) cm, OTC
- Valtrex (valacyclovir) caps, Rx

Genital: - Valtrex

Zoster: - Valtrex

Front 643

herpetic neuralgia

Back 643

Zostrix (capsaicin) cm, OTC

- Neurontin (gabapentin) caps, Rx

Front 644

Develpment and preofression of diabetes--nephropathy, neuropathy, retinopathy. Directly related to level of glycemic control.

HBA1c is proportional to average blood glucose over last 3-4 mos.

Target HBA1c?
Things that decrease insulin resistance?

Back 644

7

exercise and wt loss

Front 645

insulin resistance plus progressive beta cell dcline over time is?

Back 645

type 2 diabetes

Front 646

danger of insulin or oral anti hyperglycmic agents?

the tighter the glycemic control, the higher the risk of hypoglycemia

Back 646

Hypoglycemia

Neuroglycopenia

Coma


hypoglycemia

Front 647

3 classes of oral insulin drugs

Back 647

Insulin Secretagogues
- Insulin Sensitizers
- Alpha-Glucosidase Inibitors

Front 648

________help the beta cells secrete more insulin

__________make existing insulin work better
- thereby decrease insulin secretion


___________inhibit the hydrolysis of oligosaccharides
to glucose and other sugars
- thereby blunt the postprandial ↑ in BG

Back 648

secretagogues
sensitizers
glucosidase inhibitors

Front 649

tolbutamide

Back 649

sulfonylurea (secretagogue)

Front 650

glimepiride

Back 650

sulfonylurea (secretagogue)

Front 651

glipizide

Back 651

sulfonylurea (secretagogue)

Front 652

glyburide

Back 652

sulfonylurea (secretagogue)

Front 653

nateglinide

Back 653

secretagogue

Front 654

repaglinide

Back 654

secretagogue

Front 655

The ______--- are famous for causing hypoglycemia and wt gain

Back 655

secretagogues

Front 656

Insulin sensitizers are?

Back 656

metformin

glitazones (pioglitazone, rosiglitazone)

Front 657

pioglitazone

Back 657

glitazone (insulin sensitizer)

Front 658

rosiglitazone

Back 658

(insulin sensitizer)-glitazone

Front 659

considered the DOC for newly
diagnosed Type 2
- also ↓ hepatic gluconeogenesis,
which is the major source high
BG in Type 2
- may cause fatal lactic acidosis

Back 659

metformin

Front 660

metformin and glitazones increase HDL, may be used in PCOS to induce ovluation.

glitazones must be monitored for what?

Back 660

liver function

Front 661

acarbose

Back 661

glucosidase inhibitor

Front 662

miglitol

Back 662

glucosidase inhibitor

Front 663

glucosidase inhibitors will cause no hypoglycemia, but do cause what?

Back 663

GI distress

Front 664

symptomatic hypoglycemia is usually treated with?

Back 664

usually treated with any source
of sucrose or fructose:
- Soda or juice
- an Orange
- Candy or sugar

Front 665

Glucosidase inhibitors may be used with
other agents…insulin, sulfonylureas etc…which
may cause hypoglycemia, in which case the treatment must be some form of ______ itself, because the glucosidase inhibitor will prevent or delay the absorption of sucrose or fructose

Back 665

glucose

Front 666

If a diabetic is so hypoglycemic that s/he cannot take
anything by mouth, the only options are

Back 666

Glucagon i.m.
- or Glucose i.v.

Front 667

physiologic insulin secretion is either basal (background, consant) or prandial (increased secretion with meals).

Different insulins are targets to replace both.

Type 1 diabetics usually need ____ doses.

Back 667

divided

Front 668

basal insulin has traditionally been supplied how?

now, basal insulin often supplied how?

Back 668

Intermediate-Acting Insulins
- NPH insulin, or
- Lente insulin, or
- Ultralente insulin
Prolonged-Acting Insulins
- Detimir insulin
- Glargine insulin

Front 669

detimir

Back 669

prolonged acting insulin

Front 670

detimir

Back 670

prolonged acting insulin

Front 671

prandial insulin usually supplied by?

Back 671

by: Ultrashort-Acting Insulins
- Lispro insulin
- Aspart insulin
- Glulisine insulin

Front 672

lispro

Back 672

ultrashort insulin

Front 673

aspart

Back 673

ultrashort insulin

Front 674

glulisine

Back 674

ultrashort insulin

Front 675

intensive tx for type I diabetes

most hypoglycemic episodes due to delayed meals, physical activity, alcohol.

