Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Pharm > GI/GU case wrap up > Flashcards

GI/GU case wrap up Flashcards

1
Q

What is the common ABX for cellulitis?

A

Keflex, Bactrim, Clindamycin, Doxycycline

All can be associated with C.diff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the High risk ABX associated with C.diff?

A
  • Clindamycin
  • Cephalosporins
  • FQ
  • Augmentin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the med risk ABX associated with C.diff?

A

Amox, Macrolides, Bactrim

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the low risk ABX associated with C.diff?

A
  • Aminoglycosides
  • metronidazole
  • vanco
  • tetracyclines (DOXYCYCLINE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

If pt is admitted what should the plan be?

A
  • IVF: Start with 2L and see if he responds

When is it enough?
- Vital signs stable
- making sure he is making urine

1cc per kg per hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How much urine is he suppose to make?

A

1cc per kg per hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What meds would you give him after admit?

A
  • Antiemetics – Zofran 4mg IV Q4 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are other two antimetics and why should you be caution

A
  • Phenergan 6.25mg IV (caution liver, vaso-toxic)
  • Reglan 10mg (caution GI bleed and renal impairment)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What should you give pt case 1 for pain?

A

any are fine – morphine, dilaudid, fentanyl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What ABX will you give for pt for case 1?

A

Ceftriaxone or Fluoroquinolone – Levofloxacin

Change if necessary after culture results

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Whats the take home pt for case 1?

A
  • Patients with AKI (regardless of their underlying, acute medical issues) should be closely monitored – more often than not in the hospital for fluid replacement

Monitor, repeast labs, improve Cr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What should you be careful with AKI

A

Be careful, don’t send home, monitor to make sure they bounce back.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

REVIEW CHART!!!! GOING TO BE ON THE EXAM

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is one Dx you must keep in find for GERD?

A

Gastric CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is GERD?

A

The lower esophageal sphincter (LES) is designed to relax when food passes through the esophagus into the stomach, reflux occurs when the LES “tightness” decreases allowing for gastric contents to “reflux” back into the esophagus

Looses ability to stay tight, allows food to pass around.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the causes of LES pressure?

A

High fat and carbohydrate diet
ETOH
Tobacco
Acidic foods/drinks
Medications – CCB’s, nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are specific meds that causes GERD?

A

Medications – CCB’s, nitrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 4 med class of medications used in GERD?

A
  • Antacids
  • Sulcralfate
  • H2 receptor antagonists (H2RTs)
  • PPI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the MOA of Antacids for GERD?

A
  • Increases the pH of the gastric refluxate by neutralizing gastric acid
  • Thereby decreasing its potential to cause damage to the esophageal mucosa.
  • Increase the LES tone through alkalinization of gastric contents.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the onset of Antacids?

A

Works really fast 15-30min but you have to do frequent dosing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When is antacids used?

A
  • 1st for mild-moderate sx for GERD but not in pt with esophagitis.
  • Dont decrease secretion, not prevention more symptomatic.
  • 1st line for symptom and added to other meds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What kind of antacids should you be careful in pt with CKD?

A
  • avoid mg and aluminum containing antacids
  • ONLY use calcium-based
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the MOA of sucralfate?

A

a mucosal coating agent that forms a protective barrier between esophageal tissue and gastric refluxate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Is Sucralfate approved for GERD?

A

No but approved for erosive disease and ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Can you do mono therapy for sulcralfate?

A

No!! Not mono therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What does sucralfate contain that you should be careful with?

A
  • Aluminum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the MOA for H2 receptor antagonists?

A
  • Acid-suppressive agents that inhibit the action of histamine at the H2 receptor of the parietal cell
  • Decreasing basal acid secretion

DECREASE ACID PRODUCTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

T/F All H2RTs are equally effective and all are available OTC

A

True, all the same!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

When is H2 blockers dont work, should they try another one/brand?

A

No, since they are all the same they need to try PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

H2 blockers are not helpful in what kind of GERD?

