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Pharmacotherapeutics - Fall 21 > GI/GU Case Wrap-up- Jaynstein > Flashcards

GI/GU Case Wrap-up- Jaynstein Flashcards

1
Q

Case A: Colitis
42 yo man – abd pain and diarrhea after eating red meat 3 days ago. Currently on ABX for cellulitis (Keflex, Bactrim, Clindamycin, Doxycycline)

-etiology? (list potential pathogens)

A

Salmonella? E. Coli?

doxy- is low risk!!! this abx is NOT known to cause c-diff

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2
Q

ABX’s associated with c-diff:

List HIGH risk Abx

A

Clindamycin, Cephalosporins, fluoroquinolones, Augmentin

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3
Q

ABX’s associated with c-diff:

List moderate-risk abx

A

Amox, Macrolides, tetracycline

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4
Q

ABX’s associated with c-diff:

list low-risk abx

A

Aminoglycosides, metronidazole, vanco , Bactrim

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5
Q

V/S: BP-99/56, HR 124, K += 3.2

Issues?

CT scan shows evidence of colitis.

SHOULD this Pt be admitted?

A

HypoTN (99/56), Tachy (124) - multiple sxs of dehydration
Leukocytosis, mild hypoK, AKI, ? Mild liver dysfunction

ETOHism
APAP use – getting high, liver dys, ETOH use

YES, admit

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6
Q

Case A: colitis

Plan:

  • admit?
  • fluids?
  • antiemetics?
  • Pain meds?
  • Abx?
A

admit, IVF’s – start with 2 L’s and see if he responds hemodynamically

When is enough? VSS & Pt makes urine

Antiemetics: Zofran 4mg IV Q4 hours or Phenergan 6.25mg IV (caution liver, vaso-toxic)
Reglan 10mg (caution GI bleed and renal impairment)
  • Pain: any are fine–>morphine, dilaudid, fentanyl
  • ABX–>Start now, def evidence of bacterial colitis: Cipro–> Change if necessary after culture results
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7
Q

Case A: colitis
patients with AKI (regardless of their underlying, acute medical issues) should be closely monitored–more often in a hospital setting for _______

A

**fluid replacement

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8
Q

C. diff:

  • main symptoms?
  • Major risk factors?
A
  • main sx= diarrhea
  • Positive stool C diff test
  • Previous Abx usage(high risk=clindamycin, penicillins and cephalosporins)
  • Advanced age
  • Previous hospitalization
  • Nursing home resident
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9
Q

C.diff infection= presence of Sx in the form of 3 or more unformed stool over 24 hours for 2 consec. days with positive stools for _________

A

**pseudomembrane

Sx: Watery diarrhea,
15-30 BMs/day,
Abd pain or cramps,
Fever-low grade,

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10
Q

C. diff tx?

-prevention?

A

first line tx of C diff= **oral vancomycin (PO) KNOW– 125 mg PO QID x 10 days

  • Environmental control and hand hygiene
  • Spores can live up to 5 months on a surface
  • -Health care worker important vector
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11
Q

Salmonella:

  • s/Sx?
  • causes/risks?
  • tx?
A
  • Gram negative rod: Salmonella enteriditis
  • -Carried in GI tract of reptiles, bird, (usually get salmonells from eating **contaminated meat/eggs)
  • fever/diarrhea= MC sx
  • tx: most cases self-limiting, if uncomplicated- NO abx. If complicated–cipro=TOC, 2nd-bactrim
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12
Q

Shigella:
s/sx?
-causes/risk factors?

A
  • fecal oral spread, **linked to day care centers, changing diapers and poor hand washing.
  • sx: diarrhea (bloody, watery, pus, mucus–secretory, fever, N/V, dehydration
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13
Q

Shigella:

tx?

A
  • Rehydration
  • 1st line abx: **Ciprofloxacin
  • Bactrim or Azithromycin alternate
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14
Q

Campylobacter:
S/Sx?
-causes/risks?

A
  • Sx start 2-5 days after ingestion and last 1 week
  • sausages, hard meats, undercooked chicken
  • prodrome: fever, HA, myalgia/malaise
  • Ascending paralysis= guillian barre –association
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15
Q

Campylobacter:

tx?

