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IPAP JUNIOR SEM. > PHARM III All Lectures > Flashcards

PHARM III All Lectures Flashcards

1
Q

What are the two direct/ peripherally acring antispastic agents

A

Dantrolene and Botulium toxin A

They both alter function of nicotinic-muscle receptors or skeletal muscle fibers

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2
Q

What is the durantion of use and Clin/Ind for cyclobezaprine

A

Short term in combination with physcial therapy

Do not use for cerebral palsy or spinal cord injury

Has the potentail to lower the SZR threshold, DO NOT USE with tramadol

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3
Q

Can you use cyclobenzaprine and tramadol together

A

No! Both lower the SZR threshold

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4
Q

Since Cyclobenzaprine is like a TCA, what are its ADE and C/I

A

DROWSINESS , dry mouth, urinary retention, increadsed occular pressure

SERTONIN SYNDROME

C/I: Recent MI, any heart problems, DO NOT USE w/in 14 days of a MAOI
Hyperthyroidism
Caution in preg.

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5
Q

Orphenadrine is an analog of what other drug and is indicated for what condition

A

Diphenhydramine

Clinical Use: Treatment of muscle spasm associated with acute painful musculoskeletal conditions
Used short term (2-3 weeks)

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6
Q

Since orphanadrine is an anticholinergic what are its ADE and C/I

A

Anticholinergic effects: dry mouth (1st to appear); tachycardia, urinary hesitancy or retention, blurred vision, nausea/vomiting, etc.
High risk for confusion in elderly

Contraindications: glaucoma, pyloric or duodenal obstruction, stenosing peptic ulcers, prostatic hypertrophy or obstruction of the bladder neck, and myasthenia gravis

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7
Q

Carisoprodol is metabalized to what.. which is what gives it its anziolytic and sedative effects

A

Meprobamate

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8
Q

What is the clinical indication of carisoprodol

A

Relief of discomfort associated with acute, painful musculoskeletal conditions in adults

Used short term (2-3 weeks)

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9
Q

What are the ADE and C/I of carisoprodol

A

Withdrawl, sedation, dizzyness, HA, SZR,
Caution with ETOH and depressants
High risk of confusion in elderly

DO NOT USE IN PREGNANCY

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10
Q

Can Carisoproldol be used in pregnancy

A

NO , adverse events have been observed in animal reproduction studies

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11
Q

What is the clinical use and ADE of metaxalone

A

Clinical Use:
Relief of discomforts associated with acute, painful musculoskeletal conditions
Appears to cause less drowsiness than others

Adverse Effects:
Nausea, gastrointestinal upset, sedation, dizziness, headache, anxiety, or irritability

Serotonin Syndrome

Caution combining with alcohol and other CNS depressants

High risk for confusion in elderly

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12
Q

What is the Clin/use and ADE of methocarbamol

A

Adjunctive treatment of muscle spasm associated with acute painful musculoskeletal conditions

Treat muscle spasticity associated with tetanus (toxin) poisoning

ADE: BLACK BROWN OR GREEN URINE!
Caution in use wtih ETOH or depressants

C/I iv formulations in pts with renal impairment and hepatic impairment

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13
Q

A pt presents with tetanus poisoning, what Antispasmodic can you use to Tx

A

Methocarbamol

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14
Q

What is the clin use and ADE of tizanidine

A

Clinical Use:
Muscle spasticity
Short acting agent

Adverse Effects:
Drowsiness is the most prominent adverse effect
Start low and titrate the dose up (2mg TID)

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15
Q

What is the most prominent ADE of tizanidine

A

Drowsiness

Can also cause drymouth, HOTN, asthenia, and hepatotoxic (A2 agonist)

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16
Q

Baclofen inhibits the release of what substance in the spinal cord

A

Substance P

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17
Q

Which is better, baclofen or diazapem

A

Baclofen casues as much antispamodic activity as diazapem with out the same amount of sedation which can be a good thing

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18
Q

Can you use baclofen in SZR pts

A

Increased seizure activity reported in epileptic patients, therefore withdraw slowly

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19
Q

Can you use Diazapam in preg. Pts

A

Cat D, no

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20
Q

A pt presetns with post herpatic neuralgia, what medication can help

A

Gabapentin and Gabapentin enacarbil (prodrug)

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21
Q

Can Gabapentin Enacarbil be used for epilespy

A

prodrug for gabapentin and is indicated for post herpetic neuralgia and restless leg syndrome, NOT epilepsy

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22
Q

How are gabapentin and pregabalin eliminated

A

eliminated renally; adjustments may be necessary for renal dysfunction and hemodialysis

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23
Q

What are the ADE of Gabapentin and pregabalin

A

Dizziness, and wt gain

Gaba: drowsiness and fatigue
Pre: Sex Dyf., angioedema,

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24
Q

What is the antidote to Botulinum Toxin

A

Equine Botulinum Antitoxin

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25
Q

Do NMBA effect the CNS

A

NO! Only act periphearlly

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26
Q

A female pt presents with a unilateral severe HA, desribes it as pulsating that is aggrevated by physical activity
Complains of Nauseas, photophobia, and phonophobia, tyopically lasting up from 4-72 hours

What kind of HA is this

A

Migraine

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27
Q

A female ptr presents with cc of HA x 1 day

States pain is Bilateral and has a pressing/ tighting sensation, is not effected by physical activity, denies nausea, but sometimes has photo/phono phobia

