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Pharmacology > Lecture 12 (Pulm)-Exam 6 > Flashcards

Lecture 12 (Pulm)-Exam 6 Flashcards

1
Q

General info-LY

Smoking cessation - COPD
* What is the most important intervention?
* Only intervention is?
* Decrease what (2)?
* What are the issues around smoking?

A
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2
Q

Heparin, LMWH, fondaparinux: Indirect inhibition
* Heparin and low molecular weight heparins (LMWH) bind to what?
* What is ATIII?

A
  • Heparin and low molecular weight heparins (LMWH) bind to antithrombin III and accelerates its activity
  • ATIII is a natural anticoagulant that inactivates factors Xa and thrombin
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2
Q
A
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3
Q

What is the MOA:
* Heparin:
* LMWH:
* Fondaparinux:

A

Heparin
* Accelerates Xa and thrombin inactivation

LMWH
* Selectively accelerates Xa inactivation; minimal effects on thrombin

Fondaparinux
* Specifically accelerates Xa inactivation; no effects on thrombin

Indirect inhibition

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4
Q

How does heparin, and LMWH look like?

A
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5
Q

What can the large molecule (unfractionated)-> Heparin do?

A

able to interact with both antithrombin III and thrombin

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6
Q

What are the indications of heparin? (4)

A
  • Short time anticoagulation
  • Immediate anticoagulation – rapid onset (seconds)
  • MC life or limb threatening clots; surgical bridging therapy, DVT prophylaxis if other medications contraindicated
  • Safe in pregnancy – does not cross the placenta (since so big)
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7
Q

What is the dosing of heparin?

A
  • IV or subcutaneously (SC)
  • IV: given as bolus plus continuous IV infusion (short half-life)
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8
Q

What are the monitoring parameter of heparin?

A
  • aPTT [goal = 1.5 to 2.5 times normal (30 to 40 seconds)]
  • Antifactor Xa level (goal=0.3 to 0.7)
  • CBC (hemoglobin, hematocrit, platelets)
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9
Q

What are the adverse effects of heparin?

A
  • Bleeding
  • Osteoporosis – long-term therapy
  • Heparin induced thrombocytopenia
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10
Q

What is the antidote for heparin?

A
  • Protamine sulfate 1mg neutralizes ~ 100 units heparin
  • Continuous infusions: use heparin dose from preceding 2 to 3 hours
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11
Q

Heparin induced Thrombocytopenia
* What happens with the immune system? What does that cause?

A

Immune system makes antibodies that bind to heparin-platelet factor 4 complexes
* Platelet activation – aggregation (clumping)
* Clots
* Thrombocytopenia

Platelets are dropping but clots are forming

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12
Q

Heparin induced Thrombocytopenia
* What are the risk?
* What is the onset?
* How do you dx it? (3)

A
  • Risk: unfractionated heparin > 7 to 10 days (also occurs with LMWH)
  • Onset: 5 to 10 days after heparin initiation

Diagnosis:
* Check 4T score – probably of HIT
* Low score (≤ 3 rules out HIT); look for additional diagnoses
* High score; stop heparin, give alternative, order additional testing

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12
Q

HIT – alternative treatments*
* What do you give more critcally ill patients?
* What do you give stable patients?

A
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13
Q

Enoxaparin, Dalteparin, Fondaparinux
* What are the precautions?

A
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14
Q

What is the dosing of enoxaparin (DVT treatment and prophylaxis)

A
  • DVT treatment: 1 mg /kg SC Q12H
  • DVT prophylaxis: 30 to 40 mg SC daily
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15
Q

Enoxaparin, Dalteparin, Fondaparinux
* What are the SE?

A
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16
Q

Enoxaparin, Dalteparin, Fondaparinux
* What do you need to monitor?
* What is the antidote?

A
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17
Q

What can be used for HIT?

A

Fondaparinux

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18
Q

Warfarin
* What is the moa?

A
  • Factors II, VII, IX and X dependent on vitamin K for synthesis
  • Warfarin inhibits vitamin K recycling and synthesis
  • Not available for factor production
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19
Q

Warfarin
* What are the indications? (2)

A
  • DVT, atrial fibrillation, prosthetics valves
  • Only oral anticoagulant indicated for patients with mechanical heart valves
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20
Q

Warfarin-Pharmacokinetics:
* What is half life? What is onset?
* Requires what?
* How is metabolized?