A

No helpful with true esophagitis but good for mild-mod GERD

Erosive or ulcer dz, H2 blocker is not strong enough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is ADE of H2 blocker?

A
  • HA and Hepatitis (rare)
  • Safer than PPI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is examples of H2 blocker?

A
  • Cimetidine
  • Famotidine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Whats the MOA of PPI

A
  • irreversibly bind to the H+/K+-ATPase pump of the parietal cell
  • thereby inhibiting the final step of acid secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

T/F Both PPI and H2 blocker inhibit acid production

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Does tolerance occur with PPI?

A

No, only with H2 blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Which is more effective at treating erosion/esophagitis? PPI or H2 blocker?

A

PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Whats the ADE for PPI?

A
  • Increased risk of c-diff
  • Increased fracture risk
  • Vitamin B12 deficiency
  • CKD
  • Worsen PNA prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is one DDI with PPI?

A

(CYP2C19 inhibition)

Plavix, diazepam, phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is one FDA warning with PPI and other meds?

A

Caution anticoags/anti-platelets with omeprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are names of PPI?

A
  • Omeprazolen (Prilosec)
  • Pantoprazole (Protonix)
  • Dexilant
  • Lansoprazole (Prevacid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are good options for break-through gerd

A

Sodium bicarb anti-acids

or

H2 blocker (likely not erosive/ulcer so H2 is ok)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are all the drug option for GERD in pregnancy

A
  • Antacids – except those containing sodium-bicarb
  • H2RTs are category B
  • PPIs are category B with the exception of omeprazole which is category C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Which is one PPI that is category C?

A

Omeprazole which is category C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

T/F If pt has _____(3), they have to be on PPI

A
  • H.pylori
  • GIB
  • Erosive esophagitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Our case 2 GERD pt is on plavix, which is a DDI, what are other PPI she can take?

A

Prevacid and Protonix ok

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the goals for pt with Renal disease?

A
  • Start ACE-I and ARB (Both are equally effective)
  • Avoid nephrotoxic drugs
  • Avoid drugs/dc that contribute to renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the drugs that contribute to renal impairment?

A
  • Metformin
  • Cetirizine
  • Vitamin C & D
  • HCTZ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

If pt is DM with kidney disease, whats A1c goal?

A

~7% within 6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How can we decrease CV risk factors for pt with CKD?

A
  • Control HTN with in 2-4 weeks
  • Hyperlipidemia
  • Obesity
  • Smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Whats one of the most common problems with initiation meds in CKD?

A

Inappropriate drug selection or dosing of medications with renal elimination pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

T/F We must

A

Know our patients GFR to evaluate all medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Is Naproxen CI in DKD?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Why is naproxen CI in CKD?

A

Nephrotoxic and worsens renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

At what lvl of Crcl should naproxen be used with caution?

A

<60mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What lvl of Crcl is naproxen CONTRAINDICATED

A

<30mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Naproxen is CI in those that are on _____? (3)

A
  • Diuretics
  • ACE-I
  • ARBS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

T/F Metformin DOES NOT HAVE the potential for toxicity with in patients with a decreased GFR

A

False, it does!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

At what GFR should metformin
- reduced
- discontinued

A

Reduced at GFR 45
D/c <30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What should you do in pt before starting metformin?

A

Assess GFR prior to initiation of metformin and at least annually in patients using metformin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Whats the MOA for metformin?

A
  • inhibits the production and release of glucose from the liver (gluconeogenesis and gluconeolysis)
  • enhances insulin sensitivity in muscle and fat.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Metformin is safe in pt as long as their GFR is ___?

A

> 45, if its lower then d/c

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How much will metformin decrease A1c by?

A

1-2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

T/F metformin is weight neutral

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is recommended addition to metformin?

A

Addition to lifestyle intervention as initial therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is the max dose of metformin?

A

2000 mg per day, divided 2-4 doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the mc s/e of metformin?

A

GI intolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

When is metformin contraindicated? (not related to GFR lvls)

A
  • Hepatic impairment
  • Cardiac failure
  • Increase risk of lactic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are example of sulfonylureas?

