2 Exam - Yonts

Front 1

What are cations, list them?

Back 1

The cations are sodium (Na+), Potassium (K+), Calcium (Ca2+) and Magnesium (Mg2+) with others being a few normally occurring serum proteins, and some pathological proteins (e.g., paraproteins found in multiple myeloma)

Front 2

What are anions, list them?

Back 2

Likewise, the anions are chloride (Cl-), bicarbonate (HCO3-) and phosphate (PO3-), with others being sulphates and a number of serum proteins (predominantly albumin).

Front 3

What numbers are PaCO2 acidic?

Back 3

41-45/46

Front 4

What numbers are PaCO2 basic?

Back 4

39-35/34

Front 5

What numbers are HCO3- basic?

Back 5

25-26/-29

Front 6

What numbers are HCO3- acidic?

Back 6

23-22/-20

Front 7

List the normal blood gas values for:
PaO2
PaCO2
SaO2
HCO3
ph

Back 7

PaO2- 75-100 mmHg
PaCO2- 40 mmHg (35-34)
SaO2- 94-100% (O2 sat)
HCO3- 24 mEq/L (22-26)
ph: 7.35-7.45

Front 8

metabolic acidosis

Back 8

state that has a low pH and a low bicarbonate level.

Front 9

state that has a low pH and a low bicarbonate level.

Back 9

metabolic acidosis

Front 10

Metabolic alkalosis

Back 10

state that has a high pH and a high bicarbonate level.

Front 11

state that has a high pH and a high bicarbonate level.

Back 11

Metabolic alkalosis

Front 12

Respiratory acidosis

Back 12

a state that has a low pH and a high PCO2 level

Front 13

a state that has a low pH and a high PCO2 level

Back 13

Respiratory acidosis

Front 14

Respiratory alkalosis

Back 14

state that has a high pH and a low PCO2 level

Front 15

state that has a high pH and a low PCO2 level

Back 15

Respiratory alkalosis

Front 16

2 types of metabolic acidosis

Back 16

1. Anion Gap Acidosis: Addition of Anions that bring H+ into the body causing an acidosis

2. Hyperchloremic Acidosis:
Loss of bicarbonate (HCO3-)

Front 17

Loss of bicarbonate (HCO3-)

Back 17

Hyperchloremic Acidosis:
type of metabolic acidosis

Front 18

Excess of Bicarbonate (HCO3-)

Back 18

Metabolic Alkalosis

Front 19

Increased amount of PaCO2

Back 19

Respiratory Acidosis

Front 20

Reduced amount of PaCO2

Back 20

Respiratory Alkalosis

Front 21

what 2 forms of acid base problem can't exsist in the same time?

Back 21

Hyperchloremic Acidosis
(Loss of bicarbonate (HCO3-)
and
Metabolic Alkalosis (Excess of Bicarbonate (HCO3-)

Front 22

Metabolic Acidosis and signs and symptoms

Back 22

There are two types of acidosis. There is a hyperchloremic acidosis and a high anion gap acidosis.
Hyperchloremic acidosis is also called non-gap acidosis. The retention of acid stores overcomes endogenous bicarbonate stores.
pH = pKa + log [HCO3-/PaCO2]
Secondary response is increased ventilation with decreased PCO2
Signs and symptoms include fatigue, dyspnea, abdominal pain, vomiting, Kussmaul respirations, hyperkalemia

Front 23

Signs and symptoms include fatigue, dyspnea, abdominal pain, vomiting, Kussmaul respirations, hyperkalemia

Back 23

Metabolic Acidosis

Front 24

Hyperchloremic Acidosis mnemonics.
What causes it?

Back 24

"DD HEART CCU"
D – Dilutional – rapid infusion of normal saline (which has no bicarb)
D – Drugs – amiloride, triampterine, spironolactone, B-blockers
H – Hyperalimentation
E – Enteral fistula (pancreatic fistula causing loss of bicarb), ileostomy
A – ARF (Acute Renal Failure)
R – RTA, including acidosis of aldosterone deficiency
T – Turds (Diarrhea) – causing intestinal loss of bicarb
C – Carbonic anhydrase inhibitors (acetazolamide), Cholestyramine
C – Consumption of exogenous acids – ammonium chloride, cystine, methionine, calcium chloride.
U – Ureterosigmoidostomy

Front 25

In Hyperchloremic Acidosis mnemonics.
DD stands for what?