A
  • Generally long half-life; prolonged onset
  • Requires bridging therapy with heparin or LMWH-> if INR therapeutic for two days then then you can stop
  • Metabolized by CYP2C9 – many drug interactions
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21
Q

CYP2C9 inducers and inhibors? What do they cause to the levels of warfarin?

A
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22
Q

Monitoring Warfarin
* What levels do you need to look at?
* Adjuct dose to what?
* _ algorithms
* initial dose for most patients?
* What do you need to check daily intil therapeutic?

A

PT/INR – goal 2 to 3 in most cases
* Adjust dose to INR
* Evidence-based algorithms
* Initial dose for most patients: 5mg PO daily
* INR daily until therapeutic (then decrease interval of checking)

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23
What are the diet issues with warfarin?
Vit K needs to be stabilized with txt * for example: winter vs summer months
24
Warfarin * What are the SE? (3) * What is CI (1)?
25
Warfarin overdose: * Txt based on what?
Treatment depends on INR level and if patient is bleeding
26
Warfarin overdose: * What do you with a patient who is not bleeding? (3)
* Hold warfarin * Give vitamin K (1 to 5 mg PO) * Resume warfarin at lower dose once INR is 2 to 3
27
Warfarin overdose: * What do you with a patient who is bleeding? (2)
4-factor prothrombin complex concentrate [PCC (Kcentra)] plus vitamin K -> PCC will not work without vit k OR Fresh frozen plasma (FFP)
28
Direct inhibitors * What are the two types and their MOA?
Factor Xa inhibitors * Directly bind factor Xa * Prevent conversion of prothrombin to thrombin Thrombin inhibitors * Bind to and inhibit thrombin
29
Direct oral anticoagulants (DOACS) * First oral agent since what? * What is dadigratran? * What are the types of oral factor Xa inhibitors (4)
30
Direct oral anticoagulants (DOACS) * What are the benefits over warfarin?
* Faster onset of action * **No direct monitoring required** * Minimal drug-food interactions * Comparable bleeding rate * Less drug-drug interactions * **Fixed dose per indication** – varies by indication, age, renal and hepatic function * ± parenteral anticoagulation bridging
31
Direct oral anticoagulants (DOACS)-Indications * Reduce risk of what? * What does it treat? * Prophylaxis if what? * Not recommened as alternative when? * Contraindicated when? ⭐️
* Reduce risk of stroke any systemic embolism in patients with nonvalvular atrial fibrillation * Treat DVT and PE * Prophylaxis if DVT (hip and / or knee replacement) * Not recommended as alternative to UFH or LMWH in patients with PE who are hemodynamically unstable * **Contraindicated as anticoagulation for mechanical heart valves**
32
Fill in for DOACS
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34
Fill in for DOAC reversal agents
35
What is the HAS BLED Score? What is the scoring system?
36
* What is an Acute pulmonary embolism (PE)? * It is critical that therapy be administered when?
* Acute pulmonary embolism (PE) is a common and sometimes fatal disease with a highly variable clinical presentation. * It is critical that therapy be administered in a timely fashion so that recurrent thromboembolism and death can be prevented
37
PE: * What is the most common symptom? * What type of CP? * What does isolated dyspnea of rapid onset mean? * What does Retrosternal angina-like symptoms mean? * What are other sx? * What will the lung exam sound like?
38
What is the wells score?
39
Diagnostics PE: * What is the Dx test? What is it contraindicated with? * What are other tests?
40
Fill in
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Fill in
42
What is the perc rule?
Every single one needs ot be true
43
PE: * how do you stablize a patient?
* Oxygen * Monitor * IV fluids * ± empiric anticoagulation
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PE - Stable patient * If PE excluded, what are the next steps? * If PE confirmed, what are the next steps?
If PE excluded * No further anticoagulation If PE confirmed * Continue anticoagulation if started * Change to guideline recommended anticoagulation * Consider need for thrombolysis
46
continuation therapy of PE * Stable patients: What do you give to patients for short hospitalized stay? Why do you keep them in the hospital?
