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Pharmacotherapy > RLP > Flashcards

RLP Flashcards

1
Q

Name 5 medications that can lead to folic acid deficiency

A
  • MTX
  • Phenytoin
  • Trimethoprim long term – UTI prophylaxis, PJP prophylaxis
  • Sulfasalazine
  • Triamterene
  • Alcohol use
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2
Q

What is the usual supplemental dose of folic acid?

A

1 to 5 mg daily. Intake is from food is usually 200mcg per day or 0.2mg

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3
Q

Is folic acid a water soluable vitamin?

A

Water soluble vitamin. You don’t have to worry about accumulation.

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4
Q

What is the mechanism of action of sacubatril?

A

Naprolysin inhibitor. Naprolysin breaks down Naturetic peptides; if you inhibit this enzyme, stop breakdown and get more peptides hanging around. End result is more vasodialation, fluid loss, lower BP

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5
Q

What are the 3 Entresto doses?

A

Initial 24/26 BID – not on ACE/ARB or on low dose
49/51 – for those on greater than 10mg enalapril
Titrate up to 97/103 BID

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6
Q

What is the interaction between lithium and ARBs?

A

Lithium + Arbs can raise lithium concentrations

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7
Q

What is the ACE washout period with Entresto and why is it critical?

A

36 hour washout of ACEI before starting Entresto

Greater risk of angioedema when used together

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8
Q

What is normal and geriatric dosing of cetirizine?

A

10mg per day; high dose is 10mg BID, potential for sedative, anticholinergic effects. Maximum of 5mg in 77 years or older, per manufacturer

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9
Q

What receptors does aripiprazole work on?

A

Activity on dopamine receptors; not as strong a dopamine receptor agonist as others.

Schizophrenia is attributed to excessive dopamine,
reducing activity of dopamine is part of treatment. Also has action on serotonin re-uptake, mild histamine, mild alpha blocking.

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10
Q

Name 5 ADRs from aripiprazole

A

Extrapyramidal, weight gain, anticholinergic effects, sedation, QTC prolongation, hypotension, prolactin elevation, akathisia.

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11
Q

Name a prominent ADR from aripiprazole

A

akathisia – more pronounced than other meds – restlessness, fidgety, can’t sit still, or have internal feelings of crawling out of their skin

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12
Q

Name 3 boxed warnings for Conjugated Estrogens

A
  • alone without progestin, increases risk of endometrial cancer (need intact uterus)
  • Risk of DVT, PE, stroke (blood clots)
  • Increased risk of breast cancer
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13
Q

Name two interacting medications with Conjugated Estrogens

A

Anti-estrogen medications like Anastrazole

Warfarin or Apixaban – patient is already at clot risk

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14
Q

What questions should you assess with estrogen replacement?

A

Not for excessive amount of time, or high doses. Do they continue to need it?

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15
Q

Describe tiotropium’s mechanism of action

A

Blocks acetylcholine action at M3 receptors. When acetylcholine binds that contributes to airway constriction. Preventing binding, promotes relaxation, better breathing

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16
Q

Name a counseling tip for ziprasidone

A

Need to take ziprasidone with a meal. Greater than 500 calories. Absorption goes down without a meal. (watch out in non-responders)

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17
Q

Ziprasidone mechanism of action

A

Mechanism: blockade of dopamine receptors. May have anti-histamine, alpha blockade

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18
Q

Describe tiotropium’s systemic ADRs

A

Other anticholineric ADRs come from systemic absorption; some systemic absorption (19%) but not significant. If patients complain of these it’s probably from another medication. Elderly may be more prone to have these, especially with renal impairment.

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19
Q

Notable ADR from ziprasidone

A

One of the worst for QTc prolongation – avoid in electrolyte imbalances, other meds

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20
Q

Name most common ADR from tiotropium

A

Dry mouth

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21
Q

Name 4 ADRs from ziprasidone

A

QTc prolongation, metabolic syndrome, sedation, CNS depression, extrapyramidal symptoms, falls, Elevation of prolactin, drop in BP

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22
Q

What is the mechanism of hydralazine?

A

Direct stimulation of the arterioles to dialate

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23
Q

If you have DM and HTN, no CKD, do you need an ACE/ARB?

A

Follow ACC/AHA guidelines (HCTZ, chlorthalidone, etc.); If develop proteinuria, then you need to switch

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24
Q

Name 3 dapagliflozin ADRs.

A

Ketoacidosis, UTIs, genital infections, low BP

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25
Q

What is a unique ADR for hydralazine?

A

Lupus-like reaction (fever, muscle pain, arthritis)

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26
Q

If you have DM, and HTN and CKD, do you need an ACE/ARB?