Back 25

D – Dilutional – rapid infusion of normal saline (which has no bicarb)
D – Drugs – amiloride, triampterine, spironolactone, B-blockers

Front 26

In Hyperchloremic Acidosis mnemonics.
H stands for what?

Back 26

H – Hyperalimentation (overeating)

Front 27

In Hyperchloremic Acidosis mnemonics.
E stands for what?

Back 27

E – Enteral fistula (pancreatic fistula causing loss of bicarb), ileostomy

Front 28

In Hyperchloremic Acidosis mnemonics.
A stands for what?

Back 28

A – ARF (Acute Renal Failure)

Front 29

In Hyperchloremic Acidosis mnemonics.
R stands for what?

Back 29

R – RTA (renal tubular acidosis), including acidosis of aldosterone deficiency

Front 30

In Hyperchloremic Acidosis mnemonics.
T stands for what?

Back 30

T – Turds (Diarrhea) – causing intestinal loss of bicarb

Front 31

In Hyperchloremic Acidosis mnemonics.
CC stands for what?

Back 31

C – Carbonic anhydrase inhibitors (acetazolamide), Cholestyramine
C – Consumption of exogenous acids – ammonium chloride, cystine, methionine, calcium chloride

Front 32

In Hyperchloremic Acidosis mnemonics.
U stands for what?

Back 32

U – Ureterosigmoidostomy
A ureterosigmoidostomy is a surgical procedure where the ureters which carry urine from the kidneys, are diverted into the sigmoid colon. It is done as a treatment for bladder cancer, where the urinary bladder had to be removed

Front 33

Normal anion gap acidosis

Back 33

Hyperchloremic metabolic acidosis) is the result of excess bicarbonate losses from either renal or gastrointestinal sources.

Front 34

is the ion that is the marker for a normal anion gap acidosis. It is elevated as bicarbonate is lost. It helps maintain electrical neutrality

Back 34

Cl-

Front 35

Chloride is the ion that is the marker for a

Back 35

normal anion gap acidosis. It is elevated as bicarbonate is lost. It helps maintain electrical neutrality.

Front 36

Gap acidosis is a phenomenon in which

Back 36

organic acids are introduced and are the H+ is paired with HCO3 leaving the anions.
The anions are the previous acids that have donated their proton and now they are added to the category of negatively charged anions.

Front 37

abnomal anion number

Back 37

>12 mEq/L

Front 38

How do you calculate the anion gap, what ions are used and what is the normal range?

Back 38

Conventionally only Na+, Cl- and HCO3- are used for calculation of the anion gap in clinical settings.

Anion Gap = Na - (Cl + HCO3)

Normal is 9 -12 mEq/L
change the normal value range.

Front 39

gap acidosis that is caused by large amounts of ketoacids
List ion numbers:

Back 39

Na+= 138, (nl )
K+= 3.4, (nl )
Cl - = 105, (nl )
HCO3-= 9, (nl )
Anion Gap= 24, (nl 9-14)

The electrolytes to the left demonstrate a gap acidosis that is caused by large amounts of ketoacids from a patient in Diabetic Ketoacidosis. The ketoacids are a part of the equation in electroneutrality, but they are the disruption in the pH

Front 40

Causes of Gap Metabolic acidosis

Back 40

Ketoacidosis
Uremia (Renal failure)
Lactic Acidosis (high in sepisemia)
Toxins; Ingestion of toxins (paraldehyde, methanol, salicylate, ethylene glycol)

Front 41

Ingested toxins that cause metabolic acidosis (gap>12)

Back 41

Paraldehyde found in resins and solvents, was a prescribed drug.
Methanol used as a solvent, antifreeze, and a fuel.
Salicylates are a class of medications that are used to reduce fever and pain. The most common is aspirin.
Ethylene glycol is an odorless, colorless, sweet tasting chemical used for antifreeze. forms calcium oxalate crystals in the urine.

Front 42

used as a solvent, antifreeze, and a fuel

Back 42

Methanol
ingested toxin

Front 43

found in resins and solvents, was a prescribed drug

Back 43

Paraldehyde
ingested toxin

Front 44

are a class of medications that are used to reduce fever and pain. The most common is aspirin.