Severe hyperglycemia can cause ____

Back 675

Insulin 3 to 5 times per day

HBA1C 7% = Av BG 154


DKA

Front 676

Nausea, Vomiting & Abdominal pain
- Signs of severe dehydration ……………………….……………….. from osmotic diuresis & polyuria
- Fruity breath ( acetone ) ……………………………………………..……………… from ketogenesis
- Deep breathing ( Kussmaul ), slow, normal or rapid …………….. from ketoacids  Metab. Acidemia
- Stuporous or Comatose

- Slight hypothermia
- Hypotension & tachycardia ………………………………………… from dehydration ( 4 to 5L deficit )
- 4+ Glucosuria plus ketonuria
- BG 250 to 1000
- Leukocytosis as high as 25,000 without infection
- Low arterial pH ( 7.1 ? ) ……………………………………….……………………….… from ketoacids
- Low arterial HCO3- ……………………………………………………………………….. from ketoacids

- Possible High serum K+ ……………………………..…..…………………….. because as H+ moves into
cells, K+ comes out
& enters plasma.

- But total body K+ depletion………………………………..…… from vomiting & new urinary loss of K

- High serum osmolality ( 320 ? ) ……………………………………. from hyperglycemia & dehydration

Back 676

DKA

Front 677

DKA tx

Back 677

- Immediate Regular Insulin i.v…………………………..……………...- 0.1 Unit / kg bolus
- plus 0.1 Unit / kg / hr infusion

- Immediate fluid replacement……………………………………………………….... i.v. Normal saline

- K+ replacement @20 mEq/hr i.v. starting
about 2 to 3 hours into therapy……………………………………….……- because of K+ losses above. - because correction of the
acidemia causes K+ to
move back into the cells.

- Glucose i.v. 5% ………………………………………………………...when BG has fallen to 250 mg/dl

- i.v NaHCO3 to correct acidemia…………………………………….…… only if pH falls to 7.0 or lower

Front 678

mild intermittent asthma is?

Back 678

<2/wk
>80% nl peak flow
rescue drug only---short beta 2

Front 679

mild persistent asthma-long term control

Back 679

low dose inhaled steroid

Front 680

moderate persistent asthma tx

Back 680

daily attacks\

medium dose linhaled steroid plus long acting beta 2

Front 681

albuterol

Back 681

short acting beta 2 agonist

Front 682

terbutaline (brethine)

Back 682

short acting beta 2 agonist

Front 683

Stop bronchospasm
- Work in 15 to 30 minutes
- Work for 4 to 6 hours
- No anti-inflammatory effect
- Little or no α or β1 agonism

Back 683

short acting beta 2 agonists

Front 684

salmeterol (serevent)

Back 684

long acting beta 2 agonists

Front 685

formoterol (foradil)

Back 685

long acting beta 2 agonists

Front 686

have slow onset
- are not for Rescue
- work for at least 12 hours

Back 686

long acting beta 2 agonists

Front 687

The DOCs for moderate or severe asthma

Back 687

are inhaled glucocorticoids (steroids),
which are anti-inflammatory and
reduce airway reactivity to
allergens, irritants, cold air and
exercise

Front 688

fluticasone

Back 688

inhaled steroid

Front 689

triamcinolone

Back 689

inhaled steroid

Front 690

the combo of an inhaled steroid plus a long beta 2 Creates better control of moderate
and severe asthma than all other
options ( i.e. doubling doses ) or
combinations, i.e adding cromolyn
theophylline, or anti-leukotrienes to
either beta-2 or steroid therapy.


for severe asthma, sometimes need po steroid (_______) or IV steroid (________)

But inhaled steroids will reduce or eliminate the need for po steroids

risk of growth retardation in children is negligible.