A

Yes, need ACE/ARB

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27
Q

Watch out for in SGLT2 use in immunosuppressed?

A

More likely to have UTI, genital infections so watch out.

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28
Q

Is it unsafe to use SGLT2s with a low GFR?

A

No, but mechanism takes place in the kidney. So, if poor function, isn’t going to work well.

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29
Q

If you have DM, no HTN, no CKD, do you need an ACE/ARB?

A

No, you don’t need an ACE or ARB

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30
Q

What is the mechanism of dapagliflozin?

A

SGLT2 inhibitor. Inhibits reabsorption of glucose and sodium (water goes with it) in the kidney. Works better with higher glucose levels.

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31
Q

Name 3 ADRs from diphenhydramine

A

Confusion, fall risk, dry eyes, dry mouth, urinary retention, constipation. Peds – can get paradoxical effect of activation

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32
Q

Name 3 ADRs from levetiracetam

A

fatigue, dizziness, psychiatric changes (agitation, anxiety), hypersensitivity – skin reactions, BP elevation (peds)

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33
Q

Name 3 electrolytes depleted by torsemide

A

K, Na, Mg

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34
Q

What is the indication for Palivizumab?

A

Monoclonal antibody for preventing RSV infections in pediatric patients. AAP Guidelines for administration: less than 32 weeks gestation, especially those less than 29 weeks, significant risk factors, lung disease

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35
Q

If you have DM, no HTN and CKD, do you need an ACE/ARB?

A

Use proteinuria to direct your therapy

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36
Q

What are the triad of medications that can cause renal issues?

A

NSAID – ACE/ARB – Loop diuretic

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37
Q

Name 3 ADRS from palivizumab

A

monoclonal antibody injection; skin reactions, low chance for anaphylaxis, fever, antibody development to the medication

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38
Q

What is the conversion from bumetanide, furosemide, torsemide?

A

oral furosemide 40mg = torsemide 20mg = bumetanide 1mg

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39
Q

What are three drugs that can cause edema?

A

pregabalin, gabapentin, amlodipine, pioglitazone

40
Q

What is the mechanism of torsemide?

A

Prevents reabsorption of Na, Cl in the ascending loop of Henle. Water goes with it.

41
Q

Name 3 ADRs from torsemide

A

Urinary frequency, depletion of electrolytes (K, Na, Mg), electrolyte imbalances, dehydration, can cause ototoxicity, BP

42
Q

What is the dosing of palivizumab?

A

weight based dosing; IM injection once monthly – max of 5 doses per season. RSV is seasonal in the fall and winter

43
Q

Is hydralazine OK to use in pregnancy?

A

Yes, it can be used in pregnancy

44
Q

For patients with type 1 diabetes, what is the typical insulin requirement at the time of diagnosis?

A

Usually prandial and basal

Usually 50% prandial and 50% basal; Usually 0.4 to 1 unit per kg per day

45
Q

Compare stent thrombosis to in-stent re-stenosis

A

stent thrombosis – lumen is fine, but thrombosis forms in stent. Catastrophic. 1-2%
In-stent restenosis – scar tissue? Proliferation of cells caused by the injury in placement of the stent. Drug eluting stents are designed to stop this. Return of stable angina after stent procedure
“DAPT has no role in re-stenosis””

46
Q

Describe variability in HgbA1c

A

Testing variability of 0.5% – A1c of 7 might be either 6.5 or 7.5 (but standarization process is underway):
Can be falsely elevated or lowered by health conditions where the longer Hgb sits around, will have more sugar build up, Iron deficiency, Sickle cell, recent bleeding could be low
African Americans have tendency to run about 0.5% higher A1c when compared to CGM readings”

47
Q

For patients with type 2 diabetes, what is the typical insulin requirement?

A

Estimate about 0.1 units per kg, start around 10

48
Q

What 3 patient groups should be on DAPT?

A

ACS - unstable angina or MI. Dual antiplatelet needed for anyone with an MI, regardless of going to cath lab, or getting a stent
New stent, whether ACS or not can have stent thrombosis – lumen is fine, but thrombosis forms in stent. Catastrophic. 1-2%
Third group on DAPT – PAD, TIA, CVD, etc – huge burden on atheroschlerosis especially PAD - Used to prevent other events

49
Q

How do you prevent microvascular complications in DM?

A

Microvascular disease – prevented by glucose control
Macrovascular disease – prevented by controlling HTN, HLD
PAD, strokes, CAD
Glucose is a minor player

50
Q

What are the considerations in ticagralor for post PCI?

A

It’s BID – is this too hard for you to take? 10% have adenosine mediated dyspnea. What’s the co-pay, can they afford it? $400 a month

51
Q

What is a BBW for GLP1 agonists

A

History of Medullary thyroid cancer (people usually have papullary)

52
Q

What is the dosing of semaglutide for DM2?