A
  • **Ciprofloxacin drug of choice

- Azithromycin alternate

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16
Q

80% of traveler’s diarrhea is caused by _____

A

(E. coli) Enterotoxigenic-shiga toxin + or - non 0157 strains
–>80% of traveler’s diarrhea

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17
Q

What is the main cause of hemolytic uremia in the US?

A

E. coli 0157:H7

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18
Q

E. coli 0157:H7 :

  • linked to ______
  • sx?
A

Linked to undercooked ground beef, drinking of unpasteurized juices and milk, working with cattle (1% of cattle in US carry)

Sx: bloody diarrhea, severe cramping, nausea/vomiting

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19
Q

E. coli infection:

tx?

A
  • supportive
  • abx use is controversial
  • 5-20 % mortality
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20
Q

Vibrio cholera:

  • etiology?
  • incubation?
A
  • cholera, waterborne–> poor water sanitation, eating raw oysters/shellfish
  • Incubation: 12-72 hours
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21
Q

Vibrio:

sx?

A

**rice water stools” and RAPID dehydration,

watery diarrhea, N/V, fever/chills, abd cramping

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22
Q

Vibrio:

abx?

A

not always recommended, can use doxy or cipro, main tx: push lots of fluids!!!

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23
Q

Giardia:

S/sx?

A

diarrhea, foul-smelling greasy poop that floats, stomach pain, N, dehydration

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24
Q

Giardia:
-risk factors/exposures?
tx?

A
  • children in daycare, travelers to areas w/ poor sanitation

- tinidazole and nitazoxamide

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25
Q

Case B: GERD

  • 68yo F c/o heartburn and regurgitation 5x/week for 5 months
  • currently taking OTC Prevacid (PPI) ? (Adequate trial?)
  • ETOH: 1-2 glasses most nights
  • Mother– gastric cancer
  • Current meds: PLAVIX, DILT
  • EGD shows: erosive esophagitis, H/ Pylori neg

what DDIs should you be aware of concerning this Pt’s current meds?

A

-DDIs can occur with Plavix and Diltiazem

plavix + PPI–> combo may decrease clopidogrel active metabolite levels and efficacy

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26
Q

Describe how reflux occurs with 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

-Affects upwards of 7 million American’s

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27
Q

List Causes of lowered LES pressure

A
  • High fat and carbohydrate diet
  • ETOH
  • Tobacco
  • Acidic foods/drinks
  • Medications – CCB’s, nitrates–**diltiazem, nitrates ALL relax smooth m
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28
Q

Antacids:

  • MOA?
  • Onset and duration?
A

=Increases the pH of the gastric refluxate by neutralizing gastric acid, thereby decreasing its potential to cause damage to the esophageal mucosa. These agents also increase the LES tone through alkalinization of gastric contents.

-Onset 15-30 minutes, duration 1-3 hours

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29
Q

Antacids are 1st line therapy for which group of Pts?

A
  • Pts with mild intermittent Sx of GERD without esophagitis. (TUMs are a great option! they are usually effective, BUT require frequent dosing)
  • They may also be used for breakthrough Sx in patients receiving H2-blockers or PPI’s.
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30
Q

Antacids should be AVOIDED with ______

A

**mg and aluminum containing antacids in CKD, may use calcium-based antacids

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31
Q

GERD meds:

-Sucralfate MOA?

A

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

–Not FDA approved in tx of GERD – but has been demonstrated to provide some sx relief in these Pts

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32
Q

Sucralfate:
-how should this be prescribed? (dosing)

-which Pts should AVOID this med?

A
  • dosing is 4x a day, this is NOT mono therapy

- Contains aluminum and therefore should be avoided in Pts with CKD

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33
Q

GERD meds:

-H2 antags MOA ?

A

Acid-suppressive agents that inhibit the action of histamine at the H2 receptor of the parietal cell, decreasing basal acid secretion

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34
Q

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

A

True

-cimetidine, ranitidine, famotidine

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35
Q

H2 receptor antags:

  • symptom relief is experienced in ___% of Pts
  • How effective are they in tx of esophagitis? GERD?
A
  • 50-70%
  • Not as effective in tx of patients with true esophagitis, but adequate for mild-moderate GERD
  • Patients can become tolerant– switching to a different one does not help
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36
Q

H2 receptor antags:

-adverse effects?