Inhaled steroids can cause oral candidiaz

Back 690

prednisone

methylprednisolone

Front 691

The alternative drugs used for moderate/severe
asthma when beta-2 agonist plus inhaled steroid
is inadequate or not well tolerated

Back 691

po Anti-leukotrienes
2) inhaled Anticholinergics
3) po Theophylline
4) inhaled Cromolyn & Nedocromil
5) sc inj. Monoclonal Ab to IgE

Front 692

montelukast (singulair)

Back 692

leukotriene receptor blocker)

Front 693

2) The inhaled anticholinergic that causes
bronchodilation and ↓mucus secretion

Back 693

ipratropium (atrovent)

Front 694

is a bronchodilator with
slight anti-inflammatory effect

Back 694

theophylline

Front 695

are mast cell stabilizers
used to block both allergen-
and exercise-induced bronchospasm

Back 695

cromolyn and nedocromil

Front 696

the monoclonal Ab that binds
IgE and prevents IgE from binding to mast cells


but it is expensive and not first line

Back 696

omalizumab (xolair)

Front 697

COPD causes airway obstruction that is
only partially reversible by
bronchodilators

___________ is a long-acting anticholinergic
used for bronchodilation
in COPD


beta 2 agonists are also used.

Often, this regimen is used?

What has little use?

Back 697

tiotropium

combination of long-acting
anticholinergic plus a long beta-2
( tiotropium + salmeterol )


inhaled steroids used only a little--mainly in severe exacerbation

Front 698

Infection with H. pylori
- ↑gastric HCl secretion
- Inadequate mucosal defense

Back 698

cause PUD

Front 699

to confirm H pylori infection

Back 699

use either: - endoscopic biopsy
- serologic test
- urea breath test

Front 700

abx treatment for h pylori permits rapid healing of ulcers, low recurrence rate.

antibiotic regimen? (TWO of)

what is added?

to increase the secretion of FI mucus, the therapy sometimes also includes what?

Back 700

Clarithromycin
- Amoxicillin
- Flagyl
- Tetracycline

PPI or H2 blocker
bismuth subsalicylate

Front 701

formulary for peptic ulcer that contain a combination of two abx + PPI or H2 blocker or bismuth

Back 701

pylera

Front 702

_ is not associated with h pylori and does not respond to abx. Gastric acid secretion is stimulated by what?

Back 702

GERD


ach, gastrin, histamine

Front 703

____________ is secreted by gastric mucosa. _______ block production of prostaglandins

Back 703

prostaglandins
NSAIDS

Front 704

About 90% of all gastric acid secretion,
including, basal, food-stimulated & nocturnal
is blocked by what?

Back 704

any H2 blocker

tagamet (cimetidine)
zantac (ranitidine)

Front 705

tagament (cimetidine)

Back 705

h2 blocker

Front 706

zantac (raniditine)

Back 706

H2 blocker

Front 707

H2 blockers and PPIs take about 45 minutes
to work, so for immediate relief

Back 707

recommend an antacid
or ½ glass of skim milk

Front 708

Cimetidine inhibits the liver’s mixed function oxidase
system

Back 708

so, it affects the metabolism of
of many other drugs…Be Careful !
Ranitidine does not.

Front 709

Because H2 blockers fail in about 50% of people with GERD, ___ are now the DOC for GERD, PUD, esophagitis, zollinger ellison.

_____ also reduce risk of blooding caused by ASA, NSAID ulcers

Back 709

PPIs

Front 710

aciphex (rabeprazole)

Back 710

PPI

Front 711

prostaglandin analogue used to prevent PUD in those who must take NSAIDs

Back 711

cytotec (misoprostol)

Front 712

are two other cytoprotectants used
for PUD. They coat the mucosa
and/or

Back 712

Sucralfate (carafate ) & Colloidal Bismuth

Front 713

is used for diarrhea-predominant
Irritable bowel syndrome ( IBS )

Back 713

immodium (loperamide)

Front 714

tx for c diff

Back 714

first Flagyl ( metronidazole )
then vancomycin if Flagyl fails.

Front 715

fiber supplements for constipation predominant IBS may cause bloating and discomfort, so what are often used?