A

Starting dose 0.25mg x 4 weeks (not therapeutic) then 0.5mg weekly

53
Q

What is the relationship between obesity and DM2?

A

Obesity – once you’ve put on fat in the SQ space then body puts fat on liver, pancreas. Fat on the liver is not normal. Causes inflammation in the liver; NAFL. Fats in the pancreas causes toxicity. When fasting is over 126, or over 200, person has lost more than 50% of beta cell mass. TZD – move visceral fat to SQ compartment

54
Q

Which GLP1s have highest efficacy for weight loss?

A 
In order:
"	Semaglutide
	Liraglutide
	Dulaglutide
	Exenatide
	Lixasenatide"
55
Q

Who should have early initiation of insulin?

A

Those with symptoms of hyperglycemia, catabolism, Hgba1c >10%

56
Q

What is the definition of PAD?

A

Atherosclerotic involvement of peripheral arteries that causes flow limiting blockages in peripheral arteries
Lower extremities, but also includes carotid and renal arteries
Illiac, femoral popliteal, (outside of coronary circulation)

57
Q

Describe treatment for PAD

A 
"Exercise regimen for all; very important. Medical based therapy: All PAD should be on low dose aspirin 81mg, reduce risk of MI and Stroke
Atorva80 or rosuva40mg Irrespective of LDL level; even if 70 add high potency statin
PAD specific – cilastozol; FDA approved to increase walking distance; Contraindicated in CHF, if class III or class IV, HFpEF and HFrEF; ADR palpitations, headache, diarrhea"
58
Q

What is the threshold for starting a fixed dose combination for HTN?

A

In US if 20/10 over goal then start fixed dose combination

59
Q

Pt BP is 135/85mmHg. ASCVD – 2.9% - confirmed Stage 1 HTN. Is it time for medical therapy?

A

No, Lifestyle modifications first. BP control is 70% lifestyle and 30% medications. If don’t change lifestyle then won’t be successful and have side effects

60
Q

What is the role of sodium in HTN?

A

Sodium plays big role in HTN. Most high yield counseling point in a clinical appointment
General thresholds: AHA – 1500mg. Others less than 2300mg
If cooking everything fresh, 1 teaspoon of salt (2300mg) Ham, sausage, Salad dressing, cheese, bread,
Also BP meds might not work as well on high salt diet”

61
Q

What is the relationship between GFR and HCTZ?

A

“Lower GFR, lower efficacy of HCTZ. Under GFR of 45 don’t use HCTZ so much
Chlorthalidone use all the way down to GFR of 30
Add loop in CKD 4”

62
Q

Describe the dual action of albuterol and ipratropium

A

“Albuterol kicks in earlier, doesn’t last long vs ipratropium – longer to start 20m lasts longer
As SABA wears off, SAMA sticks around
Time of bronchodilation is extended by using both products”

63
Q

Favor ARBs or ACEIs in HTN?

A

ARBs - fewer SE, seem to be better at lowering BP

64
Q

What is recommended combination of HTN medications for Caucasians?

A

CCB/ARB. ARB will help eliminate edema from CCB

65
Q

Favor spironolactone or eplerinone?

A

Consider eplerinone is generic now and fewer ADRs

66
Q

What is the difference between new onset or chronic HTN in pregnancy?

A

“Cut off of 20 weeks – if you develop before that’s chronic HTN
After 20 weeks – then that’s gestational HTN”

67
Q

How often should you screen for HTN?

A

“Hx of gestational HTN, need to screen annually. Higher risk of HTN
Everyone – screen every 3 to 5 years

68
Q

Describe the difference between albuterol and levalbuterol.

A

“Levalbuterol – active isomer of albuterol
Racemic agents – one is more active than another, or only one is active
No evidence that there is a difference between the two products
Claims that levalbuterol nebs last longer
3x the cost; Dose is ½ of the racemic mixture”

69
Q

What levels are considered hyperkalemia?

A

Depends on institution
K Above 5.5 Or above 5.1
When it gets to 6 or 7 can get symptoms. Above 7 is a medical emergency
Some dialysis patients might be able to tolerate higher levels than others

70
Q

What is the danger of taking a LABA and experiencing an asthma exacerbation?

A

if have asthma exacerbation and taking LABA
LABA is on the beta2 receptors
Can’t give albuterol because receptor is taking
What are you doing to do to bronchodialate?

71
Q

Is nebulizer delivery better than MDI?

A

Inhaler + spacer and nebulizer are equally efficacious
Nebulizer exposes to more drug
Including in the eyes which can increase interocular pressure
Can cause pupil dilation – blurred vision

72
Q

What’s the #1 treatment for hyperkalemia in the hospital setting?