A

serious ADRs very uncommon!

  • HA
  • Rarely hepatitis
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37
Q

PPIs:
-MOA: irreversibly bind to the ________

-do Pts build a tolerance to PPIs?

A

H+/K+-ATPase pump of the parietal cell, thereby inhibiting the final step of acid secretion

  • ->Tolerance does NOT occur
  • ex’s: Omeprazole, pantoprazole, Dexilant, lansoprazole
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38
Q

Which medication is more effective at treating erosion/esophagitis than H2RTs?

A

PPIs

PPIs are first line for erosive esophagitis and H pylori

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39
Q

PPIs are linked to increased risk of _____

A

of c-diff, increased fracture risk, vitamin B12 deficiency, CKD, and worsen PNA prognosis

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40
Q

PPIs have many DDIs (CYP2C19) inhibitors:

-list ex’s of meds they interact with

A

Plavix, diazepam, phenytoin

FDA warning: Caution anticoags/anti-platelets with omeprazole

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41
Q

How often does heartburn occur in pregnancies?

A

30-50% of pregnancies

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42
Q

Heartburn tx options for pregnant Pts (list ex’s)

A
  • Antacids: BUT NOT those containing sodium-bicarb
  • H2RTs are category B
  • PPIs are category B with the exception of omeprazole (Prilosec) which is category C
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43
Q

CASE B - GERD: considerations for this Pt–>

  • H Pylori neg (if positive = ____ )
  • No GIB (if positive = _____ )
  • Endoscopy demonstrates grade B esophagitis (any evidence of esophagitis = ____)
  • Patient is on Plavix (multiple PPIs contraindicated)
  • should ASA be continued?
A
  • PPI
  • PPI
  • PPI

YES ASA should be cont, but make sure it’s enteric coated

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44
Q

Case C: CKD
38yo AA female with DM-II with progressive kidney disease

  • what are some of the goals for this Pt?
  • what meds should be modified or d/c in Pts with CKD?
A
  • Halt progression of renal disease
  • An ACE-I or ARB should be initiated
  • Discontinuation/avoidance of nephrotoxic drugs

Modify or d/c meds that contribute to renal impairment such as:

  • Metformin (cant give to Pts with CrCl <30)
  • -Vit C and D
  • -Cetirizine (Zyrtec)
  • -HCTZ

-Improve glycemic control–> Achieve A1C ~7% within 6 months

-Decrease CV risk factors-->HTN
Target of <140/90 mm Hg within 2–4 weeks
-Hyperlipidemia
-Inadequate stain dosing - adjust
-Obesity
-Smoking
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45
Q

One of the most common drug-related problems in chronic renal failure is: ?

A

inappropriate drug selection or dosing of meds with renal elimination pathways.

**Must know our Pt’s GFR to evaluate all medications

46
Q

Our patient:
ACR is 673 (>300 = severe)
BUN 43, cr 2.8
3+ protein on UA

IBW = 131, CrCl = 26mL/min,

CKD stage: ?

A

stage 4

47
Q

List the stages of CKD

A 
stage 1: 90% or more
stage 2: 60-89%
stage 3: 30-59%
stage 4: 15-29%
stage 5: <15%
48
Q

In which Pt populations is Naproxen contraindicated?

-Naproxen is contraindicated in Pt’s with GFR < ______

A
  • contraindicated in **diabetic related kidney disease (DKD), as it can be nephrotoxic and worsen renal impairment.
  • Naproxen should be used with caution in Pts with decreased kidney function (<60 mL/min) and is contraindicated when <30 mL/min.
  • Naproxen also contraindicated in Pts on diuretics (which she is presently using) and ACE inhibitors or ARBs (which she should be using) due to risk of worsening renal function.
49
Q

Metformin has the potential for toxicity with in patients with _______

A

**a decreased GFR

50
Q

Current guidelines suggest metformin re-evaluation and dose reduction at GFR

A

<45 mL/min and discontinuation at GFR<30 mL/min.

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

51
Q

DM control in CKD:
Biguanides (metformin) inhibits the production and release of glucose from the liver (gluconeogenesis & gluconeolysis) and enhances ________

A

**insulin sensitivity in muscle and fat.

52
Q

Are biguanides (metformin) safe in CKD Pts?

