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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
Q

What are the diet issues with warfarin?

A

Vit K needs to be stabilized with txt
* for example: winter vs summer months

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24
Q

Warfarin
* What are the SE? (3)
* What is CI (1)?

A
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25
Q

Warfarin overdose:
* Txt based on what?

A

Treatment depends on INR level and if patient is bleeding

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26
Q

Warfarin overdose:
* What do you with a patient who is not bleeding? (3)

A
  • Hold warfarin
  • Give vitamin K (1 to 5 mg PO)
  • Resume warfarin at lower dose once INR is 2 to 3
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27
Q

Warfarin overdose:
* What do you with a patient who is bleeding? (2)

A

4-factor prothrombin complex concentrate [PCC (Kcentra)] plus vitamin K -> PCC will not work without vit k

OR

Fresh frozen plasma (FFP)

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28
Q

Direct inhibitors
* What are the two types and their MOA?

A

Factor Xa inhibitors
* Directly bind factor Xa
* Prevent conversion of prothrombin to thrombin

Thrombin inhibitors
* Bind to and inhibit thrombin

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29
Q

Direct oral anticoagulants (DOACS)
* First oral agent since what?
* What is dadigratran?
* What are the types of oral factor Xa inhibitors (4)

A
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30
Q

Direct oral anticoagulants (DOACS)
* What are the benefits over warfarin?

A
  • 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
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31
Q

Direct oral anticoagulants (DOACS)-Indications
* Reduce risk of what?
* What does it treat?
* Prophylaxis if what?
* Not recommened as alternative when?
* Contraindicated when? ⭐️

A
  • 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
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32
Q

Fill in for DOACS

A
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33
Q
A
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34
Q

Fill in for DOAC reversal agents

A
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35
Q

What is the HAS BLED Score? What is the scoring system?

36
Q
  • What is an Acute pulmonary embolism (PE)?
  • It is critical that therapy be administered when?
A
  • 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
Q

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
Q

What is the wells score?

39
Q

Diagnostics PE:
* What is the Dx test? What is it contraindicated with?
* What are other tests?

40
Q

Fill in

41
Q

Fill in

42
Q

What is the perc rule?

A

Every single one needs ot be true

43
Q

PE:
* how do you stablize a patient?

A
  • Oxygen
  • Monitor
  • IV fluids
  • ± empiric anticoagulation
45
Q

PE - Stable patient
* If PE excluded, what are the next steps?
* If PE confirmed, what are the next steps?

A

If PE excluded
* No further anticoagulation

If PE confirmed
* Continue anticoagulation if started
* Change to guideline recommended anticoagulation
* Consider need for thrombolysis

46
Q

continuation therapy of PE
* Stable patients: What do you give to patients for short hospitalized stay? Why do you keep them in the hospital?

A

Short hospitalization (LMWH or UFH)
* Right ventricle dysfunction
* Elevated troponins

47
Q

Continuation therapy: DC home
* What do you give?
* What is the criteria do you need to in order to dischard home?

48
Q

Fill in for Venous Thromboembolism treatment

49
Q

Unstable patients (PE)
* What is the criteria?

A
  • SBP < 90 mmHg
  • Require vasopressors to maintain MAP ≥ 65
  • Signs/symptoms of shock
50
Q

Unstable patient(PE):
* What is the txt?

A
  • Oxygen ≥ 90%
  • IV fluids
  • Vasopressors – Norepinephrine DOC
  • Intubation
51
Q

Unstable patients-> Tissue plasminogen activator (tpa):
* what is the MOA?
* What is the pharmacokinetics?

A

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
Q

Tissue plasminogen activator (tpa)
* What are the SE?

A

Bleeding
* Increased risk with recent hemorrhage, trauma, surgery; uncontrolled hypertension or advanced age

53
Q

What are the 5 groups of Pumonary hypertension? What are the general txts?

A
  • Specific drug therapy for Group 1
  • Some therapies for group 4
  • Groups 2, 3, and 5 = treat underlying disorder
54
Q

Group 1 therapies
* What test do you need to do FIRST?