Back 715

osmotic laxatives (milk of magnesia)

Front 716

levsin (hyoscyamine)

Back 716

anticholinergic

Front 717

For the patient with IBS who has crampy
abdominal pain

Back 717

anticholinergic / antispasmodic
Levsin ( hyoscyamine ) may be used

Front 718

stool softener laxative

Back 718

colace (docusate sodium)

Front 719

stimulant laxative

Back 719

senokot (senna)

Front 720

softener and stimulant laxative

Back 720

Peri-Colace ( docusate + senna ) ( OTC )

Front 721

bulk forming laxative

Back 721

citrucel (methylcellulose)

Front 722

osmotic laxative

Back 722

kristalose

Front 723

for IBD, an ASA like drug is used. Ex:

collectively, they are known as the ____. They work TOPICALLY on the bowel, not systemically

Back 723

5 ASA

mezalmanies

Front 724

first line drugs for UC and crohns

Back 724

mesalamines

Front 725

pentasa

Back 725

mesalamine

Front 726

asazol

Back 726

mesalamine

Front 727

rowasa

Back 727

mesalamine-enema, for rectum and sigmoid colon

Front 728

___ compounds are also used for UC and crohns

Back 728

Azo

Front 729

azufidine (sulfasalazine)

Back 729

Azo compound

Front 730

colaza (balsalazide)

Back 730

azo compound

Front 731

_________ enemas, foam, suppositories may also be used for UC or proctitis

Back 731

hydrocortisone

Front 732

for severe flare ups of either UC or crohns, this may be sued

Back 732

po or IV steroids

Front 733

two classes of drugs used specifically for crohns

Back 733

Flagyl or Cipro, for their anti-inflammatory effects,
and Remicade ( infliximab ) ..a TNF-α blocker

Front 734

remicade (infliximab)

Back 734

TNF alpha blocker

Front 735

Tension H/A
- Migraine “
- Cluster “
- Hangover “
- Caffeine withdrawal H/A
- Rebound H/A
(aka Medication Overuse H/A)

ex of what kind of HA

Back 735

primary

Front 736

Glaucoma
- Temporal arteritis
- Meningitis
- Intracranial: - hemorrhage
- abscess
- mass lesion

ex of what kind of headache?

Back 736

secondary

Front 737

Sinusitis
- Severe HTN
- Lyme or other bite
- Influenza


varying importance, cause what type of HA

Back 737

seoncdary

Front 738

If a pt comes for help with migraines

It’s another migraine
& s/he needs your
drug-help….or…

2) Something is weirdly
new about this
headache and YOU
better pay attention.


Get a full history
and get a FULL NEURO

because: 1) If it’s a NON-benign H/A, whatever is causing it is
often poking some other structure(s) in the brain,
so you may find some neurologic deficit(s) that
help you conclude this H/A is serious.

2) If there are no neurologic deficits, it is about
85% probable that it is a benign H/A , which helps
you reassure the patient.

Back 738

.

Front 739

When a patient complains of recurrent
headaches with no hint of etiology in the H&P,
and/or they do not respond to your treatment, do this

Back 739

CT the head

Front 740

for common tension HA, pt usually uses what?

If that doesnt work, suggest this?

often dont work while awake, but if the pt can get to sleep, it will

Back 740

OTC: - Aspirin
- Acetaminophen
- Advil or Motrin


Rx naproxen (anaprox) or other rx NSAIS

Front 741

If NSAIDs alone dont work for headaches, try this?

Back 741

try adding
- a sedative antihistamine………………………………………………diphenhydramine (Benadryl )
- or…a sedative anti-emetic……………………………………………prochlorperazine ( Compazine )

Front 742

If there is vidence of pericranial or neck
muscle tension, you could
try

Back 742

muscle relaxant-flexeril (cylobenzaprine)

Front 743

cyclobenzaprine (flexeril)

Back 743

muscle relaxant

Front 744

The next level of treatment for
tension H/A may be to try a
barbiturate combination

ex?

If that doesnt work, a migraine specific drug is often tried with success

Back 744

Fioricet ( butalbital + APAP + caffeine )

Front 745

Migraines are considered to be vascular HA. Arteriolar constriction is believed to be correlated with the _____

spontaneous re dliation of the arterioles is believed to be correlated with the throbbing HA

The H/A pain itself is believed to be
due to release of the neuropeptide inflammatory
mediators, which irritate the pain endings of the trigeminal nerve in the meninges. That's why NSAIDs, esp ______ work for many migraines

drug induced vasoconstriction seems to prevent and or relieve migraines

Back 745

auras

toradol

Front 746

Drug classes employed to cause
vasoconstriction, by different mechanisms

Back 746

ergotamines
triptans

Front 747

new migraine pts should keep a log of triggers. If she comes in progress, ask if she knows what works, then give it to her.

Good choices for mild/moderate migraines or severe migraines that has responded to these agents before

migraine specific drug are for moderate/severe migraines or migraine that does not respond to the above

Back 747

NSAIDS
excedrin migraine
midrin

Front 748

ex of ergotamine

Back 748

cafergot (erfotamine + caffeine)

Front 749

imitrex (sumatriptan)

Back 749

triptan

Front 750

zomig (zolmitriptan)

Back 750

triptan

Front 751

The Ergotamines and Triptans are all
serotonin ( 5-HT ) agonists which cause
vasoconstriction in the brain and ELSEWHERE, so they are contraindicated in cardiovascular conditions such as pregnancy, uncontrolled HTN, CAD and PAD, variant angina, CVA.

;this is sometimes used to treat migraines in the ED

Back 751

toradol (ketorolac)

Front 752

cocktails for migraine termination

Back 752

NSAID……. Toradol
+ Sedative……Benadryl
+ Antiemetic…Reglan

To
Be
Right

Front 753

Beta-blocker………propranolol
Ca Ch. Blocker……verapamil
TCA……………….amitriptyline
Anticonvulsants……Depakote Topamax
all sometimes work for _____ prophylaxis

Back 753

migraine

Front 754

_________ HA is by chronic use of any type of analgesic,
typically > 3 x per week

Back 754

rebound HA

Front 755

analgesics that cause rebound HA are?

Back 755

APAP
- Asa & other NSAIDs
- All opioids
- Barbituates
- Ergotamines
- Triptans

Front 756

Transformed Migraine-Substance Overuse,
in which increased frequency of migraines causes Pt
to take analgesic > 3 x per week is the most common cause of ____HA. Over time, not taking the analgesic causes the HA, next the HA becomes refractory to the analgesic.

Back 756

rebound

Front 757

rebnoud HA is daily or almost daily, persists all day. The critical factor is not the amount per day, but how many days per week.

Treatment for benoud HA is to do what?--stop all analgesics immediately, with 1 exception.


The Exception is that abrupt cessation of
any butalbital formulary, which may cause a generalized seizure

Back 757

f

Front 758

For intolerable H/A after cessation,
the rescue medication is

Back 758

D.H.E 45 ( dihydroergotamine

Front 759

______over a period of days to months,
then disappear for 1 or more
years.

Back 759

cluster

Front 760

- often awaken the Pt
- usually start in or around the eye - cause any of: - tearing
- corneal injection
- nasal congestion
- facial flushing
- Horner’s syn.

Back 760

cluster HAs

Front 761

tx of cluster HA

Back 761

similar to that of migraine:
- D.H.E. 45 ( dihydrogertomine ) self injection
- or...Imitrex ( sumatriptan ) self injection

Front 762

_______ can abort a cluster HA

Back 762

oxygen

Front 763

Muscle relaxants are used often used for “the aching back “ or other area of unexplained, localized muscle spasm. They are also used for more generalized spasticity, typically caused by stroke, cerebral palsy or multiple sclerosis

Back 763

s

Front 764

A sedative or anxiolytic for generalized anxiety

Back 764

diazepam (valium)

Front 765

DOC for status epilepticus

Back 765

valium (diazepam)

Front 766

THis is a major muscle relaxant, also cause major sedation

Back 766

valium (diazepam)

Front 767

lioresal (baclofen) is as good as valium, but causes less ____. May also cause what side effect?

Back 767

sedation
lowers seizure threshold in epileptics, so withdraw slowly

Front 768

lioresal (baclofen)

Back 768

muscle relaxant

Front 769

_______ is an alpha 2 agonist similar to clonidine. It is a muscle relaxant

Back 769

zanaflex (tizanidine)

Front 770

side effects of zanaflex (tizanidine)

Back 770

sedation, dry mouth, hypotension

Front 771

________ is not centrally acting. It is a muscle relaxant that inhibits excitation contraction coupling within muscle fibers themselves.