-A1c % reduction?

A
  • Safe for CKD pts as long as: GFR >45 mL/min
  • Expected A1C decrease is 1–2%
  • **Metformin is weight neutral and is recommended in addition to lifestyle intervention as initial therapy in type 2 DM.
53
Q

Max recommended dose of metformin is ________

A

2000 mg per day given in 2–4 divided doses or as an extended-release.

54
Q

Metformin:

  • S/E?
  • Contraindicated in: ?
A
  • *GI intolerance is common
  • Contraindicated in hepatic impairment and cardiac failure and can increase the risk of lactic acidosis
  • Metformin should be discontinued in this patient
55
Q

DM control in CKD: Sulfonylureas

  • list ex’s ?
  • MOA?
A
  • glyburide, glimepiride, glipizide–> are insulin secretagogues that promote pancreatic β-cell secretion of insulin and potentiate insulin action on extra-hepatic tissue.
  • They may increase peripheral glucose use, decrease hepatic gluconeogenesis, and increase the # and sensitivity of insulin receptors
56
Q

For Pt’s with DM, they must have _______ insulin production in order to be started on Sulfonylureas

A
  • **endogenous (ie, pancreatic secretion of insulin); therefore, efficacy is reduced in later stages of DM.
  • Expect A1C lowering of 1-2%
57
Q

Sulfonylureas:

  • weight gain?
  • contraindications?
A
  • Hypoglycemia and weight gain (2kg/year) possible
  • Glyburide is contraindicated in renal failure & glimepiride should be used with caution
  • Glipizide is the preferred sulfonylurea in renal disease, but NEEDS renal dosing

(Metformin-1st
Sulfonylureas- 2nd line for A1c reduction)

58
Q

DM control in CKD:
α-Glucosidase inhibitors (AGI)

  • list ex’s ?
  • MOA ?
  • effect on blood sugar control and weight?

-Cr MUST be

A
  • acarbose, miglitol
  • MOA: delay GI break-down and absorption of carbs

-Have only a modest effect on blood sugar control (0.5–0.8% reduction in A1C)

  • Weight neutral, relatively **expensive and patient acceptance is limited by GI side effects (eg, flatulence, bloating, and diarrhea)
  • Cr less than 2.0
59
Q

An AGI is contraindicated in our patient due to _____

A

her renal dysfunction – also, they are unlikely to make enough of a difference in a patient with significant A1C levels.

60
Q

DM control in CKD: TZDs

  • list ex’s
  • MOA ?
A
  • TZDs= rosiglitazone (Avandia), pioglitazone
  • MOA: insulin sensitizers that reduce insulin resistance by decreasing hepatic glucose release and promoting skeletal muscle glucose absorption.
61
Q

TZDs:

  • contraindicated in ?
  • cost? weight gain?
  • a1c reduction?

Is this a good agent for out Pt?

A

**contraindicated in hepatic dysfunction and cardiac failure

  • Expensive, assoc. w/ weight gain, fluid retention, and increased fracture risk in women
  • A1C: 0.5–1.4%
  • No renal adjustment

-w/ existing cardiovascular risks, weight concerns, and availability of other, safer therapeutic options, TZDs are not optimal agents for our Pt but could be considered for second/third lines

62
Q

DM control in CKD:
DPP-4 inhibitors

  • list ex’s
  • MOA?
A
  • alogliptin, linagliptin, sitagliptin (Januvia), and saxagliptin
  • MOA=oral inhibitors of the DDP-4 enzyme, which breaks down proteins that trigger the release of insulin. Their MOA is via increased incretin (GLP-1 and GIP) levels, inhibiting glucagon secretion, decreasing blood glucose, increasing insulin secretion, and decreasing gastric emptying.
63
Q

DPP-4 inhibitors:

  • A1c reduction?
  • weight gain?
  • adverse s/e?
  • renal dosing?
A
  • A1C reduction 0.5–1%
  • Weight neutral, generally well tolerated and low risk of hypoglycemia
  • Expensive
  • **Can cause pancreatitis
  • Can be used in ESRD with appropriate dosing
  • Any of the DPP-4 inhibitors may be suitable alternatives for our patient, taking into account dose adjustment for renal dysfunction. **Linagliptin may represent the best option as it does not require dose adjustment.
64
Q