A

First: vasoreactivity test
* Short-acting vasodilator: nitric oxide, epoprostenol, or adenosine

55
Q

Group one:
* What is a positive and negative vasoreactive?
* What do you tx for negative vasoreactive?

A

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
Q

What are the WHO Group 1 functional classes with txt??

A
  • Mild – asymptomatic, no medications needed
  • Slight limitation of activity – PO medications
  • Moderate limitation of activity – PO medications
  • Severe – IV medications
57
Q

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
Q

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
Q

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
Q
  • 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
Q

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
Q

Small cell lung cancer (SCLC) – 15%
* What is it?
* What is common at dx?
* More often associated with what?

A
  • Aggressive, smokers
  • 80% metastatic at diagnosis
  • More often associated with paraneoplastic syndromes
63
Q

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
Q

What are the areas in the body that lung cancer metastasises to?

A

brain, bone, liver, adrenal

65
Q

SVC
* What is SVC syndrome?

A
  • Tumor compression of SVC
  • Thrombus from central venous catheter
66
Q

SVC:
* What is grade one and two dx test?
* What is grade 3 and 4 dx test?

A

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
Q

What are the findings for SVC grade 1 and 2?

68
Q

Carcinoid tumors
* What is it from?
* What is the MC location?
* What are local symptoms and what is less common?

A

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
Q

Carcinoid tumors
* carcinoid syndrome (CS) is from what? What are the most common ones?

A

CS results from secretion of multiple hormones (>40) from the tumors
* MC serotonin, bradykinin, histamine, kallikrein, prostaglandins

70
Q

Carcinoid tumors
* What do you need to do to dx?

A
  • 24-hour urinary 5-hydroxyindoleacetic acid (5-HIAA) excretion
  • End product of serotonin metabolism
  • Sensitivity > 90%; specificity 90%
71
Q

What are the sx of carcinoid tumors and carcinoid syndromes?

72
Q

Carcinoid syndrome - treatment
* What do you need to txt?
* What is the firt line symptomatic treatment? What is the MOA?
* What improves

A

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

73
Q

somatostatin analogs – octreotide / lantreotide
* What are the SE?

A
  • Nausea, abdominal discomfort
  • Bloating
  • Fat malabsorption
  • Gallstone formation
  • Transient
74
Q

Lung CA treatment goals:
* Depends on what?
* What is early stage?
* What is late stage?
* What should be discussed with patients?

A
  • 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
Q

NSCLC txt: fill in

76
Q

Pembrolizumab
* What is the MOA?

A

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
Q

2016 trial compared monotherapy pembrolizumab to platinum doublet
* What were the results?

A
  • 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
Q

What is recommended first line with pembrolizumab?

A

Recommended first-line for PD-L1positive advanced NSCLC

79
Q

SCLC: fill in

80
Q

What are the agents that can cause Pneumonitis and fibrosis? Hypersensitivity lung disease? Noncardiogenic pulmonary disease? Bronchospam?

A
  • Pneumonitis and fibrosis: Amidoarone, nitrofurantoin
  • Hypersensitivity lung disease: NSAIDs
  • Noncardiogenic pulmonary disease: Amiodipine
  • Bronchospam: ACE inhibitors and NSAIDs
81
Q

Hypersensitivity reactions: type one
* What is the mediator?
* What is the MOA?
* What is the time course?
* What are examples?

82
Q

Hypersensitivity reactions: type two
* What is the mediator?
* What is the MOA?
* What is the time course?
* What are examples?

83
Q

Hypersensitivity reactions: type three
* What is the mediator?
* What is the MOA?
* What is the time course?
* What are examples?

84
Q

Hypersensitivity reactions: type four
* What is the mediator?
* What is the MOA?
* What is the time course?
* What are examples?

85
Q

Type 1
* What is the mediator?
* MC what?
* When does the reaction happen?
* What does the histamine cause?
* What is the late reaction?

A

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)

86
Q

Type I
* What are the mild reactions? What about anaphylaxis?

87
Q

Type I - Treatments
* What is inital therapy?

A
  • IV fluids
  • Airway management
  • Medication administration
  • Monitoring
  • Home therapy
88
Q
  • 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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