3P APEA exam study > Pharm essentials/overview > Flashcards

Pharm essentials/overview Flashcards

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1
Q

Phases of drug pharmacokinetics

A
  1. absoprtion- site of administration into circulation. factors include route of admin, and GI ph.
  2. distribution- spread of the drug to plasma concentrations
  3. metabolism- primary occurs in the liver (first pass).
    very dependent on CPY450 (CYP3A4) enzyme.
  4. Elimination- excretion of drug from the body. Half life concept is critical to elimination.
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2
Q

Antihypertensive drugs (5)

A
  1. ACE inhibitors
  2. ARBs
  3. Beta blockers
  4. calcium channel blockers
  5. diuretics
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3
Q

MOA ACE inhibitors + side effects

A

inhibits angiotensin 1 from becoming angiontensin 2.
(angiontension 2 is a strong vasoconstrictor)
thereby causing vasodilation

SE- accumulation of bradykinin, increased K+

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4
Q

MOA ARB + Side effects

A

Block angiotension 2 at the AT1 receptor. Preventing vasoconstriction and aldosterone-secreting actions.

SE: Dizziness + increased K+
*Kidney protecting!

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5
Q

MOA beta blockers + SE

A

Block beta-1 receptors in the cardiac tissue–> causing negative chronotropic effect and negative myocardial contractility

SE: bradycardia, hypotension, fatigue, depression

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6
Q

DO NOT USE _________ for patients with reactive airway disease/asthma + why

A

Beta blockers!

Beta blockers are non-selective in blocking beta-1 and also impact beta-2 receptors in the bronchial smooth muscle causing increased risk of bronchoconstriction

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7
Q

Do not use ____________ (antihypertensive) with pregnant patients

A

ACE inhibitors

beta blockers are safest in pregnancy

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8
Q

MOA calcium channel blockers + Side effects

(also examples of each)

A

Two types
1- Dihydropyridines (e.g., amlodipine, nifedipine) for blood vessels

non-dihydropyridines (e.g., diltiazem, verapamil) for both the heart and vessels- used more for arrhythmias

MOA: hinder calcium ions in cardiac calcium channels causing decreased cardiac contractility and arterial dilation

Side effects: peripheral edema (due to arterial dilation), fatigue, dizziness

+ Don’t take with grapefruit juice

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9
Q

MOA Diuretics + SE

A
  1. Thiazide diuretics: Act on the distal convolted tubule
  2. Loop diuretics: target the ascending loop of Henle
  3. Potassium sparing: Effects the collection ducts…

SE: Thiazide + Loop cause hypokalemia!

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10
Q

Respiratory drug classes (4)

A
  1. Beta agonists (SABA and LABA)
  2. Inhaled corticosteriods (Fluticasone and budesonide)
  3. Leukotriene receptor antagonists (Montelukast)
  4. Antihistamines (1st generation v. 2nd generation)
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11
Q

MOA beta-agonists (SABA + LABA) MOA + SE

A

SABA: binding to beta 2 receptors in the bronchial smooth muscle cells.
-Increase cAMP
-Smooth muscle relaxation
*albuterol

LABA: (Salmeterol) Provide bronchodilation for prolonged periods. LABAs must be prescribed with ICS to prevent asthma related death!!!

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12
Q

Inhaled Corticosteroids (ICS) MOA + SE

A

ex. Fluticasone and budesonide
MOA: powerful anti-inflammatory effects. Suppression of cytokine production, inhibits eosinophil recruitment and reduces airway hyperresponsiveness.

SE: ORAL THRUSH (use with spacer),

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13
Q

Can you prescribe a long acting beta agonist (ex. salmererol) alone for asthma?

A

LABA: (Salmeterol) Provide bronchodilation for prolonged periods. LABAs must be prescribed with ICS to prevent asthma related death!!!

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14
Q

BLACK BOX WARNING LABA

A

Black Box Warning: Single-ingredient LABAs (like salmeterol or formoterol alone for asthma) are associated with an increased risk of asthma-related death and are not recommended for asthma treatment without an ICS.