Think what kind of HA

A

Tension

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28
Q

A male pt present with cc of HA x 45 minutes

Describes it as unilateral severe piercing sensation
States he has ipsilateral nasal congestion, miosis, and ptosis, and frequently the HA occur at night

What kind of HA

A

Cluster

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29
Q

What does the acronym snooping refer to with HA

A

S: systemic symptoms or signs (e.g., fever, weight loss), or systemic disease (e.g., cancer)

N: neurologic symptoms or signs

O: onset sudden (e.g., thunderclap headache)

O: onset late in life (> 40 years)

P: pattern change (progressive with loss of headache-free periods; change in type)

Go SNOOP for an alt cause

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30
Q

What does the Acronym POUNDing mean when it comes to HA

A 
Pulsatile 
One day duration or less 
Unilateral 
N/V 
Disabling intensity

POUNDING=migraine

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31
Q

What is the criteria to Dx a Migraine without aura

A 
Al least 5 attacks that last 4-72 hours with at least 2 of the follwoing: 
Unilateral 
Pulsating 
Mod-severe pain 
Aggrivated by phycical activity

During the HA at least 1 of the follwing s/s:
N/V, photo or phonophobia

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32
Q

WHat is the Dx criteria for Migrain with aura

A

A least TWO HA with at least 1 S/s of aura ( Visual, sensory, speach, language, motor, brainstem, or retinal)

With at least two of the following:

  • One aura symptom spreads gradually over ≥5 min, and/or two or more symptoms occur in succession
  • Each aura symptom lasts 5-60 min
  • At least one aura symptom is unilateral
  • The aura is accompanied, or followed within 60 min, by headache
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33
Q

What is the gene that is associated with genetic predisposition of migraines

A

50% of cases of familial hemiplegic migraine (FHM) are caused by mutations within the CACNL1A4 gene on chromosome 19

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34
Q

What is the important mediator in Migraines

A

Seretonin (5-HT)

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35
Q

What is the neuronal theroy of Migraines

A

Migraine aura may be explained by the neuronal theory in that the positive (e.g., light around the edges of the field of vision) and negative (e.g., blind spots or tunnel vision) symptoms of the migraine aura are caused by neuronal dysfunction, not ischemia

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36
Q

Activation of what system is the reason for pain in a migraine

A

Pain results from activity within the trigeminovascular system

Activation of trigeminal sensory nerves triggers the release of vasoactive neuropeptides:

  • Calcitonin gene-related peptide [CGRP]
  • substance P
  • neurokinan A

These Produce vasodilation and dural plasma extravasation leading to neurogenic inflammation

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37
Q

What are the 4 phases of a Migraine

A
  1. Premonitory S/s
    (phono/photophobia, hyperosmia, anxiety, depression , euphoria, polyuria, diarrhea, stiff neck, tawning, food cravings, ect)
  2. Aura
    (Positive or negative visual (most often), sensory, or motor symptoms that develop over 5-20 minutes and last for usually 60 minutes, with the headache usually following within 60 minutes)
  3. HA
    ( Generally begins with a dull ache that intensifies over a period of minutes to hours to a throbbing headache, which worsens with each arterial pulse)
  4. Resolution
    (Fatigue, irritable, impaired concentration, scalp tenderness, mood changes (e.g., refreshed and euphoric or malaise and depression))
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38
Q

What are the short term goals of Migraine Tx

A

Treat attacks rapidly and consistently without recurrence

Restore the subject’s ability to function

Minimize the use of backup and rescue medications

Optimize self-care and reduce subsequent use of resources

Cause minimal/no adverse effects

Be cost-effective

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39
Q

What are the long term goals of Migraine Tx

A

Reduce migraine frequency, severity, and disability

Improve quality of life

Prevent headache

Avoid escalation of headache medication use

Educate and enable patients to manage their disease

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40
Q

What is the primary end point of Migraine Tx

A

Headache response (pain-relief or pain-free within 2 hours) (Primary endpoint)

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41
Q

What is the MIDAS

A

Migraine disabilty assesment

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42
Q

What is a MIDAS grade I

A

MIDAS score of 0-5

Means little or no disability

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43
Q

What is a MIDAS grade II

A

Score of 6-10

Means mild disability

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44
Q

What is a MIDAS grade III

A

Score from 11-20

ind. moderate disabilty

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45
Q

What is a MIDAS grade IV

A

Score greater than 21+

Ind. severe disability

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46
Q

A score of less than 2 on the Monitoring Headache Response Migraine-ACT Questionnaire means what

A

Score of ≤ 2 may indicate a need to change the patient’s acute medication therapy

Score of ≤ 1 may indicate that the change is mandated

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47
Q

What is the Sterp care across migraine Tx

A

HA 1 = treat with NSAID
HA 2= Tx w/ NSAID
HA 3= Tx with NSAID

If unsuccessful response in more than 2 HA Tx with NSAID then treat HA 4 with triptan

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48
Q

What is the Step Care within Migriane Tx

A

HA treated with an NSAID yet unsuccesful after 2 hrs

Then treat with a triptan

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49
Q

What is the stratified Care approach to Migraine Tx

A

PTs with MIDAS grade II= NSAID

MIDAS grade III-IV= triptan

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50
Q

What are the two specific therapies for migraines

A

Ergotamines and Triptans

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51
Q

Is acetaminophen better or worse at treating HA than NSAIDs

A

Pain-free response at 2hrs found inferior to other commonly used NSAIDs and aspirin

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52
Q

Are there any studies supporting the use of Butabital for HA

A

NOPE

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53
Q

Can pts taking MAOI take Midric C-IV

A

NO!