DM control in CKD: Incretin mimetic/glucagon-like peptide-1 (GLP-1) agonists

  • list ex’s
  • MOA ?
A

-albiglutide, exenatide (byetta), liraglutide (victoza))

  • mimics the action of the hormone incretin, which helps regulate both fasting and postprandial glucose levels.
  • –>These agents stimulate GLP-1 receptors enhancing glucose-dependent insulin secretion by the pancreatic β-cell, suppressing inappropriately elevated glucagon secretion and slowing gastric emptying.
65
Q

GLP-1 agonists:

  • are they assoc. with hypoglycemia?
  • how do they help w/ appetite?
A

-Insulin production is only increased in response to high blood glucose levels; SO they are NOT assoc. w/ hypoglycemia

  • GLP-1 agonists also curb appetite and delay gastric emptying leading to weight loss
  • given subQ and they are EXPENSIVE, but can be dosed weekly
66
Q

GLP-1 agonists cannot be prescribed with _______ & cant be used in Pts with CrCl < _____

A
  • DPP-4 inhibitor

- CrCl <30

67
Q

DM control in CKD: Sodium-glucose transport protein 2 (SGLT2) inhibitors

  • list ex’s
  • MOA ?
A

-SGLT2) inhibitors= canagliflozin (Invokana), dapagliflozin, and empagliflozin (Jardiance)

MOA: reduce tubular glucose reabsorption (pee out glucose), therefore reducing blood glucose levels and the need for insulin release.

68
Q

SGLT2 inhibitors should be considered in which Pts?

A
  • *obese and HTN Pts
  • assoc with weight loss (2-8# in 18 weeks) and antihypertensive (up to 7mmHg systolically) properties
  • Conflicting data on Lipid control–> may increase HDL and LDL
  • Moderate A1C reduction of 0.75% on average
69
Q

SGLT2 inhibitors:
are assoc w/ which adverse S/E ?
-contraindicated with GFR < _____

A

***euglycemic DKA, increased UTIs, pancreatitis

  • <45 ml/min
  • An SGLT2 inhibitor is not an option for our patient due to only modest A1C effects and her CKD
70
Q

DM control in CKD: Injectable insulin

  • A1c reduction?
  • weight effects?
A

**has potential for the greatest A1C reduction and allows the tightest glucose control

-assoc w/ weight gain and hypoglycemia

71
Q

For patients with more advanced renal failure, how should you adjust their insulin doses?

A

may require lower doses of insulin due to decreased renal clearance, thus close monitoring and dose adjustment is required with declining GFR – but insulin is the ***best option for patients with severe renal dysfunction.

-Case C Pt: Although initiation of basal insulin may be the best alternative in this patient due to high A1C and decreased renal function, acceptability of insulin may be poor because the patient has expressed an aversion to needles. MUST CONVINCE PT!

72
Q

Basal insulin is used for ____

A

fasting glucose control and includes intermediate acting NPH insulin, long-acting glargine (Lantus, Basaglar) and detemir (Levemir) and ultra-long acting degludec (Tresiba) and high concentration glargine U-300 (Toujeo).

-Basal insulin is generally dosed once or twice daily.

73
Q

Bolus insulin includes:

A

rapid-acting aspart (NovoLog, NovoRapid), glulisine (Apidra) lispro (Humalog), and the inhaled insulin Afrezza as well as short-acting regular insulin (Humulin R, Novolin R). Bolus insulin is used for mealtime glucose control and requires multiple daily injections.

