Y2S1B1 - Cs - Copd And Acid-Base Disorders

Front 1

T/F

In normal people, lung function does not decline with age, but it does in COPD.

Back 1

False!

Normal people's lung function declines, but at a SLOWER rate than those with COPD

Front 2

T/F

With treatment, COPD patients' lung function can return to where they were prior to an exacerbation.

Back 2

False!

COPD is an exacerbative disease, and they can never return to where they were. Goal is to decrease exacerbations!

Front 3

What are some risk factors for COPD?

Back 3

Smoking (80-90%)
Passive smoke
Ambient air pollution
Occupational dusts and chemicals
Multiple infections
Hyperresponsive airways/allergy
Elderly white males
Alpha-1 antitrypsin deficiency (<1%)

Front 4

What is the mean pack-year hx of a smoker with COPD?

Back 4

20 pack-year (20/day x 10 yrs)

Front 5

In COPD, which begins earlier, large or small airway disease?

Back 5

Small

Front 6

Why is there usually exercise avoidance in COPD?

Back 6

b/c of dyspnea on exertion

Front 7

Hx of dyspnea and wheezing in COPD can lead to an erroneous diagnosis of what?

Back 7

Asthma

(ask them when asthma started, as a kid, or older?)

Front 8

How does COPD usually present?

Back 8

5th decade of life with dyspnea on exertion, productive cough, or acute chest illness

-large, barrel shaped chest
-low, flat diaphragm
-diminished breath sounds (w/ occasional rhonchi)
-prolonged expiratory phase
-horizontal ribs
-peripheral cyanosis

Front 9

Define COPD.

Back 9

Preventable and treatable disease that isn't fully reversible, with progressive (usually) airflow limitation a/w an abnormal inflammatory response to irritants. Also produces systemic problems.

Front 10

What is the pathophys of COPD?

Back 10

-Cough and sputum production (increased mucous, reduced clearance)
-Airway collapse (loss of elastic recoil)
-increased smooth muscle tone
-pulm hyperinflation
-hypoxemia and/or hypercapnia

Front 11

What is an early change of peripheral airways in COPD?

Back 11

Inflammation of peripheral airways (won't see on xray!)

This leads to TISSUE REMODELING and scarring, which is irreversible!
Leads to lumen narrowing and FIXED OBSTRUCTION
-> Inflammation leading to edema and mucus hypersecretion ADDS to obstruction

Front 12

Damage (dilation and destruction) to the lung parenchyma (respiratory bronchioles and alveoli) occurs more in the upper lobes, except for when?

Back 12

Lower lobes in alpha1-antitrypsin deficiency COPD

Front 13

How does damage to the lung parenchyma occur?

Back 13

Overproduction of endogenous proteinases in response to repeated & prolonged inflammation, with INABILITY of antiproteinases to neutralize.

Destruction of alveoli attachments to outer wall of PA inhibits ability of PA to remain patent
(air blowing out causes traction which pulls the airway shut, because it is no longer secured by alveoli! - thanks Pathoma guy)

Destruction of alveoli causes loss of elastic recoil
(big shopping bags full of air instead of little balloons - again, thanks Pathoma guy)

Front 14

How does cigarette smoke damage the pulm vasculature?

Back 14

Causes endothelial dysfx, thickening of intima, increased smooth muscle cells and tone.

-> Chronic hypoxemia causes further vasoconstriction and secondary erythrocytosis AND tachycardia

--> Can lead to pulm HTN d/t increased afterload and increased viscosity in right ventricle

END RESULT: Cor pulmonale

Front 15

Gas exchange problems in COPD usually occur when FEV1 is less than what?

Back 15

1 liter

Front 16

What is the main cause of hypoxemia?

Back 16

V/Q mismatch

Loss of surface area can reduce diffusion capacity

Front 17

Pulmonary capillaries near damaged alveoli in emphysema have ____ O2 content and ______ flow.

Back 17

Low, very low

Front 18

Pulmonary capillaries near damaged alveoli in chronic bronchitis have ____ O2 content and ______ flow.

Back 18

Low, relatively normal

Front 19

What are some CXR findings in emphysema?

Back 19

-overexpanded - blacker than normal (more air)
-flat diaphragm
-tenting
-vertical heart (stretched out)

Front 20

What are some CXR findings in emphysema with chronic bronchitis?

Back 20

-alveoli congolomerate -> decreased surface area
-black with white around inflamed airway

Front 21

In COPD, what is decreased more - FVC or FEV1?

Back 21

FEV1 -> therefore decreased FEV1/FVC

Front 22

Define chronic bronchitis!

Back 22

-Submucosal hypertrophy and inflammation of bronchi
-Chronic cough for 3 months in each of 2 successive years w/o discernible cause
-Destruction of acinus or secondary lung lobule distal to the terminal bronchus

Front 23

What's the physical appearance of a typical emphysema patient?

Back 23

"Pink Puffer"

tripod, skinny, breathe fast
look like marathon runner

(maintain oxygenation (stay pink) by pursing lips and increasing pressure to prevent airway collapse)

Front 24

What's the physical appearance of a typical chronic bronchitis patient?

Back 24

"Blue Bloater"

bigger

(can't maintain oxygenation as well - shopping bags!)

Front 25

T/F

With COPD, it is usually either emphysema or chronic bronchitis, not both.

Back 25

False!