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54
Q

Can pts with HTN take Midrin C-IV

A

No, isometheptane causes vasocon

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55
Q

What should pts who take Excedrin be cautioned of with daily use

A

Caution of caffeine withdrawal headaches if taking daily

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56
Q

How long can NSAIDs be used in HA tx

A

Limit use to < 15 days per month to prevent drug overuse headache

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57
Q

How do NSAIDS help Tx migraines

A

magraines: prevents neurogenically mediated inflammation in the trigeminovascular system

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58
Q

Should NSAIDS be used in pts with PUD, Renal insuf, bleeding D/o

A

No can cause bleeding and remember renal trifecta

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59
Q

What is the most effective route for ergotamines

A

Rectal !

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60
Q

What is ergotism

A

Ergotism: intense vasoconstriction resulting in peripheral vascular ischemia and possible gangrene, as well as possibly tonic-clonic convulsions accompanied by mania and hallucinations

From taking ergotamine

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61
Q

Can preg pts take ergotamine

A

NO! Cat X

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62
Q

Ca Triptans and ergotamine be used together

A

Do not use within 24 hours of a triptan

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63
Q

Can ergotamines be used in pts with CVDz, Hepatic or Renal Dz

A

No!

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64
Q

Long term use with ergotamines can cause what valvular heart problems

A

Fibrotic valve thickening (e.g., aortic, mitral, tricuspid) with long-term use

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65
Q

Can you give ergotamine alone

A

No, cuases N/V so need to premedicate

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66
Q

What medication is used to treat status migraniosus

A

Dihydroergotamine IV (45)

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67
Q

What is the advantage of using Dihydroergotamine vs ergotamine

A

Dihydroergotamine has less ADE

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68
Q

Can you use dihydroergotamine and Triptans together

A

Do not use within 24 hours of a triptan

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69
Q

What are the highest likely hood of success triptans when treating migraines

A

The highest likelihood of consistent success was found with rizatriptan, eletriptan, and almotriptan

ERA!

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70
Q

How many times per month can a pt use triptans

A

Limit use to ≤ 9 days per month

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71
Q

What pts can Triptans NOT be used in

A

Patients with a history of ischemic heart disease (e.g., angina, previous MI, etc.), uncontrolled hypertension, and cerebrovascular disease (e.g., stroke)

Do not use in patients with hemiplegic and basilar migraines

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72
Q

How should the 1st does of triptans be administered

A

Patients at risk of coronary artery disease should have 1st triptan dose in the clinic with vitals ± ECG

Consider administering the 1st triptan dose in the clinic with vitals ± ECG in patients with a likelihood of unrecognized coronary disease (i.e., significant hypertension, hypercholesterolemia, obese patients, diabetics, smokers, etc.)

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73
Q

If a pt is taking a triptan for HA, can you also give then an ergotaine

A

Do not use within 24 hrs of ergotamines

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74
Q

Can triptans and SSRIs be used together

A

Caution with other serotonin active medications serotonin syndrome

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75
Q

What is seretonin syndrome

A

A potentially life-threatening drug reaction resulting from excess serotonin
Presents as a clinical triad of abnormalities:
-Cognitive effects
-Neuromuscular dysfunction
-Autonomic dysfunction

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76
Q

A pt presents to the ED with AMS, myoclonus/ hyperreflexia, and hyperthermia

What triad of S/s if this reflecting

A

Seretonin syndrome

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77
Q

What is the Tx approach to seretonin syndrome

A

Withdrwal offending agent

Supportive care
Cyporheptadine

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78
Q

Which Triptan contains a sulfa group and can not be given to pts with sulfa ALLRGY

A

Almotriptan

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79
Q

If a pt is taking propranolol, what adjustmnet must be made to Rizatriptan Rx

A

Decreased the dose to 5 mg in pts taking propranolol

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80
Q

If a pt is taking clarithromycin ( a CYP3A4 Inh.) how must they take eletriptan

A

Can not be used with in 72 hours

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81
Q

Can preg. Pts used butophanol

A

When used in pregnancy, abnormal fetal heart rate was noted

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82
Q

Butorphanol as a partial Mu agonist has what ADE

A

HOTN, N/V, blurred vision, sedation

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83
Q

What is the best way to prevent Medication over use headaches

A

Prevention is best: limit use of migraine therapies to 2 days/week

Treat by discontinuing the offending agent

  • Takes 3 to 8 weeks following medication withdrawal to evaluate efficacy
  • May bridge with prophylactic HA medications
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84
Q

What are the thresholds to start a pt on migraine prophylaxis

A

Frequency and duration (generally accepted thresholds):
> 4 HA/month or
Last >12 hours

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85
Q

What is an adequate trial time frame for a migraine prophylaxis tx

A

1-2 months

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86
Q

How is Treatment generally administered for migraine prophylaxasis

A

Treatment is generally continued for 3-6 months after the frequency and severity of headaches decrease, and then is tapered gradually (over 2-4 weeks) and discontinued

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87
Q

A pt presents with recurring headaches that are in a predicatble pattern (menstral migraines)

What is an approaprite prophylaxis

A

NSAID at the time of the HA

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88
Q

When can BB be used in Migraine Tx

A

In healthy or comorbid HTN, angina, or anxiety

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89
Q

A pt with comorbid depression or insomina, with migraines should get what meds

A

TCAs

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90
Q

A pt with SZR and Migraines should get what Dx

A

Anticonvulsants

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91
Q

Topiramate causes a 2-4 fold increase in what condition

A

Kidney stones

Can also cause Met Acidosis

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92
Q

If a pt has astham or raynouds can they take BB

A

NO!