A

glyburide, glimepiride, glipizide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the MOA of Sulfonylureas?

A
  • Insulin secretagogues that promote pancreatic β-cell secretion of insulin and potentiate insulin action on extra-hepatic tissue.
  • Increase peripheral glucose use, decrease hepatic gluconeogenesis, and increase the number and sensitivity of insulin receptors.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Sulfonylureas will not work if _____?

A

they have zero insulin production, they must have endogenous insulin production

71
Q

How much does sulfonylureas decrease A1C by?

A

1-2%

72
Q

What are the S/e of sulfonylureas?

A
  • hypoglycemia
  • Weight gain
73
Q

Which type of sulfonylurea is CI in renal failure?

A
  • Glyburide
  • Glimepiride
74
Q

Which sulfonylurea is the choice in pt with renal dx?

A

Glipizide but also needs renal dosing

75
Q

What is the MOA of α-Glucosidase inhibitors?

A

delay GI break-down and absorption of carbohydrates

76
Q

What is example of α-Glucosidase inhibitors

A

(acarbose, miglitol)

77
Q

What is the reduction of A1c for a-glucosidase inhibitors?

A

0.5–0.8% reduction in A1C

78
Q

Does α-Glucosidase inhibitors cause weight gain?

A

No, they are weight neutral

79
Q

What is the s/e of α-Glucosidase inhibitors?

A

GI side effects and expensive

80
Q

What must Cr be for α-Glucosidase inhibitors?

A

LESS than 2.0

81
Q

What are the MOA of TZDs?

A
  • insulin sensitizers that reduce insulin resistance by decreasing hepatic glucose release and promoting skeletal muscle glucose absorption.
82
Q

What are examples of TZDs?

A

rosiglitazone, pioglitazone

83
Q

When are TZDs contraindicated?

A
  • Hepatic
  • Cardiac
84
Q

What are the s/e of TZDs?

A

weight gain, fluid retention, and increased fracture risk in women

85
Q

Whats the average A1c reduction in TZDs?

A

0.5-1.4%

86
Q

Which type 2 DM meds do not need renal adjustment?

A

TZDs (Rosiglitazone and Pioglitazone

87
Q

What are the different DPP-4 inhibitors?

A

alogliptin, linagliptin, sitagliptin (Januvia), and saxagliptin

88
Q

Whats the MOA of DPP-4 Inhibitors?

A
  • Increased incretin
  • Inhibiting glucagon secretion, decreasing blood glucose, increasing insulin secretion, and decreasing gastric emptying.
89
Q

What is the A1c reduction for DPP-4 Inhibitors?

A

0.5-1%

90
Q

Which DM2 meds can cause pancreatitis?

A

DPP-I

91
Q

Can DPP-4 -I be used in pt with ESRD?

A

Yes you can!

92
Q

What are example of GLP-1 Agonist?

A
  • Albiglutide
  • Exenatide
  • Liraglutide
93
Q

What is the MOA for GLP-1 agonist?

A
  • Enhancing glucose-dependent insulin secretion by the pancreatic β-cell, suppressing inappropriately elevated glucagon secretion and slowing gastric emptying.
94
Q

Which DM2 meds cause weight loss?

A

GLP-1

95
Q

How is GLP-1 given?

A

SubQ so easier

96
Q

Which two DM2 meds CANNOT be prescribed together

A

GLP and DDP

97
Q

At what Crcl cant you not give your pt GLP-1?

A

CrCL < 30

98
Q

What are example of SGLT-2 Inhibitors?

A

canagliflozin
dapagliflozin
empagliflozin

99
Q

What is MOA of SGLT-2 Inhibitors?

A
  • Reduce tubular glucose reabsorption (pee out glucose), therefore reducing blood glucose levels and the need for insulin release.
100
Q

Whats a good DM2 med for obesity and HTN pt?

A

SGLT-2

101
Q

What may increase in pt on SGLT?

A

HDL and LDL

102
Q

Which DM2 is at risk for DKA?

