GI/GU case wrap up Flashcards

(173 cards)

1
Q

What is the common ABX for cellulitis?

A

Keflex, Bactrim, Clindamycin, Doxycycline

All can be associated with C.diff

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2
Q

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

A
  • Clindamycin
  • Cephalosporins
  • FQ
  • Augmentin
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3
Q

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

A

Amox, Macrolides, Bactrim

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4
Q

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

A
  • Aminoglycosides
  • metronidazole
  • vanco
  • tetracyclines (DOXYCYCLINE)
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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

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6
Q

How much urine is he suppose to make?

A

1cc per kg per hour

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7
Q

What meds would you give him after admit?

A
  • Antiemetics – Zofran 4mg IV Q4 hours
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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)
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9
Q

What should you give pt case 1 for pain?

A

any are fine – morphine, dilaudid, fentanyl

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10
Q

What ABX will you give for pt for case 1?

A

Ceftriaxone or Fluoroquinolone – Levofloxacin

Change if necessary after culture results

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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

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12
Q

What should you be careful with AKI

A

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

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13
Q

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

A
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14
Q

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

A

Gastric CA

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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.

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16
Q

What are the causes of LES pressure?

A

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

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17
Q

What are specific meds that causes GERD?

A

Medications – CCB’s, nitrates

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18
Q

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

A
  • Antacids
  • Sulcralfate
  • H2 receptor antagonists (H2RTs)
  • PPI
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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.
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20
Q

What is the onset of Antacids?

A

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

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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
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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
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23
Q

What is the MOA of sucralfate?

A

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

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24
Q

Is Sucralfate approved for GERD?

A

No but approved for erosive disease and ulcer

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25
Can you do mono therapy for sulcralfate?
No!! Not mono therapy
26
What does sucralfate contain that you should be careful with?
- Aluminum
27
What is the MOA for H2 receptor antagonists?
- Acid-suppressive agents that inhibit the action of histamine at the H2 receptor of the parietal cell - Decreasing basal acid secretion DECREASE ACID PRODUCTION
28
T/F All H2RTs are equally effective and all are available OTC
True, all the same!
29
When is H2 blockers dont work, should they try another one/brand?
No, since they are all the same they need to try PPI
30
H2 blockers are not helpful in what kind of GERD?
No helpful with true esophagitis but good for mild-mod GERD Erosive or ulcer dz, H2 blocker is not strong enough
31
What is ADE of H2 blocker?
- HA and Hepatitis (rare) - Safer than PPI
32
What is examples of H2 blocker?
- Cimetidine - Famotidine
33
Whats the MOA of PPI
- irreversibly bind to the H+/K+-ATPase pump of the parietal cell - thereby inhibiting the final step of acid secretion
34
T/F Both PPI and H2 blocker inhibit acid production
True
35
Does tolerance occur with PPI?
No, only with H2 blocker
36
Which is more effective at treating erosion/esophagitis? PPI or H2 blocker?
PPI
37
Whats the ADE for PPI?
- Increased risk of c-diff - Increased fracture risk - Vitamin B12 deficiency - CKD - Worsen PNA prognosis
38
What is one DDI with PPI?
(CYP2C19 inhibition) Plavix, diazepam, phenytoin
39
What is one FDA warning with PPI and other meds?
Caution anticoags/anti-platelets with omeprazole
40
What are names of PPI?
- Omeprazolen (Prilosec) - Pantoprazole (Protonix) - Dexilant - Lansoprazole (Prevacid)
41
What are good options for break-through gerd
Sodium bicarb anti-acids or H2 blocker (likely not erosive/ulcer so H2 is ok)
42
What are all the drug option for GERD in pregnancy
- Antacids – except those containing sodium-bicarb - H2RTs are category B - PPIs are category B with the exception of omeprazole which is category C
43
Which is one PPI that is category C?
Omeprazole which is category C
44
T/F If pt has _____(3), they have to be on PPI
- H.pylori - GIB - Erosive esophagitis
45
Our case 2 GERD pt is on plavix, which is a DDI, what are other PPI she can take?
Prevacid and Protonix ok
46
What are the goals for pt with Renal disease?
- Start ACE-I and ARB (Both are equally effective) - Avoid nephrotoxic drugs - Avoid drugs/dc that contribute to renal impairment
47
What are the drugs that contribute to renal impairment?
- Metformin - Cetirizine - Vitamin C & D - HCTZ
48
If pt is DM with kidney disease, whats A1c goal?
~7% within 6 months
49
How can we decrease CV risk factors for pt with CKD?
- Control HTN with in 2-4 weeks - Hyperlipidemia - Obesity - Smoking
50
Whats one of the most common problems with initiation meds in CKD?
Inappropriate drug selection or dosing of medications with renal elimination pathways.
51
T/F We must
Know our patients GFR to evaluate all medications
52
Is Naproxen CI in DKD?
Yes
53
Why is naproxen CI in CKD?
Nephrotoxic and worsens renal impairment
54
At what lvl of Crcl should naproxen be used with caution?
<60mL/min
55
What lvl of Crcl is naproxen CONTRAINDICATED
<30mL/min
56
Naproxen is CI in those that are on _____? (3)
- Diuretics - ACE-I - ARBS
57
T/F Metformin DOES NOT HAVE the potential for toxicity with in patients with a decreased GFR
False, it does!
58
At what GFR should metformin - reduced - discontinued
Reduced at GFR 45 D/c <30
59
What should you do in pt before starting metformin?
Assess GFR prior to initiation of metformin and at least annually in patients using metformin.
60
Whats the MOA for metformin?
- inhibits the production and release of glucose from the liver (gluconeogenesis and gluconeolysis) - enhances insulin sensitivity in muscle and fat.
61
Metformin is safe in pt as long as their GFR is ___?
>45, if its lower then d/c
62
How much will metformin decrease A1c by?
1-2%
63
T/F metformin is weight neutral
True
64
What is recommended addition to metformin?
Addition to lifestyle intervention as initial therapy
65
What is the max dose of metformin?
2000 mg per day, divided 2-4 doses
66
What is the mc s/e of metformin?
GI intolerance
67
When is metformin contraindicated? (not related to GFR lvls)
- Hepatic impairment - Cardiac failure - Increase risk of lactic acidosis
68
What are example of sulfonylureas?
glyburide, glimepiride, glipizide