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15
Q

Leukotriene receptor antagonists (LTRAs) MOA + SE

A

ex. Montelukast
MOA: inhibit cysteinyl leukotriene receptor

SE: cold s/s + sinustitis

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16
Q

Which asthma/COPD medication is best for patient with aspirin-induced respiratory disease

A

Leukotriene antagonists
(Montekulast)

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17
Q

Black box warning for Montelukast

A

AKA singulair

Neuropsychiatric: Agitation, anxiety, depression, confusion, aggression, hallucinations, memory problems, suicidal thoughts/actions, vivid dreams, sleepwalking.

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18
Q

Antihistamines MOA + SE

A
  1. First generation (benadryl)/hydroxyzine
  2. Second generation loratadine or cetirizine

MOA: Lower Histamine reaction

SE: 1st generation crosses blood brain barrier= sedation

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19
Q

Types of Insulin and their dosing schedule

A

Short acting- lispro, aspart (begin in 15 minutes)

Intermediate:

Long acting: Glargine and detemir- 24 hour dosing

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20
Q

MOA biguanides + SE:

A

Biguanides (Metformin): Considered the first-line treatment for DM 2,

it decreases liver glucose production and increases insulin sensitivity.

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21
Q

MOA Sulfonylureas + SE:

A

Stimulate pancreatic beta cells to release more insulin (e.g., Glipizide, Glyburide, Glimepiride).

SE: HYPOGLYCEMIA + weight gain

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22
Q

DPP-4 Inhibitors MOA + SE

A

Increase insulin release and reduce glucagon levels
(e.g., Sitagliptin, Saxagliptin, Linagliptin).

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23
Q

SGLT2 Inhibitors MOA + SE

A

SGLT2 Inhibitors: Promote glucose excretion through urine (e.g., Dapagliflozin, Canagliflozin). Ex. Jardiance

SE: mild weight LOSS,
Rare side effect: Fournier’s Gangrene

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24
Q

Diabetic meds that cause weight gain

A

insulin,
sulfonylureas (like glipizide, glyburide),
thiazolidinediones (TZDs) (like pioglitazone)
meglitinides (like repaglinide)