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93
Q

What is the NSAID used for Mentrual migraines

A

Naproxen

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94
Q

What electrolyte is a useful prophylaxis of migraines in pregnancy

A

Magnesium

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95
Q

What expensive medication can be considered for pts with 15 or more HA a month

A

Botulism toxin A

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96
Q

Is a pt is pregnant, what is the best Tx of their migraines

A

Acetaminophen for active attacks

Mag for prophylaxis

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97
Q

What is the most common type of primary HA

A

Tension HA

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98
Q

What seperates a tension HA from a migriane

A

Differences:
Lacks premonitory symptoms and aura

Pain usually mild to moderate in intensity, bilateral, and described as dull, non-pulsatile tightness or pressure that occurs in a hatband distribution around the head

Disability minor in comparison to a migraine

Routine physical activity does not affect headache severity

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99
Q

What is the criteria for Dx of a Acute Tension HA

A

At least TEN episodes occuring more than 1 day a momth lasting form 30minutes to 7 days

With at least 2 of the followingL 
Bilateral 
Pressing/tightning 
Mild to mod pain 
Not aggrevated by physical activity

Can not have N/V or either photo/phonophobia

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100
Q

What is the critera for chronic tension HA

A

HA more than 15 days per month for more than 3 months
Lasting hours or continous

Meeting at least 2: 
Bilateral 
Pressing/ tightning 
Mil-mod pain 
Not aggrevated by phys. Activity

Can not have N/V or photophobia+phonophobia

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101
Q

When should prophylaxis be considered for tension HA

A

Consider if headache frequency (> 2/week), duration (> 3-4 hours), or severity results in medication use or significant disability

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102
Q

What are the ADE of using a TCA (amitryptyline) for tension HA

A

: anticholinergic side effects, weight gain, orthostatic hypotension, and arrhythmia concerns

Should be taken at night

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103
Q

1st degree relatives of people with cluster HA have what risk of having it as well

A

1st degree relatives have a 14-fold increased risk for also having cluster headaches

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104
Q

A pt presents to the exam room , pacing back and forth holding his head, states that the pain is only one one side of his head, and is severe ..
what kind of HA could this be

A

Cluster HA

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105
Q

What is the criterea to Dx a cluster HA

A

A least FIVE attacks that are severe with unilateral eye pain lasting 15-180 minutes if untreated

HA is accompanied by at least 1 ipsilateral S/s

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106
Q

What is the Tx appraoch to Cluster HA

A

O2 is the 1st line Tx

Sumatriptan is the most effective Rx

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107
Q

What is T1DM

A

results from β-cell destruction, usually leading to an absolute insulin deficiency

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108
Q

What is T2DM

A

results from a progressive insulin secretory defect often in the presence if insulin resistance (i.e., a relative insulin deficiency exists)

109
Q

What fasting glucose indicated Diabetes

A

126 mg/dL

110
Q

What Oral Glucose Tolerance Test value indicated DM

A

Greater than 200mg/dL

111
Q

What A1C value indicated DM

A

Greater than 6.5

112
Q

What is the 7th leading cause of deaith in the US

A

DM

113
Q

Reducing Hypertension in DM pts has what profoudn effect

A

In general, for every 10 mmHg reduction in SBP, the risk for any complication related to diabetes is reduced by 12%

Reducing DBP from 90 to 80 mmHg reduces the risk of major cardiovascular events by 50%!!!

114
Q

What is the leading cause of new cases of blindness among adults

A

DM

115
Q

What week of pregnancy are pts screened for DM

A

24th-28th week

116
Q

What are the BG goals for a pt with GDM

A

Goal:
Preprandial: ≤95 mg/dl
1 hr postprandial: ≤140 mg/dl
2 hr postprandial: ≤120 mg/dl

117
Q

A preg pt presents to the clinc, she has no Hx of DM or GDM, when should she be screened for GDM

A

At 24-28 weeks

118
Q

A pt has risk factors for DM and GDM and is pregnant, when should she be screened for GDM

A

At the 1st prental visit

119
Q

Women with GDM should be screened for DM how many weeks post partum

A

6-12 weeks

120
Q

Which two DM Rx are preg cat C

A

Glargine and glulisine

All other DM medications are labeled B

121
Q

What is the threshold that defines hypoglycemia

A

Less than 70

122
Q

A pt presents with tachyHR, tremors, sweating, anxiety and complains of hunger

What should you check

A

BG

123
Q

What is level 1 hypoglycemia and what is the Tx appraoch

A

BG of 60-70 mg/dL

15-15-15 rule

124
Q

What is level 2 hypoglycemia and what is the Tx approach

A

BG 41-59 mg/dL

30-15-30 rule

125
Q

What is level 3 hypoglycemia and what is the Tx approach

A

BG less than 40 mg/dL

Glucagon 1mg subQ
Or 50mls of D50W IV

126
Q

How do most T1DM pts present initially

A

DKA

127
Q

What are the hallmark Dx labs for DKA

A

Hyperglycemia
Acidosis
Anion Gap
Ketonemia or Ketouria

128
Q

What is the inital approach to Hyperglycemic emergencies

A

Check BG, serume/urine ketones, CMP, start IV fluids of 1 L per hr

129
Q

If the potassium level is below 3.3

How should you admin inulin

A

DONT!