69
What is the MOA of Sulfonylureas?
- 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.
70
Sulfonylureas will not work if _____?
they have zero insulin production, they must have endogenous insulin production
71
How much does sulfonylureas decrease A1C by?
1-2%
72
What are the S/e of sulfonylureas?
- hypoglycemia - Weight gain
73
Which type of sulfonylurea is CI in renal failure?
- Glyburide - Glimepiride
74
Which sulfonylurea is the choice in pt with renal dx?
Glipizide but also needs renal dosing
75
What is the MOA of α-Glucosidase inhibitors?
delay GI break-down and absorption of carbohydrates
76
What is example of α-Glucosidase inhibitors
(acarbose, miglitol)
77
What is the reduction of A1c for a-glucosidase inhibitors?
0.5–0.8% reduction in A1C
78
Does α-Glucosidase inhibitors cause weight gain?
No, they are weight neutral
79
What is the s/e of α-Glucosidase inhibitors?
GI side effects and expensive
80
What must Cr be for α-Glucosidase inhibitors?
LESS than 2.0
81
What are the MOA of TZDs?
- insulin sensitizers that reduce insulin resistance by decreasing hepatic glucose release and promoting skeletal muscle glucose absorption.
82
What are examples of TZDs?
rosiglitazone, pioglitazone
83
When are TZDs contraindicated?
- Hepatic - Cardiac
84
What are the s/e of TZDs?
weight gain, fluid retention, and increased fracture risk in women
85
Whats the average A1c reduction in TZDs?
0.5-1.4%
86
Which type 2 DM meds do not need renal adjustment?
TZDs (Rosiglitazone and Pioglitazone
87
What are the different DPP-4 inhibitors?
alogliptin, linagliptin, sitagliptin (Januvia), and saxagliptin
88
Whats the MOA of DPP-4 Inhibitors?
- Increased incretin - Inhibiting glucagon secretion, decreasing blood glucose, increasing insulin secretion, and decreasing gastric emptying.
89
What is the A1c reduction for DPP-4 Inhibitors?
0.5-1%
90
Which DM2 meds can cause pancreatitis?
DPP-I
91
Can DPP-4 -I be used in pt with ESRD?
Yes you can!
92
What are example of GLP-1 Agonist?
- Albiglutide - Exenatide - Liraglutide
93
What is the MOA for GLP-1 agonist?
- Enhancing glucose-dependent insulin secretion by the pancreatic β-cell, suppressing inappropriately elevated glucagon secretion and slowing gastric emptying.
94
Which DM2 meds cause weight loss?
GLP-1
95
How is GLP-1 given?
SubQ so easier
96
Which two DM2 meds CANNOT be prescribed together
GLP and DDP
97
At what Crcl cant you not give your pt GLP-1?
CrCL < 30
98
What are example of SGLT-2 Inhibitors?
canagliflozin dapagliflozin empagliflozin
99
What is MOA of SGLT-2 Inhibitors?
- Reduce tubular glucose reabsorption (pee out glucose), therefore reducing blood glucose levels and the need for insulin release.
100
Whats a good DM2 med for obesity and HTN pt?
SGLT-2
101
What may increase in pt on SGLT?
HDL and LDL
102
Which DM2 is at risk for DKA?
SGLT-2 inhibitors
103
What DM2 med in CI in GFR less than <45?
Metformin SGLT-2
104
Which has the highest reduction of A1c?
injectable insulin
105
Which allows the highest glucose control
Injectable insulin
106
What is the BEST option with severe renal dsyfn?
Injectable insulin
107
What are the best HTN in CKD?
ACE inhibitors
108
What are example of ACE inhibitors ?
captopril, enalapril, lisinopril, ramipril, benazepril, perindopril, and quinapril
109
Whats the MOA of ACE-I?
inhibit conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion
110
Does ACE-I effect lipid lvls?
No
111
T/F ACE-I reduce proteinuria and the rate of renal disease progression in patients with diabetic nephropathy
True
112
Example of ARBs
losartan, irbesartan, valsartan, telmisartan, candesartan, and eprosartan
113
MOA of ARBs?
impair the vasoconstrictive effect of angiotensin II and block the stimulation of aldosterone secretion
114
What is s/e of ACE-I and ARBs?
HyperK!!!!!
115
What CKD stages is HCTZ recommended?
Stage 1-3, dont use for stage 4 and 5!!
116
What is s/e of HCTZ?
- hyperglycemia - Decrease GFR - Increase TG and total cholesterol
117
What is beneficial for pt with CKD stage 4 & 5?
Loops (furosemide)
118
Can you put pt on a loop diuretic as monotherapy in pt with CKD?
NOT mono therapy but can be added to ACE-I/ARBS as second agent
119
Is it recommended to use potassium-sparing diuretics?
No, be careful
120
How can b-blocker help in HTN for DM2?
Reduce mortality
121
Why should you be careful with Bblocker?
- Masks hypoglycemia, very concerning - decrease GFR - Affect lipid pannel
122
Which HTN have neutral effect on lipid and glucose?
CCB and also reduce proteinuria
123
whats 3rd line of HRN control in CKD?
CCBs
124
What is 1st line for dyslipidemia in CKD?
Statins, mod-high dose is recommended
125
Why is moderate statin recommended?
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
When should you re-check lipid levels in CKD?
3 months
127
What are other meds used in dyslipidemia for CKD?
- Bile acid sequestrants/binding resin - Fibrates
128
What are examples of bile acid sequestrants?
colestipol, cholestyramine, and colesevelam
129
How much does colestipol, cholestyramine, and colesevelam reduce LDL by?
15-20%
130
What are examples of fibrates?
bezafibrate, gemfibrozil, and fenofibrate
131
What does fibrates reduce?
TG levels
132
Can fibrates be used in CKD?
yes but statin is 1st line
133
What combo that is contraindicated in pt with CKD with dyslipidemia?
Fibrate/Statin because increase in Rhabdo!!
134
What can be added to statin tx for CKD pt with dyslipidemia?
Maybe bile acid sequestrants
135
What is the med of choice for BPH?
α-Adrenergic antagonists (α-blockers)
136
What is the MOA for α-Adrenergic antagonists (α-blockers)?
- competitively antagonize α-adrenergic receptors - relaxation of the bladder neck, prostatic urethra, and prostate smooth muscle Less obstruction to flow
137
How long does it take for a-blocker to work
days to weeks but patients might require titration up for full effect, might need increase dose
138
When is α-blockers recommended?
patients with normal prostate size and PSA
139
What is S/e of a-blocker?
hypotension and syncope, with immediate-release terazosin and doxazosin
140
Combined use with antihypertensives, diuretics, or phosphodiesterase type 5 inhibitors can lead to
low BP!
141
How often should you titrate a-blocker?
every 2 weeks
142
is mono therapy ok for a-blocker for BPH and HTN?
NO!
143
What is the MOA of 5a-reductase inhibitors?
shrinkage of an enlarged prostate by approximately 20% to 25% after 6 months.
144
How long should pt be on 5a-Reductase inhibitors?
6 months!
145
Which meds is used in pt with elevated prostate and PSA?
5a-reductase inhibitors
146
example of 5a-reductase inhibitors
finasteride and dutasteride
147
By what % will 5a reductase inhibitors decrease PSA by?
50%
148
What are the S/e of finasteride and dutasteride?
- Decreased libido - erectile dysfunction - ejaculation disorders
149
Which 5a reductase inhibitors only takes 1 month to work?
Dutasteride
150
Is combo therapy with α-adrenergic antagonist and 5α-reductase possible?
Only if MONO-therapy didn't work OR high risk of BPH complications
151
What is the combo therapy s/e with α-adrenergic antagonist and 5α-reductase ?
Weight risk
152
Why should you be caution with a-blocker for BPH with HTN?
Orthostatic hypotension Not contraindicated but be careful
153
T/F 5-alpha reductase inhibitors CAN'T cause orthostasis
False, it can, just less than alpha-blocker
154
Look at slide 40!! exam question
155
What are chronic medical condition that cause ED?
Hypertension Diabetes mellitus BPH
156
What are lifestyle rf that causes ED?
- Smoking - Excessive alcohol consumption - Obesity - Poor overall health and reduced physical activity
157
Which HTN meds is associated with ED?
B-blockers
158
Which antidepressants/antipsych is associated with ED?
TCA
159
which BPH med can cause ED?
5a-reductase inhibitors
160
Before you start meds for ED, what should you do?
PE, history and assess if they are safely perform sexual activity
161
Whats the med for ED?
Phosphodiesterase Type 5 Inhibitors
162
What is the MOA for Phosphodiesterase Type 5 Inhibitors?
- 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
T/F PDE inhibitors are only effective in the presence of sexual stimulation
True
164
are PDE facilitators of an erection OR initiators?
facilitators of an erection
165
What are S/E of PDE?
Hypotension, headache, facial flushing, nasal congestion, dyspepsia, myalgia, back pain, and, rarely, priapism.
166
What are the example of PDE?
Avanafil (Stendra) Sildenafil (Viagra) Tadalafil (Cialis Vardenafil (Levitra)
167
if pt get erection for more than 4-6 hours from PDE, what should they do?
go to the ER!
168
Which PDE meds can be used with BPH and ED meds?
Tadalafil
169
What is the CI for PDE?
Nitrates
170
How many trials need to be made to say the PDE isn't working?
6-8 trial
171
What is injection/ transurethral suppository med for ED?
Alprostadil
172
What is the MOA for alprostadil?
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