A

SGLT-2 inhibitors

103
Q

What DM2 med in CI in GFR less than <45?

A

Metformin
SGLT-2

104
Q

Which has the highest reduction of A1c?

A

injectable insulin

105
Q

Which allows the highest glucose control

A

Injectable insulin

106
Q

What is the BEST option with severe renal dsyfn?

A

Injectable insulin

107
Q

What are the best HTN in CKD?

A

ACE inhibitors

108
Q

What are example of ACE inhibitors ?

A

captopril, enalapril, lisinopril, ramipril, benazepril, perindopril, and quinapril

109
Q

Whats the MOA of ACE-I?

A

inhibit conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion

110
Q

Does ACE-I effect lipid lvls?

A

No

111
Q

T/F ACE-I reduce proteinuria and the rate of renal disease progression in patients with diabetic nephropathy

A

True

112
Q

Example of ARBs

A

losartan, irbesartan, valsartan, telmisartan, candesartan, and eprosartan

113
Q

MOA of ARBs?

A

impair the vasoconstrictive effect of angiotensin II and block the stimulation of aldosterone secretion

114
Q

What is s/e of ACE-I and ARBs?

A

HyperK!!!!!

115
Q

What CKD stages is HCTZ recommended?

A

Stage 1-3, dont use for stage 4 and 5!!

116
Q

What is s/e of HCTZ?

A
  • hyperglycemia
  • Decrease GFR
  • Increase TG and total cholesterol
117
Q

What is beneficial for pt with CKD stage 4 & 5?

A

Loops (furosemide)

118
Q

Can you put pt on a loop diuretic as monotherapy in pt with CKD?

A

NOT mono therapy but can be added to ACE-I/ARBS as second agent

119
Q

Is it recommended to use potassium-sparing diuretics?

A

No, be careful

120
Q

How can b-blocker help in HTN for DM2?

A

Reduce mortality

121
Q

Why should you be careful with Bblocker?

A
  • Masks hypoglycemia, very concerning
  • decrease GFR
  • Affect lipid pannel
122
Q

Which HTN have neutral effect on lipid and glucose?

A

CCB and also reduce proteinuria

123
Q

whats 3rd line of HRN control in CKD?

A

CCBs

124
Q

What is 1st line for dyslipidemia in CKD?

A

Statins, mod-high dose is recommended

125
Q

Why is moderate statin recommended?

A

Moderate dose statins are generally recommended in renal dysfunction to reduce the risk of potential toxicity, although patients tolerating higher doses do not require change in therapy.

126
Q

When should you re-check lipid levels in CKD?

A

3 months

127
Q

What are other meds used in dyslipidemia for CKD?

A
  • Bile acid sequestrants/binding resin
  • Fibrates
128
Q

What are examples of bile acid sequestrants?

A

colestipol, cholestyramine, and colesevelam

129
Q

How much does colestipol, cholestyramine, and colesevelam reduce LDL by?

A

15-20%

130
Q

What are examples of fibrates?

A

bezafibrate, gemfibrozil, and fenofibrate

131
Q

What does fibrates reduce?

A

TG levels

132
Q

Can fibrates be used in CKD?

A

yes but statin is 1st line

133
Q

What combo that is contraindicated in pt with CKD with dyslipidemia?

A

Fibrate/Statin because increase in Rhabdo!!

134
Q

What can be added to statin tx for CKD pt with dyslipidemia?

A

Maybe bile acid sequestrants

135
Q

What is the med of choice for BPH?

A

α-Adrenergic antagonists (α-blockers)

136
Q

What is the MOA for α-Adrenergic antagonists (α-blockers)?

A
  • competitively antagonize α-adrenergic receptors
  • relaxation of the bladder neck, prostatic urethra, and prostate smooth muscle

Less obstruction to flow

137
Q

How long does it take for a-blocker to work

A

days to weeks but patients might require titration up for full effect, might need increase dose

138
Q

When is α-blockers recommended?