Back 771

dantrium (dantrolene)

Front 772

this is given for malignant hyperthermia

Back 772

IV dantrium

Front 773

for acute muscle spasm, try these two muscle relaxants

Back 773

Flexeril ( cyclobenzaprine)
Skelaxin ( metaxalone )

Front 774

___ IS loss of cholinergic neurons in the nucleus basalis of Maynert,
and then in widespread other areas of the cortex .

____ is loss of dopaminergic neurons in the substantia nigra.

___ is degeneration of the frontal lobes, and of the caudate and
Not Addressed putamen (of the basal ganglia).

____ is degeneration of upper motor neurons
(corticospinal tract) and lower motor neurons (alpha motor
neurons)

Back 774

Alzheimers
PArkinsons
Huntingtons
ALS

Front 775

Signs: - Tremor - Bradykinesia
- Muscle rigidity - Posture & gait abns (no arm swinging)
- Masked face

Back 775

Parkinsons

Front 776

The substantia nigra in the brainstem sends dopaminergic neurons up to a component of the basal ganglia in the middle of the brain, the “striatum,” which is a collective term for the caudate nucleus and the outer part of the putamen. All of these structures are part of the extrapyramidal motor system (EMS), named as such because, though it is a motor system, it is separate from the corticospinal tract, which sends its upper motor neurons down through the medullary pyramids and thence down the spinal cord to synapse with the cell bodies of the alpha motor neurons. The EMS occupies a large mass of tissue in the middle of the brain, mostly basal ganglia, and helps plan, initiate and smooth out our motor actions. When something goes wrong with the EMS / basal ganglia, one develops tremors, discoordination and/or involuntary movements all known as dyskinesias.

The substantia nigra’s dopamineric neurons send inhibitory input to the excitatory cholinergic neurons of the striatum. When the inhibitory dopaminergic neurons die off in Parkinson’s disease, the excitatory cholinergic effect of the striatum is no longer balanced and the dyskinesias develop.

Back 776

Parkinsons

Front 777

Antipsychotic drugs (“neuroleptics”) block dopamine receptors.
So, they often cause dyskinesias…which are called extrpyramidal
Symptoms (EPS)

- The worst EPS are caused by the “typical” antipsychotics..

Ex?

Back 777

haloperidol ( Haldol )
- chlorpromazine ( Thorazine )
- thioridazine ( Mellaril )

Front 778

- The least severe EPS are caused by the new “atypical”
antipsychotics
ex?

Back 778

clozapine ( Clozaril )
- risperidone ( Risperdal

Front 779

Strategy of Parkinsons tx

Back 779

restore dopaminergic transmission and/or antagonize the cholinergic overbalance.

- levodopa + carbidopa anticholinergics
- MAO-B inhibitor
- COMT inhibitor
- dopamine receptor agonist

Front 780

LEVODOPA, precursor of dopamine. Dopamine itself does not cross the blood-brain
barrier, but levodopa does, where it is converted to dopamine. However, much of the
levodopa is decarboxylated to dopamine in other tissues. To prevent this, the
dopa-decarboxylase inhibitor ________ is given at the same time.
- SINEMET = levodopa + carbidopa

After 3 to 5 years of Parkinson’s, enough neurons in the substantia nigra have died
off that there are not enough left to benefit from levodopa  decline of effect.

Back 780

Carbidopa

Front 781

_______inhibits MAO-B, the enzyme which metabolizes dopamine.
The drug increases dopamine levels in the brain, enhances the effect of levodopa and
decreases the required dose of levodopa.

- MAO-A is the enzyme that enzyme metabolizes norepinephrine and
serotonin. Traditional “MAO inhibitors” inhibit MAO-A and are used
as antidepressants because they increase norepinephrine and serotonin.
Ex?

Back 781

selegiline

- phenelzine ( Nardil )
- tranylcypromine ( Parnate )

Front 782

- So, a pharmacy NO-NO is giving…

MAO-A inhibitor + SSRI or TCA


Too much norepinephrine / serotonin

=

Back 782

hypertensive crisis

Front 783

_______ is a catecholamine-O-methyltransferase (COMT) inhibitor. When
carbidopa is given to inhibit dopamine decarboxylase (above), much of the levodopa
is now metabolized by COMT into 3-O-methyldopa which competes with the
levodopa for transport into the brain and  lower brain dopamaine levels 
“wearing off” phenomenon of the benefit of levodopa. __________prevents this.

Back 783

entacapone

Front 784

BROMOCRIPTINE & PERGOLIDE are ergotamines and dopamine receptor
agonists. As dopamine agonists, they improve Parkinson’s symptoms, but as
ergotamines, they are also vasoconstrictors which can exacerbate peripheral vascular
disease ( Raynaud’s etc ).