Hold insulin and give K+ until K is greater than 3.3

Than give K+ in each L of IV fluid to maintain a level between 4-5 mEq/L

130
Q

What are the two Insulin approaches to hyprglycemic emergencies

A

Either

0.1 U/kg as IV bolus follwoed ob a o.1 U/Kg/Hr of IV infusion

Or 0.14U/kg pr Hr as Iv continuous infusion

In both approaches, If serum gl doesnt fall by 10% in the first hour give 0.14 bolus.

131
Q

When should Tx approach be amended in DKA

A

When serum gl reaches 200 reduce Insulin to 0.02-0.05 U

Keep serum gl between 150-200 until resolution of S/s

132
Q

WHen should Tx appraoch to HHS be ammended

A

When serum gl reaches 300 reduce Insulin to 0.02-0.05

Keep gl between 200-300 until resolution of S/s

133
Q

On sick days how often should T1DM check BG

A

Every 2-4 hours if increased

134
Q

On sick days how often shoudl T2DM pts check thier BG

A

2-4 times a day if elevated

135
Q

What is the age of onset difrences of T1 vs T2 DM

A

T1 usually before the age of 30

T2 is usually after 40

136
Q

Is there a strong familail link for T1DM

A

No, however T2 there is

137
Q

If a pt has a fasting plasma glucose of 100-125

What would we call this

A

Pre diabetic

138
Q

If a pt had a Glucose Tolerance test from 140-199

What would we call this

A

Pre DM

139
Q

An A1C of 5.7-6.4 is what

A

PreDM

140
Q

in general, every 1% drop in HbA1c reduces the risk of microvascular complications by what percent

A

40%

141
Q

What are the Common ADE of Insulin use

A

Hypoglycemia ( can be life threatening)

Wt gain (4kg)

Lipohypertrophy: fat mass occurring at the injection site

Lipoatrophy: dimpling in the skin at the injection site due to fat breakdown

142
Q

Where can Insulin not be injected

A

Into the umbilicus

143
Q

What is the site of most rapid absoprtionfor Insulin, what is the least

A

Fastest in the abdominal fat

Slowest in the superior buttocks

144
Q

How does renal failure and hepatic failure effect insulin clearnace

A

Decreased clearance

145
Q

What is the role of Bolus insulin

A

Controls post pradinal hyperglycemia

146
Q

What is the role of basal insulin

A

Controls fasting hyperglycemia

147
Q

When must rapid acting insuling be administered

A

Either 5-15 minutes before
Or withing 20 minutes after a meal

Lispro: Give SQ within 15 mins before or immediately after meals

Aspart: Give SQ 5 to 10 mins before meals

Glulisine : Give SQ injection within 15 mins before or within 20 mins after a meal

148
Q

How is afrenza administered

A

Inhaled , at the beginning of a meal

Useful for pts that dont want to stick themselves

149
Q

If switchingn to afrenza from subQ insulin what is the conversion

A

SQ mealtime insulin: round up to the nearest 4 units and converting unit-per unit

Example: 6 units of Novolog to 8 units of Afrezza

150
Q

What pts is U500 insulin used for

A

U500 (high concentration regular insulin) used for patients requiring > 200 units/day

151
Q

What kind of insulin is U500

A

Short acting (refular) insulin

152
Q

How is short acting insulins administered

A

Can be IV or SubQ

30 min beofre meals

153
Q

How is intermediate acting insulin administered

A

Not in relation to meals, can be used a basal insulin

154
Q

What does NPH insulin stand for

A

Neutral protamine hagedorn

155
Q

Of the long acting insulings, Glargine and detemir, which one is bound to albumin

A

Detemir

156
Q

Can long acting insulins be mixed with other insulins

A

Do not micx with other insulins or dilute!

157
Q

Using Regular short acting insulin after a meal increases the risk of …

A

HOglycemeia

158
Q

WHat is the major risk of U500 insulin

A

Inadvertent OD

159
Q

For basal insulin , which has the lower risk of noctural HOglycemia, NPH or Long acting?

A

Long acting, like determir and glargine have the lower risk

160
Q

What is the ave. Daily req Insulin for a T1 DM

A

O.5 units per kg

161
Q

What is the insulin to carb ration when using regular insulin

A

450/TDD

162
Q

What is the insulin to CHO ration when using rapid acting insulin

A

500/TDD

163
Q

1 unit of insulin is estimated to cover how many gm of CHO

A

15gm

164
Q

What is the rule of 1500 and 1800

A

Regular Insulin: Correction factor = 1500/TDD
Rapid-Acting Insulin: Correction factor = 1800/TDD

Correction dose= (current BG-desired blood BG)/ corretion factor

Example
Current Bg 234, desired BG is 120
Pts wt is 100kg
Assume 0.5u/kg

(234-120)/ (1500/50)= 3.8 (4)units of regular insulin

Or 114/( 1800/50)= 3.16 (3) units of rapid acting insulin

165
Q

If pre breakfast BG is high/ low what insulin adjustment

A

adjust evening basal insulin dose

166
Q

If pre-lunch blood glucose is high/low adjust?

A

adjust morning bolus insulin dose the next morning

167
Q

If pre-supper blood glucose is high/low

Adjust

A

adjust morning basal insulin and/or pre-lunch bolus dose the next day

168
Q

If pre-bedtime blood glucose is high/low

Adjust?

A

adjust supper rapid/reg insulin dose the next day

169
Q

If 2-hour post-prandial glucose is high/low

Adjust?

A

adjust pre-meal rapid/reg insulin dose the next day

170
Q

If 0300 BG is high/. Low

Adjust ?

A

adjust evening basal insulin dose the next day

171
Q

What is the difference between somogu effect and dawn phenomenon

A

Dawn: Insufficient evening basal insulin leads to AM hyperglycemia secondary to normal waking process
—0200 to 0300 SMBG results reveal a normal or elevated blood sugar

Solution: increase the evening basal insulin

Somogyi: Too much evening basal insulin leads to hypoglycemia in the middle of the night
—0200 to 0300 SMBG results reveal a decreased blood sugar
In response to the hypoglycemia, the body responds by increasing glycogenolysis and gluconeogenesis leading to AM hyperglycemia

Solution: decrease the evening basal insulin

172
Q

What are the Rsk fxs for T2DM

A 
Physical Inactivity 
Family Hx 
High Rsk Ethnicity 
Delivering a baby >9lbs 
GDM Dx 
Polycyctis ovarian syndrome 
HTN 
Hx of CVD 
Dislipidemia (HDL < 35 or TriGs>250) 
A1C > 5.7
173
Q

Define Metabolic syndrome

A

40in (men) 35in (women) waist

HDL less than 40 (men) or 50 (women)
Or Statin

TriGs > 150 or Rx
HTN or Rx
Fasting gl > 100 or Rx

174
Q

What are the 4 markers for T2 DM Dx

A

A1c greater than 6.5

Fasting gl > 126

2-hr gl > 200

Random gl> 200

175
Q

What are the goal of therapy for Type 2 Dm pts

A

A1c below 7.0
Or beolw 8.0 in eledery
(Tight control is below 6.5)

Post pradnianl bg less than 180

176
Q

What is a proper excercise regime for a pt with T2 DM

A

150 min/wk mod intensity aerobic activity
Spread over 3 days a week
With resistance training 2 times a week

177
Q

What is the primary and secondary prevention of CVD for pts with DM

A

Aspring

Or clopiogrel ( if allergy)

178
Q

What is the bp goal for a pt with DM

A

Less than 130/80

179
Q

A T2DM pt presents with an A1c of 8.8

What is the treatement approach

A
  1. Above goal? Yes= metfromin
  2. Follow up in 3 months
  3. Above goal? Add an option 1 med
    (GLP-1, SGLT2, DPP4, TZD, SU)
180
Q

If a pt is started on a GLP-1, what med can not be part of thier treaptmetn

A

DDP-4 (liptins)

181
Q

Are Sulfonyrueas usually added on to pts regiments

A

No, SU are usually started first if the pt can afford other options, but rarely added on later

182
Q

What are the 4 option 1 DM rx

A

GLP-1, SGLT-2, DPP-4, TZD

If the pt is poor then you can consider SU

183
Q

If a pt is started on a GLP 1, and is not at goal, what is the next step

A

SGLT2

184
Q

If a pt is started on an SGLT-2, and is not a goal what is the next step

A

GLP-1

185
Q

If a pt is started on a DPP-4 and is not at goal what is the next step

A

SGLT-2

186
Q

If a pt is started in a TZD, and is not at goal what is the next step

A

SGLT-2

187
Q

Can you combine DPP4s with GLP1

A

No!

188
Q

If a pt has ASCVD

What is the appraoch to Tx thier T2DM

A

Must start with either a GLP-1 or a SGLT2,
If not at goal add on which ever of the above was not started first

If still not at goal then d/c to GLP-1 and add on a DPP-4 ,

And if still not at goal start pt on basal insulin

189
Q

What is the threshold to place a pt on metfrom plus an option 1 med

A

If A1c is above 1.5% goal

190
Q

If a pt has an AIc above 10% what is the approach

A

Can start insulin right away

Using a Dual injectable therapy approach

GLP-1 + Basal insulin

If not at goal then add mealtime insulings starting at largest meal of day and adding until Goal is met

191
Q

SGLT-2i (flozins) have what major ADE

A

Can cause CHF and CKD

192
Q

GLP-1 (tides) have what major ADE

A

ASCVD risk

193
Q

What is the only labeled oral agent DM Rx for use in children

A

Metformin

194
Q

How should metformin be used in the elderely

A

Should not be titrated to max doses

195
Q

What are the ADE of metfomin

A

Gi upset , Lactic Acidosis

METfromnin acidosis

196
Q

A pt presents to the ED with signs of hyperglycemia, they have a Scr level greater than 1.5, can they be given metfromin

A

NO, Contraindicated if Scr > 1.4 in females or 1.5 in males

197
Q

A pt comes in to the ED and is a T2DM pt who takes metformin, they may need contrast later as part of thier w/u, what should be done with thier metformin

A

Hold metformin if radiographic iodinated contrast media is given and resume 2-3 days later after normal renal function documented

198
Q

Can Metformin and cimetidine be used together

A

Cimetidine (Tagamet) competes for rental tubular secretion with metformin and can increase metformin levels

199
Q

Sulfonuryeas (SU) all end in…

A

IDE

Ide take my sulfonyureas!