A

patients with normal prostate size and PSA

139
Q

What is S/e of a-blocker?

A

hypotension and syncope, with immediate-release terazosin and doxazosin

140
Q

Combined use with antihypertensives, diuretics, or phosphodiesterase type 5 inhibitors can lead to

A

low BP!

141
Q

How often should you titrate a-blocker?

A

every 2 weeks

142
Q

is mono therapy ok for a-blocker for BPH and HTN?

A

NO!

143
Q

What is the MOA of 5a-reductase inhibitors?

A

shrinkage of an enlarged prostate by approximately 20% to 25% after 6 months.

144
Q

How long should pt be on 5a-Reductase inhibitors?

A

6 months!

145
Q

Which meds is used in pt with elevated prostate and PSA?

A

5a-reductase inhibitors

146
Q

example of 5a-reductase inhibitors

A

finasteride and dutasteride

147
Q

By what % will 5a reductase inhibitors decrease PSA by?

A

50%

148
Q

What are the S/e of finasteride and dutasteride?

A
  • Decreased libido
  • erectile dysfunction
  • ejaculation disorders
149
Q

Which 5a reductase inhibitors only takes 1 month to work?

A

Dutasteride

150
Q

Is combo therapy with α-adrenergic antagonist and 5α-reductase possible?

A

Only if MONO-therapy didn’t work OR high risk of BPH complications

151
Q

What is the combo therapy s/e with α-adrenergic antagonist and 5α-reductase ?

A

Weight risk

152
Q

Why should you be caution with a-blocker for BPH with HTN?

A

Orthostatic hypotension
Not contraindicated but be careful

153
Q

T/F 5-alpha reductase inhibitors CAN’T cause orthostasis

A

False, it can, just less than alpha-blocker

154
Q

Look at slide 40!!
exam question

A
155
Q

What are chronic medical condition that cause ED?

A

Hypertension
Diabetes mellitus
BPH

156
Q

What are lifestyle rf that causes ED?

A
  • Smoking
  • Excessive alcohol consumption
  • Obesity
  • Poor overall health and reduced physical activity
157
Q

Which HTN meds is associated with ED?

A

B-blockers

158
Q

Which antidepressants/antipsych is associated with ED?

A

TCA

159
Q

which BPH med can cause ED?

A

5a-reductase inhibitors

160
Q

Before you start meds for ED, what should you do?

A

PE, history and assess if they are safely perform sexual activity

161
Q

Whats the med for ED?

A

Phosphodiesterase Type 5 Inhibitors

162
Q

What is the MOA for Phosphodiesterase Type 5 Inhibitors?

A
  • Smooth muscle relaxation
  • phosphodiesterase (PDE) type 5, which is responsible for degradation of cGMP. With prolonged cGMP activity, smooth muscle relaxation is induced, leading to an erection.
163
Q

T/F PDE inhibitors are only effective in the presence of sexual stimulation

A

True

164
Q

are PDE facilitators of an erection OR initiators?

A

facilitators of an erection

165
Q

What are S/E of PDE?

A

Hypotension, headache, facial flushing, nasal congestion, dyspepsia, myalgia, back pain, and, rarely, priapism.

166
Q

What are the example of PDE?

A

Avanafil (Stendra)
Sildenafil (Viagra)
Tadalafil (Cialis
Vardenafil (Levitra)

167
Q

if pt get erection for more than 4-6 hours from PDE, what should they do?

A

go to the ER!

168
Q

Which PDE meds can be used with BPH and ED meds?

A

Tadalafil

169
Q

What is the CI for PDE?

A

Nitrates

170
Q

How many trials need to be made to say the PDE isn’t working?

A

6-8 trial

171
Q

What is injection/ transurethral suppository med for ED?

A

Alprostadil

172
Q

What is the MOA for alprostadil?

A

prostaglandin E1 analog that induces an erection by stimulating adenyl cyclase, leading to increased cAMP, smooth muscle relaxation, rapid arterial inflow, and increased penile rigidity.

173
Q
A

Clinical Pharm (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions