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CRRAB II Week 6 > PBL Case 2 > Flashcards

Flashcards in PBL Case 2 Deck (55)
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1
Q

What are three nonpharmacologic interventions to manage asthma?

A
  1. Breathing exercises
  2. Yoga
  3. Activity
2
Q

How do breathing exercises affect asthma?

A

May reduce asthma exacerbation and improve quality of life in adults with asthma.

3
Q

What are two breathing exercises used with asthma?

A
  1. Buteyko technique

2. Papworth Method of Integrated Breathing and Relaxation Techniques

4
Q

What is the Buteyko technique?

A

Aims to correct breathing patterns by reducing hyperventilation and thus resetting CO2 levels. Involves periods of breath holding interspersed with periods of shallow breathing, accompanied by physical activities to further increase the buildup of CO2.

5
Q

What is the Papworth Method?

A

A method of integrated breathing and relaxation techniques - focuses on dysfunctional breathing including hyperventilation and hyperinflation common in patients with asthma and reducing anxiety associated with breathlessness and wheezing.

6
Q

How does activity improve asthma?

A

Aerobic training may reduce symptom frequency and improved asthma-related quality of life in adults with asthma. It is also associated with reduced frequency of exacerbation.

7
Q

What is seen on a dose response curve with competitive antagonists?

A

Competitive antagonists are drugs that bind to the receptor in a reversible way without activating the effector system for that receptor.
-In the presence of a competitive antagonist, he log dose-repose curve is shifted to higher doses (i.e. horizontally to the right on the dose axis) but the same maximal effect is reached.

8
Q

What is an inverse agonist?

A

An agent that binds to the same receptor as an agonist but induces a pharmacological response opposite the agonist.

9
Q

How does an irreversible antagonist effect the dose-response curve?

A

An irreversible antagonist causes a downward shift of the maximum, with no shift of the curve on the dose axis unless spare receptors are present.

10
Q

What types of antagonists can be overcome by adding more agonist?

A

Competitive antagonists!

Irreversible antagonists cannot be overcome by adding more agonist.

11
Q

What do Competitive antagonists increase?

A

The ED50! (mean effective dose that produces wanted effect in 50% of population)
-Irreversible antagonists do not! (unless spare receptors are present)

12
Q

How does an Agonist, Antagonist and Inverse Antagonist affect percent response of drug?

A

Agonists increase the percent (100%). Antagonists bring the percent to zero. Inverse antagonists make the response -50%.

13
Q

What are the direct benefits of patients having asthma plans?

A
  1. Decreased office visits
  2. Save Money
  3. Increases sense of self-efficacy
  4. Reduced hospital admissions and morbidity rates
14
Q

How do Asthma plans save money?

A

For every $1 you put into asthma prevention, you get $71 back

15
Q

How do Asthma plans increase sense of self-efficacy?

A

Gives patients a strategy for every phase of asthma (exacerbations, daily management, etc.)

16
Q

What do all patients with asthma need to understand?

A
  • How to use their medication and the difference between reliever and controller therapies.
  • How to recognize worsening asthma and how to set up therapy
17
Q

What can asthma education improve?

A

Compliance, especially with ICS (inhaled corticosteroids).

-All patients should be taught how to use their inhalers correctly.

18
Q

What have written asthma action plans been shown to reduce?

A
  • Hospital admissions
  • Morbidity rates in adults and children
  • -> these plans are particularly recommended in patients with unstable disease who frequently have exacerbations
19
Q

What is NOT AN ALLERGY?

A

Aspirin-induced hypersensitivity!!

20
Q

What are other names for Aspirin-induced hypersensitivity?

A
  • Aspirin-exacerbated asthma
  • Aspirin-Exacerbated Respiratory Disease (AERD)
  • Sampter’s Triad
21
Q

What is Sampter’s Triad?

A
  1. Asthma
  2. Aspirin induced bronchospasms
  3. Nasal polyps
22
Q

What is the prevalence of Aspirin-induced hypersensitivity?

A
  • Seen in 7% of asthma patients.
  • 14% of severe asthma
  • 10% of nasal polyposis or chronic rhinosinusitis
23
Q

What is the Pathophysiology related to Aspirin-induced hypersensitivity?

A
  1. Decreased prostaglandin (PGE2) synthesis
  2. Overproduction of Leukotrienes at baseline (LTC4 in particular)
  3. Bronchoconstriction, mucus secretion, nasal mucosal swelling, and airway edema, and also attracts eosinophils into the airways
    • COX inhibitors (aspirin, NSAIDS)
  4. More Leukotriene pathway
  5. Exacerbates symptoms
  6. Boom, you get the triad!!
24
Q

What is the significance of PGE2 in Aspirin-induced hypersensitivity?

A
  • It is a bronchodilator with anti-inflammatory effects
  • Usually counteracts leukotrienes (LTD)
  • Might also be an overexertion/overactivity of 5-lipoxygenase —> Increase in leukotriene synthesis
25
Q

What is the significance of bronchial mast cells and eosinophils in Aspirin-induced hypersensitivity?