Back 784

,

Front 785

________ and ______ are non-ergotamine dopamine receptor
agonists. They improve Parkinson’s and are NOT vasoconstrictors. Ropinirole now
has an off-label use for restless leg syndrome

Back 785

roprinirole and pramipexole

Front 786

_______ is actually an antiviral drug for Influenza-A that also
has anti-Parkinson’s effects

Back 786

amantadine

Front 787

_______ and __________ are anticholinergics, antimuscarinic
agents to be precise. They help eliminate the cholinergic overbalance mentioned above.
As anticholinergics, they may also cause typical side effects:

dry mouth, blurred vision, consitpation, urinary retention, mydriasis

Back 787

benztropine and trihydyxphenidyl

Front 788

These are even more PALLIATIVE-ONLY than the Parkinson’s drugs. In other
words they don’t really work, and certainly not for long.. The drugs you will be
expected to know for the Board are all anticholinesterases, i.e acetylcholinesterase
inhibitors aka indirect cholinomimetics. That is to say, they inhibit the enzyme,
acetylcholinesterase, which is normally responsible for terminating the action of Ach
in neuronal synaptic clefts. This prolongs the action of Ach and thereby increases
brain cholinergic function in the form of thinking, memory and the ability to recognize
one’s own spouse.

Back 788

drugs for AD

Front 789

What forms are supporting documentation for an inventory adjustment?

Back 789

DD Form 114, Military Pay Order; DD Form 200, Financial Liability Investigation of Property Loss; SF 364, Report of Discrepancy

Hint 789

is not a type: resolved discrepancies

Front 790

sexual stimuli become integrated in the lumbar spinal cord, efferent action potentials in certain fibers (nervi erigentes) within the pelvic splanchnic nerves, release NO synthase within the penis--NO--acitvate cGMP. THis causes muscle relaxation, penile arteriolar vasodilation, corpus cavernosum engorgement. ___________ inactivates cGMP.

Back 790

type 5 phosphodiesterase

PDE-5

Front 791

cialis (tadalafil)

Back 791

PDE5 inhibitor

Front 792

viagra (sildenafil)

At recommended doses, they have no effect without prior sexual stimulation.

Back 792

PDE5 inhibitor

Front 793

Viagra (sildenafil) works for about ___ hours.

Cialis (taldalafil) works for about ___ hours

Back 793

4
36

Front 794

Other drugs that cause vasodilation like ____ and ____ are contraindicated with PDE5 inhibitors because the combo may cause hypotension

Back 794

nitrates
alpha blockers

Front 795

One alpha blocker that may be taken with a PDE 5 inhibitor is ______ because it is selective for prostte arteriolar smooth muscle

Back 795

tamsulosin (flomax)

Front 796

fosamax(alendronate)

Back 796

bisphosphonate

Front 797

boniva (ibandronate)

Back 797

bisphosphonate

Front 798

reclast (zoledronic acid)

Back 798

bisphosphonate

Front 799

bisphosphonates:

_________ is taken once a day
__________ is taken once a month
________ is given once a year IV

All decrease osteoclast activity

Back 799

fosamax
boniva
reclast

Front 800

The PO bisphosphonates may cause esophageal ulcers. Pts must take without food and not lie down for 30 minutes.

Back 800

.

Front 801

forteo (teriparatide)

Back 801

another drug for osteoporosis

human parathyroid hormone

Front 802

stimulates bone formation rather than bone resorption

Back 802

Forteo (teriparatide ) , a form of
human parathyroid hormone

Front 803

miacalcin (salmon calcitonin)

Back 803

another drug for osteoporosis, used to treat bone pain

Front 804

this can be used to treat bone pain

Back 804

miacalcin (salmon calcitonin)

Front 805

evista (raloxifene)

Back 805

SERM for osteoporosis

Front 806

most effective therapy to prevent osteoporosis

disadvantages?

Back 806

HRT

but it increases the risk of:
- Breast & Uterine CA
- Stroke & CAD
- DVT

Front 807

______ is not as good as HRT in the prevention of osteoporosis, but is not as good as HRT in the
prevention of osteoporosis, but:
- no ↑risk of uterine CA
- same risk of DVT

Back 807

evista (raloxifene)