Usually mixed, with one being predominant

Front 26

The overall strategy in treatment of COPD is...

Back 26

Minimize progression of air flow obstruction (delay rate of decline of FEV1)!!

Front 27

What are some ways to prolong life in COPD?

Back 27

SMOKING CESSATION
Oxygen (if hypoxic)
Reduce exacerbations
Pulm rehab, aka exercise
LVRS (in select patients, controversial)
Lung transplant

Front 28

What are some symptomatic treatments for COPD?

Back 28

MDI therapy (SA beta-2 agonists, LA beta-2 agonists, SA and LA anticholinergics)
Theophylline
Corticosteroids (inhaled or oral)
Combos (SABA + anticholinergic, LABA + coritcosteroids)

Front 29

Postbronchodilator FEV1/FVC is less than 70% in what stages of COPD?

Back 29

ALL STAGES

*important

Front 30

What is the postbronchodilator FEV1% of predicted in the following stages of COPD?

a) At risk
b) Mild
c) Moderate
d) Severe
e) Very severe

Back 30

a) >80
b) >80
c) 50-80
d) 30-50
e) <30

Front 31

What is the recommended treatment in Stage 0: At Risk COPD (risk factors, chronic cough and sputum, no spirometric abnormalities)?

Back 31

Adjust risk factors (smoking cessation, exercise pollution avoidance, weight loss)

Immunizations (influenza, pneumococcal)

Front 32

What is the recommended treatment in Stage 1: Mild COPD (FEV1 >80%, w/ or w/o symptoms)

Back 32

Short-acting bronchodilator as needed

Front 33

What is the recommended treatment in Stage 2: Moderate COPD (FEV1 50-80%, w/ or w/o symptoms)?

Back 33

-One or more long-acting bronchodilators
-Rehab

Front 34

What is the recommended treatment in Stage 3: Severe COPD (FEV1 30-50%, w/ or w/o symptoms)?

Back 34

-One or more long-acting bronchodilators
-Rehab
-PLUS inhaled glucocorticoid steroids if repeated exacerbations (>3/yr)

Front 35

What is the recommended treatment in Stage 4: Very Severe COPD (FEV1 <30% or presence of respiratory or right heart failure)?

Back 35

-One or more long-acting bronchodilators
-Rehab
-inhaled glucocorticoid steroids if repeated exacerbations (>3/yr)
-PLUS treatment of complications
-PLUS long-term O2 therapy if resp failure (if pO2 sat <88%, to prevent right heart failure)
-PLUS consider surgical options

Front 36

If someone wants a lung transplant, what do they HAVE to do first?

Back 36

QUIT SMOKING!

Front 37

What is LVRS?

Back 37

Lung Volume Resection Surgery

try to get more FUNCTIONAL lung volume by removing big dead parts of lung

controversial b/c:
-mortality = 10%
-get leaking
-dangerous procedure
-troubles getting them off ventilator after surgery
-acts like an acute exacerbation

Front 38

What are the normal values for...

a) pH
b) pCO2
c) HCO3-
d) pO2
e) %O2 sat

Back 38

a) 7.40 (7.35-7.45)
b) 40 (36-44)
c) 24 (22-26)
d) 90 (80-100)
e) 100% (>95%)

Front 39

What is the name of this equation? (don't know if this matters)

[H+] = 24 x pCO2 / [HCO3-]

Back 39

Kassirer-Bleich equation

Front 40

How does the body get rid of acid? (very generally)

Back 40

excreted by lung and kidneys as well as buffered by circulating buffers

Front 41

For every 10 mmHg CO2 change from normal (40), the pH changes _____mEq [H+] in the opposite direction from normal (7.4), and defines a purely respiratory abnormality.

Back 41

0.08

Front 42

How can metabolic acidosis occur on top of respiratory acidosis?

Back 42

They're not breathing enough, so the tissues get hypoxic and must use anaerobic metabolism -> leading to increased lactic acid

This is more acute. Chronically, the kidney will compensate by pumping out more HCO3- (metabolic compensation)

Front 43

What's the problem?

ABG: pH 7.27, HCO3- 10, pCO2 23

Back 43

Metabolic acidosis w/ resp alk compensation

If you get this wrong (or just got lucky), go back and review how to figure it out

Front 44

How do you calculate if there is an anion gap in metabolic acidosis?

Back 44

Cations minus Anions will be greater than 16 in anion gapped metabolic acidosis (or 20 if you include K+)

Na+ - (Cl- + HCO3-) > 16

Front 45

What is the DDx of gapped acidosis???

Back 45

MUDPILES!

Methanol (alcoholics, in withdrawal, delirium tremens)
Uremia (RF)
Diabetic Ketoacidosis (DKA, #1)
Paraldehyde (propylene glycol; window washer and antifreeze)
INH (rarely; TB med)
Lactic Acidosis (resp acidosis w/ poor perfusion)
Ethyline Glycol/EtOH (alcoholics - too much alcohol, not enough food)
Salicylates (aspirin overdose)

If someone has gapped acidosis, you must order all the tests (serum levels) for these! (find out INH from history)

Front 46

What can cause non-gapped acidosis?

Back 46

HCO3 losses (diarrhea, small bowel surgery via dumping)
Renal tubular acidosis
Aldosterone deficiency
Acidifying salts; NH4Cl, arginine HCl
Meds