Short hospitalization (LMWH or UFH) * Right ventricle dysfunction * Elevated troponins
47
Continuation therapy: DC home * What do you give? * What is the criteria do you need to in order to dischard home?
48
Fill in for Venous Thromboembolism treatment
49
Unstable patients (PE) * What is the criteria?
* SBP < 90 mmHg * Require vasopressors to maintain MAP ≥ 65 * Signs/symptoms of shock
50
Unstable patient(PE): * What is the txt?
* Oxygen ≥ 90% * IV fluids * Vasopressors – Norepinephrine DOC * Intubation
51
Unstable patients-> Tissue plasminogen activator (tpa): * what is the MOA? * What is the pharmacokinetics?
MOA – * binds fibrin in a thrombus and converts plasminogen to plasmin; plasmin lyses fibrin and fibrinogen breaking up the clot Pharmacokinetics: * Short half-life; less than 5 minutes; 80% cleared within 10 minutes * Bolus dose followed by continuous infusion
52
Tissue plasminogen activator (tpa) * What are the SE?
Bleeding * Increased risk with recent hemorrhage, trauma, surgery; uncontrolled hypertension or advanced age
53
What are the 5 groups of Pumonary hypertension? What are the general txts?
* Specific drug therapy for Group 1 * Some therapies for group 4 * Groups 2, 3, and 5 = treat underlying disorder
54
Group 1 therapies * What test do you need to do FIRST?
First: vasoreactivity test * Short-acting vasodilator: nitric oxide, epoprostenol, or adenosine
55
Group one: * What is a positive and negative vasoreactive? * What do you tx for negative vasoreactive?
Positive: IF MPAP decreases by ≥ 10 mmHg and the MPAP is < 40 mmHg; PAH is vasoreactive Most not reactive * Vasoreactive = treatment with calcium channel blocker (amlodipine or nifedipine) * Non vasoreactive = alternative medications
56
What are the WHO Group 1 functional classes with txt??
* Mild – asymptomatic, no medications needed * Slight limitation of activity – PO medications * Moderate limitation of activity – PO medications * Severe – IV medications
57
PAH Group 1 treatments - vasodilators * Calcium channel blockers: What is an example? When do we use it? * Endothelin receptor antagonist: What is the MOA? What are the examples? What is an example?
58
# PAH Group 1 treatments - vasodilators Phosphodiesterase type 5 inhibitors: * What is the MOA? What are the examples? * Cannot combo with what? Guanylate cyclase stimulators: * What is the MOA? What is an example? * No combo with what? * What is it approved for?
59
Prostacyclin analogues: * What is the MOA? What are the examples? * What is the route? Prostacyclin IP receptor agonist: * What is the MOA? What is an example? * When was it approved?
60
* What is the lung cnacer screening criteria? (think age, smoking, and pack year)? * What does the patient get each year if they meet the criteria
61
Lung Cancer: NSCLC * Which one is most common? * Which lung cancer is associated with smoker, large central mass, hemoptysis? * Which lung cancer is associated with aggressive tumor that rapidly doubles insize? * What is another cancer that is rare?
62
Small cell lung cancer (SCLC) – 15% * What is it? * What is common at dx? * More often associated with what?
* Aggressive, smokers * 80% metastatic at diagnosis * More often associated with paraneoplastic syndromes
63
Lung CA – Signs and symptoms * What are the local sx? * What are the consitutional sx? * What are the local invasion sx? * What are the distant metastasis sx? * What are the paraenoplastic sx?
64
What are the areas in the body that lung cancer metastasises to?
brain, bone, liver, adrenal
65
SVC * What is SVC syndrome?
* Tumor compression of SVC * Thrombus from central venous catheter
66
SVC: * What is grade one and two dx test? * What is grade 3 and 4 dx test?
Grade I or II * Contrast enhanced chest CT or chest MRI * Anticoagulate Grade III or IV * Stabilize (A, B, Cs) * Venography with endovenous intervention
67
What are the findings for SVC grade 1 and 2?
68
Carcinoid tumors * What is it from? * What is the MC location? * What are local symptoms and what is less common?
Neuroendocrine tumors arising from neuroendocrine glands * Grow slow and rarely metastasize – still problematic MC location = gi tract; lungs less common * Local symptoms = dyspnea, chest pain, hemoptysis, wheezing * Less common = carcinoid syndrome (CS)