Insulin is the best!!! Shows the greatest reduction in a1c and best glucose control

74
Q

A patient with renal insufficiency and HTN has a ____fold higher risk of progression to ESRD than a person with renal insufficiency who is normotensive

A

6

75
Q

CASE C - CKD
This patient’s BP is not controlled by hydrochlorothiazide 50 mg per day, a thiazide diuretic that may complicate glucose control
–>You rarely want HCTZ above ____mg in the first place

Target BP is

A

25 mg

<140/90 mm Hg,

  • An ACE or ARB is necessary for our patient. Would start as a single agent with initiation of life-style changes and add a second agent if BP remains >140/90 mmHg.
  • Some data has shown ACE-I in DM-I and ARBs in DM-II produce the best outcome
76
Q

HTN control in CKD:
ACEIs

  • list ex’s
  • MOA?
A

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

  • ->inhibit conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion.
  • -Neutral effects on lipid levels
  • -May improve glucose control through decreased insulin resistance
  • -Reduce proteinuria and the rate of renal disease progression in Pts w/ diabetic nephropathy
77
Q

HTN control in CKD:
ARBs

  • list ex’s
  • MOA?
A
  • Angiotensin-II receptor blockers (ARBs) (losartan, irbesartan, valsartan, telmisartan, candesartan, and eprosartan)
  • ->MOA: impair the vasoconstrictive effect of angiotensin II and block the stimulation of aldosterone secretion.

-No effect on lipid or glucose levels

78
Q

Which HTN meds are assoc with Hyper K?

A

ACEIs and ARBs

79
Q

Thiazide diuretics (hydrochlorothiazide) are an effective and inexpensive therapy for BP control; recommended in pts with CKD stages _____

A

1-3

(Thiazides are not the optimal choice in this Pt cuz they can worsen hyperglycemia, decrease GFR, and increase total cholesterol and triglyceride (TG) levels. However, they may be considered as a second-line agent if the patient needs.)

80
Q

Loop diuretics (eg, furosemide) may be beneficial in pts with CKD stage ____

A

4 & 5

81
Q

Can Loop diuretics effect blood glucose levels?

A

yes, they can increase blood glucose and alter glucose tolerance tests
-Not recommended for single drug therapy, can be added to an ACE-I or ARB

(note: lasix is 2nd line agent to ACEI’s)

82
Q

List ex’s of K+ sparing diuretics

-should they be used in Pts with renal insufficiency?

A
  • spironolactone, triamterene, and amiloride

- should be used w/ extreme caution or not at all in renal insufficiency

83
Q

β -Blockers reduce mortality in the treatment of HTN, but they can mask the signs and symptoms of ______

A

**hypoglycemia and slow recovery from hypoglycemia in diabetic patients, **decrease GFR by reducing renal blood flow, and adversely affect lipid levels by increasing TG and reducing HDL levels.

84
Q

When are CCBs considered for tx of HTN?

  • list ex’s of CCBs
  • effect on glucose levels?
A
  • IF Pt fails to tolerate tx w/ ACEI or ARB or requires intensification of therapy
  • amlodipine, diltiazem, nifedipine, and verapamil
  • have neutral effects on lipid and glucose levels and also reduce proteinuria.
85
Q

What dose of statin therapy is recommended in renal dysfunction Pts?

A

**moderate dose statins–to reduce the risk of potential toxicity, although Pts tolerating higher doses do not require change in therapy.

86
Q

CASE C - CKD
the Pt is presently receiving a statin without adequate lipid response, however dietary changes and improved medication adherence should improve lipid profile. Many different approaches to this: (list ex’s)

A
  • Serum lipids may be inaccurate in Pts with CKD
  • Guidelines vary suggesting statin dosing between 10-20 mg QD
  • Maximize lifestyle changes, recheck in 3 months
  • Increase to atorvastatin 20 mg
87
Q

Dyslipidemia in CKD:

  • list ex’s of bile acid sequestrants
  • bile acid sequestrants reduce LDL levels by ___%
A

colestipol, cholestyramine, and colesevelam

- 15–20%.

88
Q

Why are there compliance issues with bile acid sequestrants?

A
  • GI S/E and the need for frequent dosing

- Can be used in patients with CKD, but stains are considered first-line

89
Q

How are fibrates effective?

-list ex’s

A

bezafibrate, gemfibrozil, and fenofibrate

  • effective in reducing TG levels but variable efficacy in reducing LDL and raising HDL.
  • Can be used in patients with CKD, but stains are considered first-line
90
Q

Can you combine tx with fibrate and statins in Pts with CKD?

A

NO! **Fibrate/statin combinations are CONTRAINDICATED in patients with CKD as the risk of rhabo is significantly increased

91
Q

CASE C - CKD–> plan

HTN tx?

DM?

A

HTN:
-Valsartan 80mg QD, Telmisartan 40mg QD (can titrate up to 80mg QD) -or- Lisinopril 10mg to start, expect 20-40mg QD needed

-HCTZ may be discontinued

  • Maximal effect at 4 weeks to achieve a goal BP of <130/80 mm Hg
  • -**She should be monitored for hyperkalemia and Cr elevation. –If there is more than a 30% increase in Cr or serum potassium >5.5, the drug should be discontinued.

DM:
-**INSULIN is her DOC
-If the Pt refuses insulin, next line therapy is:
A sulfonylurea (glipizide 5mg QD) -OR-
A DPP-4 inhibitor (linagliptin 5mg QD)

92
Q

Case C- CKD Pt–> plan

  • uncontrolled dyslipidemia tx?
  • other recommendations?
A

Dyslipidemia: Pt currently using atorvastatin 10 mg QD, with inadequate lipid control
–Can try lifestyle changes for up to 3 months -OR-
Increase atorvastatin to 20mg QD

Others:

  • d/c Vit C, D ginseng, and naproxen
  • Reduce ASA to 81mg QD
  • Nasonex may be continued
  • Cetirizine decrease to 5mg (5mg max if CrCl less than 30)
  • Prilosec need should be readdressed- why are you on this? Is this med necessary?
  • Smoking cessation
  • Aggressive lifestyle modifications
93
Q

α-Adrenergic antagonists (α-blockers)

  • MOA?
  • onset of action?
  • recommended for?
A

MOA: competitively antagonize α-adrenergic receptors, causes relaxation of the bladder neck, prostatic urethra, and prostate smooth muscle

  • Onset: **days to weeks but patients might require titration up for full effect
  • Recommended for patients with normal prostate size and PSA
94
Q

α-Adrenergic antagonists (α-blockers):

-what are the MC dose-limiting adverse effects?

A

**hypotension and syncope, which are more common with IR terazosin and doxazosin

  • Combined use with antihypertensives, diuretics, or phosphodiesterase type 5 inhibitors can lead to additive BP–lowering effects; however, this appears to be less of a problem with tamsulosin
  • Titrate up slowly (every 2 weeks) and instruct patient to take prior to bedtime
95
Q

Can you use α-Adrenergic antagonists (α-blockers): for tx of BPH and essential HTN?

A

NO, Despite the BP-lowering property of α-adrenergic antagonists, they are not recommended as monotherapy for patients with both BPH and essential hypertension.

96
Q

5α-Reductase inhibitors:

  • MOA: ?
  • onset of action?
  • used to prevent _______
A
  • inhibit 5α-reductase, which is responsible for intraprostatic conversion of testosterone to dihydrotestosterone, the active androgen that stimulates prostate tissue growth. Thus, resulting in shrinkage of an enlarged prostate by approximately 20% to 25% after 6 months.
  • **minimum of 6 months is required to evaluate the effectiveness of tx
  • 5α-reductase inhibitors are used to prevent BPH-related complications and dz progression (these drugs shrink the size of the prostate)
97
Q

5α-Reductase inhibitors can decrease serum levels of PSA by ____%

A

50%

-finasteride, dutasteride

98
Q

5α-Reductase inhibitors:

-adverse effects ?

A

decreased libido, erectile dysfunction, and ejaculation disorders, which may persist after the drug is stopped, and gynecomastia and breast tenderness

-Drug interactions are uncommon

99
Q

Combination therapy: with α-adrenergic antagonist and 5α-reductase inhibitor may be considered in: ____

A

**symptomatic Pts who do not respond to an adequate trial of monotherapy or in those at high risk of BPH complications

  • combo therapy is more expensive and associated with the array of adverse effects
  • -Weight risk/benefit, always start with monotherapy
100
Q

CAUTION when prescribing an alpha-blocker to a patient who is being treated for HTN: (S/E)

A
  • Not a contraindication
  • Adjust antihypertensive if needed
  • Take antihypertensive medication in the AM, alpha-blocker in the PM
  • Provide good education on orthostasis

-5-alpha reductase inhibitors can cause orthostasis was well, but not as often/severe as alpha-blockers