200
Q

What is the most common ADE of SUs

A

HOglycemia and wt gain

Can also cause allergic reactions

201
Q

Which of the SUs have the highest HOglycemic potential

A

Chlorpropamide

202
Q

What are the ADE of chlopropamide

A

HOgl

SIADH, HONa+

Avoid in pts with renal dysfun. Or the eledrly

203
Q

Which of the 2nd gen SUs has the highest HOgl rsk

A

Glyburide

204
Q

What is the safest SUs for renal dysfun pts

A

Glimepiride

205
Q

Meglitidines all end in

A

GlinIDE

Ide take your Melitinides and SUs

206
Q

If repaglinide and gemfibrozil are taken together

What is the effect

A

Doubles the effectiveness

207
Q

What are the ADE of meglitinides

A

HOgl
NOT associated with Wt gain

URI and Flu like syndromes

208
Q

What is the role of meglitinides

A

To be added on to metformin in place of sulfonylureas in patients with irregular eating schedules or in those who develop late hypoglycemia with sulfonylureas

209
Q

Should meglitinides be used a mono tx

A

One of the last choices as monotherapy for patients with an A1C less than 7.5% Use with caution

210
Q

What is the receptor that TZDs work on

A

Binds the peroxisome proliferator activator receptor-γ (PPAR-γ) enhancing insulin sensitivity at skeletal muscle, liver, and fat cell

211
Q

Can TZDs be used in CHF pts

A

NO! Avoid in patients with symptomatic CHF

May result in a dilutional anemia; edema frequency increases when the TZD is combined with insulin (15%)

212
Q

What is the cancer that is associated with TZD use

A

Increased risk of bladder cancer (Pioglitazone)

213
Q

What is the saying for TZDs

A

I like to bring TXDs to the PPAR-ty ZONE

both drugs end in zone and work on the PPAR receptor

214
Q

What is the diffence between GLP-1 and GIP

A

GLP-1
Secreted from the L-cells in the distal intestine in response to meals
The insulinotropic action of GLP-1 is glucose dependent; glucose concentrations must be greater than 90 mg/dL
Low risk for hypoglycemia
Also suppresses glucagon secretion, slows gastric emptying, and reduces food intake by increasing satiety

GIP
Secreted by K-cells in the intestine
Augments insulin secretion
Has little effect on insulin secretions at glucose concentrations > 140 mg/dL
Does not affect gastric motility, or satiety

215
Q

What is the major differences of GLP-1 Agonists and DPP-4 Inhibitors

A 
GLP-1 Agonists: 
Slightly greater efficacy 
positive weight loss
Administered subcutaneously 
Slightly more ADR (e.g., N/V/D)
DPP-4 Inhibitors: 
have slightly worse efficacy 
weight neutral 
administered PO
Less ADR
216
Q

What effect do DPP-4s have on the pancreas

A

Can cause pancreatitis

217
Q

What are the ADE of DPP-4

A

Increased Rsk of URI, UTI,

May worsen HF

Pancreatitis

218
Q

Which DDP-4 does not require a renal dose adjustmetn

A

Linagliptin

219
Q

What are the ADE of GLP-1 agonists

A

HOgl, HA, N/V/D
Pancreatitis
THYROID CELL CANCER

Renal insuff.

220
Q

If a GLP-1 and a Su are used together, what must you do

A

consider decreasing the Sulfonylurea dose by 50 % to decrease the risk of hypoglycemia

221
Q

Taking GLP-1 (tide pods) can cause what effect to your wt

A

Wt loss

Especially semaglutide

222
Q

What are the ADE of using Amylin Analogues

A

Severe HOgl

Do not use in pts talking GI motility agents

223
Q

CAn you mix pramlintide with insulin

A

No

224
Q

What is a good drug to use in pts nearç target HbA1c levels with near normal FPG levels, but high postprandial levels

A

Alpha Glucosidase inhibitors

225
Q

What is the SrCr level that must be present to use Acarbose or Meglitol

A

ust be above 2mg/dl

226
Q

Which of the SGLT-2 inhibitors are approved for CVD

A

Empagliflozing and Canagliflozin

227
Q

What are the ADE of SGLT-2 (flozins)

A

genital fungal infections, UTIs

Increased urination 
Wt loss ( may be benificaial )
228
Q

How does canagliflozin effect stroke risk

A

Increases stroke risk

229
Q

Which SGLT-2 i

Is assocaited with bladder cancer

A

Dapagliflozin

230
Q

What effect do dieuretics have on gl

A

Impaire insulin secrtion and reduce sensitivity and may cause Hyper gl

231
Q

What will the admin of CRH do to a pt with cushings

A

Administration of CRH in a patient with Cushing’s Dz will result in additional ACTH and cortisol secretion as the normal negative feedback is impaired

Patient’s with ectopic production of ACTH will not respond with additional ACTH and cortisol secretion

232
Q

What is the diffenrence between sustained and pulsatile GnRH

A

Pulsatile GnRH secretion is required to stimulate the gonadotroph cell to produce and release Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH) during the fetal and neonatal period and from the age of 2yrs until the onset of puberty

Sustained non-pulsatile GnRH or GnRH analogs inhibits the release of FSH and LH via down regulation by the pituitary in both women and men resulting in hypogonadism

233
Q

What is the most common ADE of GnRH/ LHRH analogs

A

Flare ups in the 1st week of tx

Hot flashed, ED< Decreased libido

234
Q

What is the role of LHRH in prostate cancer

A

LHRH is released to the ant pit which releases LH, LH stimulate leydigs cells to make testosterone whcih increases the prostate growth of cancer cells

235
Q

GnRH/ LHRH anaolgues all end in..