A

“IV Calcium – stabilize the myocardium so that arrhythmias are less likely. Doesn’t do anything about level of K
Calcium gluconate – not as damaging to veins (1/3 potency)
Calcium chloride – more potent, use on code cart. Lasts 30-60 minutes”

73
Q

What’s the #2 treatment for hyperkalemia in the hospital setting?

A

“IV regular insulin, IV push dextrose (50%)(D50).Redistributes potassium back into the cells
Give 5 units to renal impairment IV (not SQ). Give 10 units to others
Sodium potassium ATP ase pump in skeletal muscles
Intervention lasts 4-6 hours, but dextrose won’t last that long. Might go low”

74
Q

What is the expected effect of a beta agonist on lung capacity?

A

Positive response is increase of 200mL or 12% in FEV1 compared to baseline (asthma); (COPD might be 50mL, not big response)

75
Q

What is the mechanism of action of beta2 agonists?

A

“Smooth muscle surrounds the passages inside the lungs; Needs Ca in cytosol for actin and myosin to interact and contract.
Albuterol - Increases cAMP in smooth muscle
Decreases calcium concentrations
Decreases muscle contraction thus increased relaxation”

76
Q

What is the mechanism of SAMAs/LAMAs?

A

“Smooth muscle surrounds the passages inside the lungs; Needs Ca in cytosol for actin and myosin to interact and contract.
Muscarinic agonists - Increases guaylate cyclase and cGMP in smooth muscle
Decreases calcium concentrations
Decreases muscle contraction thus increased relaxation”

77
Q

Tips for patients getting edema from CCB?

A

take at night, add diuretic

78
Q

What is the staging for albuminuria (albumin/creatinine)

A

A1 – spot urine albumin/creatinine ratio less than 30 mg/g
A2 – 30 to 299 – make sure it’s persistent
A3 – above 300 - severe, persistent

79
Q

Is protein/creatinine or albumin/creatinine the right test for determining CKD?

A

Albumin/creatinine ratio. Albumin is 60 – 70% of protein in urine

80
Q

What are symptoms of SSRI withdrawal?

A

Anxiety, stomach upset, electrical zaps

81
Q

What is the mechanism of action of calcitonin?

A

Blocks parathyroid hormone, then blocks osteoclast activity

82
Q

Name two prodrugs that might not get activated with paroxetine (CYP2D6 inhibitor)

A

Codeine and tamoxifen

83
Q

Name 3 indications for partoxetine

A

Depression, anxiety, PTSD, OCD, hot flashes

84
Q

What is the mechanism of action of dulaglutide?

A

GLP1 agonist. Slows gastric emptying; helps release insulin after eating

85
Q

What is the half life of paroxetine?

A

Half-life is shorter than others, about 20 hours. Stopping paroxetine abruptly might lead precipitate withdrawal

86
Q

What are the health risks as albuminuria increases?

A

Higher albuminuria, higher risk for AKI, progression of CKD, ESRD, higher risk of CVD

87
Q

What are 3 ADRS from HCTZ?

A

Hypercalcemia, gout exacerbation, low Na, K, Mg; frequent urination;

88
Q

What is calcitonin used for?

A

Hypercalcemia, pain with fracture, in the past for osteoporosis

89
Q

What is the dosing of dulaglutide?

A

Injections once a week. Has a 5d half life; takes about a month to get to steady state. 0.75mg; 1.5mg; 3mg; 4.5mg. Higher doses have little HgbA1c lowering but more ADRs

90
Q

Since HCTZ contains a sulfa group do you need to worry about sulfa allergies?

A

Investigate the allergy history. If there is a history of serious reaction to a sulfa drug, then use caution

91
Q

If you only have Protein/creatinine ratio how can you convert to albumin/creatinine ration?

A

“Less than 142 mg/g then probably are A1
Between 142 mg/g to 660 – A2
Above 660 – A3”

92
Q

Interpret the kidney staging of GFR 3aA1

A

low GFR, but little albuminuria – elderly, really need to intervene? Normal aging

93
Q

Name 3 ADRS from calcitonin

A

Lowers Ca levels; rhinitis; nose bleeds; irritation

94
Q

Name 2 ADRS from paroxetine that are more significant than other SSRIs

A

Sedation, Weight Gain

95
Q

Interpret the kidney staging of GFR 3aA3

A

GFR 45 to 60, high albuminuria. this person is at high risk for poor outcomes

96
Q

Is paroxetine on the Beers List?

A

Yes, risk of mild anticholinergic ADRs, low BP

Pharmacotherapy (11 decks)

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