101
Q

List ex’s of chronic medical conditions associated with ED

A
  • **Hypertension
  • **Diabetes mellitus
  • **BPH
  • Coronary and peripheral vascular disease
  • Neurologic disorders (eg,
  • Parkinson disease and multiple sclerosis)
  • Endocrine disorders (hypogonadism, pituitary, adrenal, and thyroid disorders)
  • Psychiatric disorders
  • Dyslipidemia
  • Renal failure
  • Liver disease
  • Penile disease (Peyronie disease or anatomic abnormalities)
102
Q

Surgical procedures and lifestyle habits associated with ED

A

Surgical Procedures:

  • Perineal or vascular surgeries
  • Radical prostatectomy
Lifestyle:
Smoking
Excessive alc consumption
Obesity
Poor overall health and reduced physical activity
103
Q

Trauma incidents associated with ED

A
  • Pelvic fractures or surgeries

- Spinal cord or brain injuries

104
Q

Ex’s of classes of meds that can cause ED

A 
**Antihypertensives:
β-Blockers (excluding nebivolol)
Thiazide diuretics
Centrally acting agents (clonidine, methyldopa, and reserpine)
Spironolactone
α-Blockers

**CNS Depressants:
Opioid analgesics
Benzodiazepines
Hypnotics

**Lipid Medications:
Gemfibrozil
HMG-CoA reductase inhibitors

**Antidepressants/Antipsychotics:
Tricyclic antidepressants
Monoamine oxidase inhibitors
Selective serotonin reuptake inhibitors/serotonin-norepinephrine reuptake inhibitors

**Anticonvulsants:
Carbamazepine
Phenytoin

**Gastrointestinal Agents:
Histamine 2-receptor antagonists
Proton pump inhibitors

**Antiandrogens and Hormones:
5α-Reductase inhibitors
Progesterone and estrogen
Corticosteroids

**Recreational Drugs:
Ethanol
Cocaine
Marijuana

105
Q

Before initiating tx for ED, a PE and thorough medical, social, and medication histories with emphasis on _______ must be taken to assess for ability to safely perform sexual activity and to assess for possible drug interactions.

A

cardiac disease***

-Reversible and/or modifiable factors should concurrently be addressed

106
Q

ED tx: Phosphodiesterase Type 5 Inhibitors

-MOA: ?

A

selectively inhibit phosphodiesterase (PDE) type 5, which is responsible for degradation of cGMP. With prolonged cGMP activity, smooth muscle relaxation is induced, leading to an erection.

107
Q

PDE inhibitors are only effective in the presence of ______

A

sexual stimulation to drive the NO/cGMP system, making them facilitators of an erection, not initiators.

108
Q

ED tx: Phosphodiesterase Type 5 Inhibitors

  • list ex’s of meds
  • adverse effects?
A

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

***Vardenafil and sildenafil may also cause blurred vision, difficulty in discriminating blue from green, bluish tones in vision, or difficulty seeing in dim light

Four:

  • Avanafil (Stendra)
  • **Sildenafil (Viagra)
  • Tadalafil (Cialis)
  • Vardenafil (Levitra)
109
Q

Phosphodiesterase Type 5 Inhibitors are absolutely contraindicated for use with ______. & should be used with caution with ______

A

**nitrates

Cautions: alpha-1 blockers, erythromycin, and antifungals (except Levitra –but, Levitra is the only PDE5 that can conflict with antiarrhythmics)

110
Q

What % of Pts will not respond to tx with a PDE inhibitor?

A
  • up to 1/3
  • A single trial is not adequate. It is estimated that 6-8 attempts with a medication and specific dose may be needed before successful intercourse results.
111
Q

ED tx: Alprostadil

  • MOA ?
  • formulation?
A
  • 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.
  • available as an intracavernosal injection (Caverject or Edex) or a transurethral suppository (MUSE, medicated urethral system for erection)
112
Q

CASE D - ED–> He has multiple factors that can be contributing (HTN, DM, BPH, obesity, tobacco)
–He is on several meds that have ED as a possible SE: Metoprolol and Amitriptyline (5α-Reductase inhibitor)

-tx?

A

The meds he’s currently on are working well, so don’t change them. Start the Pt on Cialis—which has been shown to improve BPH AND ED!!!!!!

Pharmacotherapeutics - Fall 21 (7 decks)

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