A

-relin

Exception leoprolide

236
Q

What is the approariate tx for Prostate cancer

A

GnRH (relins)

237
Q

A pt presents with endometriosis

What is the approatie hormone tx

A

GnRH/LHRH (relins)

238
Q

A pt presents at a 7 with puberty onset

What is the approatire hormone tx

A

GnRH/LHRH (relins)

239
Q

What two things inhibtit FSH

A

Inhibin and Estrogens

240
Q

A pt presents with excessive diaphoresis, OA, arthralgias, parasethisias, coarse facial features, with increasing hand/ finger size,

+HTN, HDz, Cardiomegaly

+/- OSA, T2DM

Think

A

ACROMEGALY

GH secreting adenoma

241
Q

What are the three agents that can be used if surgry is no indicated to treat acromegaly

A

Somatostatin Analogs

Growth Hormone Receptor Antagonist (GHRA)

Dopamine Agonists

242
Q

What is the ADE of Pegvisomant

A

Its a growth receptor antagonist
That can cuase N/V, flu like S/s

REVERISBLE elevation in hepatic transaminase

243
Q

What is the role of somatotropin in puberty

A

Stimulates longitudinal bone growth until the epiphyses close near the end of puberty

244
Q

A pt presents with turners syndrome
Or prader willi syndrome

What agent can help them grown

A

Somatatropin

245
Q

What hormone when in excess causes amenorrhea, anovulation, infertility, hirsutism, and acne in women, and erectile dysfunction, decreased libido, gynecomastia, and reduced muscle mass in men

A

Prolacitn

246
Q

What are the ADE of dopamine agonist

A

Nausea, headache, diarrhea, abdominal pain, light-headedness, orthostatic hypotension, and fatigue

247
Q

What is the ADE of desmopressin/ DDVAP

A

Hyponatremia and SZR (dilutional)

248
Q

What agent can be used to conttrol bleeding in a pt with hemophilia A or Von Willebrands Dz

A

Desmopressin

It will control bleeding by stimulating the body to release more von Willebrand factor already stored in the lining of your blood vessels, thereby enhancing factor VIII levels

249
Q

What is the Tx approach to Acute SIADH

A

The goal is to correct hyponatremia at a rate that does not cause neurologic complications (locked in syndrome/ inducing central pontine myelinolysis (CPM)) , as follows:
—Raise serum sodium by 0.5-1 mEq/hr, and not more than 10-12 mEq in the first 24 hours

Aim at maximum serum sodium of 125-130 mEq/L

Treatment Options:

  • 3% hypertonic saline (513 mEq/L)
  • Loop diuretics with saline
  • Vasopressin-2 receptor antagonists
  • Water restriction
250
Q

What is the tx appraoch to chroninc AS/s SIADH

A

Fluid restriction and Vassopressin receptro antagonists

251
Q

What is the Black Box warning for Conivaptan and Tolvaptan

A

(Used for in pt SIADH)

Black Boxed Warning: must be initiated and re-initiated in a hospital and monitor serum sodium

Too rapid correction of hyponatremia (>12mEqL/24hrs) can cause osmotic demyelination (Spastic quadriparesis, seizures, coma, and DEATH)

252
Q

If a pt has HF and SIADH, which medication can be used, tolvaptan or conivaptan

A

TOLVAPTAN!

Coni can notti be used

253
Q

What is the reflex that stimulates Oxcytocin

A

Neuroendocrine reflex

Breafeading or hearing babies cry

254
Q

What is the off label use of metoclopramide in women

A

Stimualte lactation

255
Q

What is the most common form of hypothyroidism

A

Hassimotos (autoimmune hypothyroidism)

256
Q

What 2 drugs can cause hypothyroidism

A

Amioderone and lithium

257
Q

A pt presenst with CC of wkness, and dry skin , letharrgy and slow speech

Think

A

hypothyroid ( may also have cold sensation)

258
Q

What is congenital hypothyroidism

A

Cretenism

259
Q

How often is levothyroxine treatement checked/ adjusted

A

every 6 weeks

260
Q

What is the treatment appoarch to myxedma coma

A

Levothyroxine + hydrocortisone

261
Q

A pt presents with progressive weakness, stupor, hypothermia, hypoglycemia, and hypoRR

Think of what thyroid problem

A

Myxedema coma

262
Q

A pt presents with high fever, tachyHR, tachyRR, dehydration, delirium , N/V/D, and AMS

Think of what thyroid condition

A

Thyroid storm

263
Q

What are the advantages of methimazole vs. PTU

A

Methimazole: Pregnancy Category D

PTU is associated with a higher incidence of liver failure

264
Q

What are the black box warnings of methimazole and PTU

A 
Severe liver injury 
Jaundice 
Agranulocytosis 
Leukopenia 
Arthralgias 
And rash
265
Q

When a pt is going to get iodine 131, when must iodides be stoped

A

3-4 days prior

266
Q

What can be used to prophylax for rad exposure in nuclear incidnets

A

Potassium iodide

267
Q

What is the step by step appraoch to Tx thyroid storm

A
  1. PTU or methimazole
  2. Iodide solution Tx (K+ iodide)
  3. BB tx (propranolol)
  4. Acetaminoiphen
  5. Corticosteroids (hyrdocortisone)
  6. Bile acid sequestrants (cholestyramine)
268
Q

If a pt is taking a statin, what herbal food should they avoid

A

Red yeast rice

IPAP JUNIOR SEM. (43 decks)

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