69
Carcinoid tumors * carcinoid syndrome (CS) is from what? What are the most common ones?
CS results from secretion of multiple hormones (>40) from the tumors * MC serotonin, bradykinin, histamine, kallikrein, prostaglandins
70
Carcinoid tumors * What do you need to do to dx?
* 24-hour urinary 5-hydroxyindoleacetic acid (5-HIAA) excretion * End product of serotonin metabolism * Sensitivity > 90%; specificity 90%
71
What are the sx of carcinoid tumors and carcinoid syndromes?
72
Carcinoid syndrome - treatment * What do you need to txt? * What is the firt line symptomatic treatment? What is the MOA? * What improves
Treat underlying disease First-line symptomatic treatment: somatostatin analogs – octreotide / lantreotide * MOA: binds somatostatin receptors on NETs and inhibits hormone release * Flushing and diarrhea improved in 80% of patients
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somatostatin analogs – octreotide / lantreotide * What are the SE?
* Nausea, abdominal discomfort * Bloating * Fat malabsorption * Gallstone formation * Transient
74
Lung CA treatment goals: * Depends on what? * What is early stage? * What is late stage? * What should be discussed with patients?
* Depends on type of cancer and stage of disease * Early-stage disease – goal may be cure * Late-stage disease – goal is usually prolongation of life and QOL * Risk / benefits should be discussed in detail with patient and individualized to meet needs
75
NSCLC txt: fill in
76
Pembrolizumab * What is the MOA?
PD-1 is an immune check point inhibitor * Binds to PD-1 receptors on T-cells following chronic infections or tumors * Limits T-cell response in chronic phase – not acute phase * Reactivates tumor-specific cytotoxic T-lymphocytes
77
2016 trial compared monotherapy pembrolizumab to platinum doublet * What were the results?
* 305 patients with PD-L1+ tumors (expression ≥ 50%) * Median progression-free survival 10.3 months pembrolizumab vs 6 months doublet * Larger trials with similar to superior results * Better outcomes with higher PD-L1 tumor expression
78
What is recommended first line with pembrolizumab?
Recommended first-line for PD-L1positive advanced NSCLC
79
SCLC: fill in
80
What are the agents that can cause Pneumonitis and fibrosis? Hypersensitivity lung disease? Noncardiogenic pulmonary disease? Bronchospam?
* Pneumonitis and fibrosis: Amidoarone, nitrofurantoin * Hypersensitivity lung disease: NSAIDs * Noncardiogenic pulmonary disease: Amiodipine * Bronchospam: ACE inhibitors and NSAIDs
81
Hypersensitivity reactions: type one * What is the mediator? * What is the MOA? * What is the time course? * What are examples?
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Hypersensitivity reactions: type two * What is the mediator? * What is the MOA? * What is the time course? * What are examples?
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Hypersensitivity reactions: type three * What is the mediator? * What is the MOA? * What is the time course? * What are examples?
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Hypersensitivity reactions: type four * What is the mediator? * What is the MOA? * What is the time course? * What are examples?
85
Type 1 * What is the mediator? * MC what? * When does the reaction happen? * What does the histamine cause? * What is the late reaction?
IgE mediated * MC type of allergic reaction * Immediate reaction: minutes HISTAMINE * Urticaria / hives * Bronchoconstriction * GI smooth muscle contraction * Vasodilation * Increased vessel permeability Late reaction: 8 to 12 hours later * Tryptases * Cytokines (IL-4, IL-5, leukotrienes)
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Type I * What are the mild reactions? What about anaphylaxis?
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Type I - Treatments * What is inital therapy?
* IV fluids * Airway management * Medication administration * Monitoring * Home therapy
88
* Epinephrine (Epipen): what is the action? * Antihistamines: What is the action? * Beta agonist: What are is the action? * Steroids: What are teh actions?

Pharmacology (14 decks)

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