metformin= weight neutral

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25
Monitor Metformin for what severe complication
Lactic acidosis *Monitor kidney function
26
How long to wait after metformin to have CT contrast and why
48 hours after contrast It is often recommended to stop taking it on the day of the procedure as well. This precaution prevents the risk of lactic acidosis, a rare but serious condition, which can occur if the contrast causes acute kidney injury (AKI) and metformin builds up in the kidneys
27
Normal TSH levels
0.5-5.0
28
High TSH low T4 =
hypothyroidism
29
MOA levothyroxine
Synthetic version of T4,
30
GI drugs
1. PPI 2. H2 receptor antagonists 3. Antiemtic agents 4. laxatives
31
PPI MOA and SE
ex. pantoprazole / omeprazole MOA: irreversibly bind to hydrogen-potassium enzyme on gastric parietal cells SE: Increased risk of C-diff, Osteoporosis with long term use, decreased magnesium, calcium and vitamin B12
32
H2 antagonist MOA + SE
Ex. ranitidine/famotidine MOA: Reducing gastric acid secretion by competitively inhibiting histamine receptors SE: Tachyphylaxis- reduced effectiveness
33
Ondansetron MOA + SE
MOA: blocking serotonin receptors. 5-HT3. SE: Prolonged QTC interval
34
Metoclopramide MOA + SE
(Reglan) MOA: Dopamine receptor antagonist and increases gastric emptying. SE: drowsiness, fatigue Severe: Tardive dyskinesia
35
Laxative types + MOA of each (4)
1. Bulk forming: absorb water in the intestine to increase stool bulk 2. osmotic: draw water from surrounding tissues into the bowel to soften stool and ease passage. They are highly effective but require increased fluid intake to work properly. 3. stimulant: irritate the intestinal lining, forcing muscles to contract and move stool quickly (usually within 6–12 hours) 4. stool softeners: These add moisture to the stool to soften it, making it easier to pass without straining.
36
NSAID MOA + SE
work by inhibiting COX1 and COX2 (celecoxib) which are required in the making of prostaglandins COX2 inhibitors are less likely to cause ulcers but more likely to cause cardiovascular risks -stomach ulcers -worsening kidney function -MI/HTN with COX 2
37
DMARDs MOA + SE
ex. methotrexate, hydrochloroquine humera, remicade (conventional vs biologics) MOA: suppresses the immune system for treatment of RA or psoriatic arthritis pain SE: N/V/D Increased risk of infection
38
Steroid MOA + SE
prednisone (dexamethasone stronger than prednisone) MOA- inhibit genes that produce pro-inflammatory cytokines and proteins SE: Osteoporosis, adrenal suppression
39
SSRI MOA + SE
prevents reabsorption of serotonin in the presynaptic neuron causing an increased in availability at the synaptic cleft SE: sexual dysfunction, serotonin syndrome!
40
Serotonin syndrome s/s
usually appearing within hours of starting or increasing medication. Key signs include agitation, confusion, rapid heart rate, high blood pressure, dilated pupils, muscle rigidity, shivering, goosebumps, diarrhea, and high fever (adrenaline response + fever)
41
Drugs that cause serotonin syndrome
antidepressant medications (SSRIs, SNRIs, MAOIs, TCAs) Triptans for migraines Opioids (tramadol, fentanyl), dextromethorphan (cough syrup), St. John’s Wort, Foods high in Tyramine: aged cheeses, cured meats, sauerkraut, tap beers, soy products, overripe fruit, fava beans, and excessive caffeine
42
Foods high in tyramine cause
potentially serotonin syndrome if taken with serotonin med (Adrenaline response + fever)
43
SNRI MOA + SE
Ex. venlafaxine + Duloxetine MOA: Block both serotonin and norepinephrine SE: serotonin syndrome, increased BP
44
TCA MOA + SE
ex. amitriptyline MOA: nonselectively inhibits the reuptake of norepineprhine and serotonin SE: Anticholinergi effects, ortho hypo=fall risk in the elderly
45
Benzodiazepines MOA + SE
Enhancing the inhibitory GABA neurotransmitter SE: CNS depression
46
Antipsychotics (classes) MOA +SE
Typical: Haldol, antagonize dopamine receptors which address the positive symptoms of schizoprenia but carry high risk of EPS (ex. tardive dyskinesia) Atypical: Risperidone and quetiapine target serotonin 5 HT2A receptors work best for treating negative symptoms of mood disorders. Less EPS s/s but more risk of metabolic syndrome
47
FDA warning for antipsychotics and elderly
FDA "black box" warnings indicate elevated death risks in patients with dementia-related psychosis. Studies suggest higher mortality rates for FGAs compared to second-generation antipsychotics due to cardiovascular issues. Up to 50% of adults aged 60–80 taking traditional antipsychotics experience EPS, including Parkinson-like symptoms (rigidity, tremor, bradykinesia) and dystonia.
48
ANTIBIOTICS*****
49
Common category X meds (pregnancy)
isotretinoin (Accutane), thalidomide statins warfarin methotrexate and various hormonal therapies like contraceptives and hormone replacement therapy (ACE inhibitors)
49
Antifungal MOA + SE
ex fluconazole MOA: Disrupt ergosterol synthesis SE: LIVER TOXIC
50
Common BEERs list meds
first-generation antihistamines (e.g., Diphenhydramine), NSAIDs (e.g., Ibuprofen, Naproxen), benzodiazepines (e.g., Diazepam), 1st generation antipsychotics
51
Black box warning fluoroquinolones
TENDINITIS (especially if used with corticosteriod)
52
Secondary prevention
early detection exams
53
Tertiary prevention
restoring physical or cognitive health
54
Start hearing screenings
At birth
55
Vision screenings needed
Once between age 3-5
56
lead screening
Blood test for children around age 1-2
57
Autism screening
18-24 months (M-CHAT screening)
58
Adolescent screening
Depression screening all kids starting age 12 (PHQ-9)
59
DM screening
with A1C or fasting glucose screen at age 35 y/o and every 3 years
60
Blood pressure screening
age 40+ yearly younger every 3 years
61
Lipid panel screening
start at age 20 and repeat every 5 years (fasting)
62
Mammogram screening
Start at age 50 and do it every other year (or 10 years before dx if family hx)
63
Cervical cancer screening
Start at age 21 with pap Q3 years At age 30 can switch to pap + HPV test every 5
64
Colon cancer screening
Start at age 50 fecal occult test- annual or sigmoidoscopy- every 5 years or colonoscopy- every 10 years
65
TDAP vaccine
Readminister every 10 years (5 if booster needed for exposure)
66
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