A

These cells make lots of leukotriene LTC4 (see more of these cells in patients with AERD)

26
Q

What is the enzyme LTC4 synthase?

A

It mediates the formation of LTC4, is overexposed by eosinophils and other leukocytes in both nasal and pulmonary tissues of some patients with AERD

27
Q

How is Arachidonic Acid synthesized?

A

Phospholipase A2 converts Membrane phospholipids into Arachidonic acid.

28
Q

How are prostaglandins and thromboxanes synthesized?

A

Cycloxygenase (COX) converts Arachidonic acid into prostaglandins and thromboxanes.

29
Q

How is Leukotriene A4 synthesized?

A

5-lipoxygenase and FLAP convert Arachidonic acid into Leukotriene A4.

30
Q

How is Leukotriene C4 created?

A

Leukotriene C4 synthase converts Leukotriene A4 into Leukotriene C4.

31
Q

How is Leukotriene B4 created?

A

Epoxide hydrolase converts Leukotriene A4 into Leukotriene B4.

32
Q

What is Virchow’s triad?

A

Three broad categories of factors that are thought to contribute to thrombosis.

  1. Hypercoagulable state
  2. Vessel injury
  3. Venous stasis
33
Q

What is the Hypercoagulable state?

A

Increased ability for coagulation upon stimulation.

34
Q

What things can cause a Hypercoagulable state?

A
  1. Platelet activation –> increased clot formation
  2. Malignancy –> Abnormal release of coagulation promoting cytokines
  3. Inherited disorders –> defect in coagulation cascade
  4. Trauma –> systemic injury –> activation of coagulation cascade
  5. Pregnancy/OCP/Obesity –> increased estrogen –> hypercoagulabiltiy
35
Q

How does fat promote coagulation?

A

Fat converted androgens to estrogen. And estrogen leads to hyper coagulability.

36
Q

What is venous stasis?

A

Low blood flow rate that concentrates clotting factors at certain site

37
Q

What are causes of venous stasis?

A
  1. Obesity –> sedentary –> poor venous return

2. Fracture/plane ride –> decrease muscle motion –> poor venous flow

38
Q

What is vessel injury?

A

Exposes tissue factor on damaged cell –> vWF can bind then.

39
Q

What causes vessel injury?

A
  1. Bacteria –> invades vessel wall

2. Artificial valve –> abnormal surface

40
Q

What is V/Q mismatch?

A

It describes lung ventilation in excess of perfusion.

41
Q

What are causes of V/Q mismatch?

A

Any process that increases dead space ventilation:

  • Alveolar overdistention (auto-PEEP)
  • Lung parenchymal destruction (emphysema)
  • Hypoperfusion (hypovolemia, acute RV failure)
  • Obstruction of the pulmonary arterial circulation (pulmonary embolus)
42
Q

What are two common clinical manifestations of acute PE?

A
  1. Tachypnea
  2. Respiratory distress
    - -> Marked hypoxemia is uncommon
43
Q

What is happening in patients who become hypoxemic after an acute PE?

A

They usually have a secondary lung process.

44
Q

What is the basic significance of the D-dimer test?

A

The test can help rule OUT a clot, but it is not very helpful in ruling IN a clot!

45
Q

What is the probability of DVT after negative findings on a D-dimer assay?

A

0.8%

46
Q

What is the probability of DVT after positive findings on a D-dimer assay?

A

38%

47
Q

What is the sensitivity of the D-dimer test? What does sensitivity tell us?

A
  1. 5%
    - Sensitivity looks for a true positive rate
    - Highly sensitive tests that come back negative help rule OUT a disease
48
Q

What is SNOUT?

A

Sensitivity rules OUT disease

49
Q

What is the specificity of the D-dimer test? What does specificity tell us?

A
  1. 9%
    - Specificity looks for a true negative rate
    - Highly specific tests with a positive result help rule IN a disease
50
Q

What is SPIN?

A

Specificity rules IN disease

51
Q

What is the NPV of the D-dimer test?

A

99.7%

52
Q

What is the PPV of the D-dimer test?

A

20.0%

53
Q

What is NPV in English?

A

Mr. Vu, we ordered a D-dimer test to chest for a DVT. It has a 99.7% negative predictive value regarding a DVT. This means that if the D-dimer test results come back negative, we are 99.7% sure you do NOT have a DVT.

54
Q

What is PPV in English?

A

Mr. Vu, we ordered a D-dimer test to check for a DVT. It has a 20% positive predictive value. This means that if the D-dimer test results come back positive, we are only 20% sure you actually have a clot/DVT.

55
Q

What do you need to keep in mind with NPV and DVT?

A
  • D-dimer has a better negative predictive value, but alone it does not exclude isolated distal DVT.
  • In patients with low pretest clinical probability, D-dimer had a negative predictive value of >95% for isolated distal DVT