Back 44

Salicylates
ingested toxin

Front 45

is an odorless, colorless, sweet tasting chemical used for antifreeze. forms calcium oxalate crystals in the urine.

Back 45

Ethylene glycol
ingested toxin

Front 46

Anions associated with High Anion Gap Metabolic Acidosis

Back 46

Lactic Acidosis; Lactate
Ketoacidosis; B-Hydroxybutyrate, acetoacetate
Methanol; Formate
Ethylene glycol; Oxalate, Glycolate, Glyoxylate
Salicylate; Salicylate, Lactate, Ketoacids
Renal Failure; Hippurate, Sulfate, Phosphate, Urate

Front 47

Causes of Metabolic Acidosis
Elevated Anion Gap > 12
Intoxications

Back 47

2. Intoxications
Methanol, Ethylene Glycol, Paraldehyde, Salicylates and INH

Front 48

Hyperchloremic Metabolic Acidosis

Back 48

Normal gap acidosis is caused by a loss of bicarbonate or by a gain in acid (not exogenous acids).
Urinary anion gap or net charge and urinary pH are useful in determining etiology of hyperchloremic metabolic acidosis.
To determine if there are high levels of urinary chloride, and thus a normal anion gap acidosis, you need to get spot levels of Na, K, and Cl from the urine.
Urinary Net Charge = ([Na + K]- Cl) performed from spot, or random urine studies.

Front 49

Negative urinary anion gap suggests

Back 49

GI loss of bicarbonate (-9 and more negative)

Front 50

Positive urinary anion gap suggests

Back 50

altered distal urinary acidification like renal tubular acidosis (RTA) (-8 and more positive)

Front 51

Low urinary pH and elevated plasma K in a patient with a positive urinary anion gap suggests

Back 51

selective aldosterone deficiency

Front 52

Urinary pH > 5.5 and elevated K suggests

Back 52

hyperkalemic distal renal tubular acidosis (RTA)

Front 53

hyperkalemic distal renal tubular acidosis (RTA) suggested by

Back 53

Urinary pH > 5.5 and elevated K suggests

Front 54

Urinary pH > 5.5 and normal or decreased K indicates

Back 54

classic renal tubular acidosis (RTA)

Front 55

classic renal tubular acidosis (RTA)

Back 55

Urinary pH > 5.5 and normal or decreased K indicates

Front 56

Causes of Hyperchloremic Metabolic Acidosis

Back 56

Renal Tubular Acidosis The inability of the kidney to reabsorb HCO3- or excrete H+.
Ileostomy when the small bowel is moved surgically to open on the abdominal wall secondary to some colon disorder causing it to be removed or totally ineffective.
Intestinal loss of Bicarbonate (diarrhea)
Carbonic anhydrate inhibitors (acetazolamide) the kidney can not buffer and bicarbonate is lost in the urine causing a gain in total body H+.
Dilutional acidosis (rapid infusion of bicarbonate-free isotonic fluid

Front 57

The inability of the kidney to reabsorb HCO3- or excrete H+.

Back 57

Renal Tubular Acidosis and cause Hyperchloremic Metabolic Acidosis

Front 58

when the small bowel is moved surgically to open on the abdominal wall secondary to some colon disorder causing it to be removed or totally ineffective.

Back 58

Ileostomy and cause Hyperchloremic Metabolic Acidosis

Front 59

the kidney can not buffer and bicarbonate is lost in the urine causing a gain in total body H+.

Back 59

Carbonic anhydrate inhibitors (acetazolamide)
and cause Hyperchloremic Metabolic Acidosis

Front 60

(rapid infusion of bicarbonate-free isotonic fluid

Back 60

Dilutional acidosis
and cause Hyperchloremic Metabolic Acidosis

Front 61

ammonium chloride (used as expectorant in medicine, has been used as diuretic)
cystine
calcium chloride (found in some sport drinks, and pickle brine, used medically to treat hyperkalemia or hypocalcemia)

Back 61

Ingestion of exogenous acids
and cause Hyperchloremic Metabolic Acidosis

Front 62

(when the ureters are diverted to the sigmoid colon in those who have had bladder cancer and do not have functioning bladder)

Back 62

Ureterosigmoidostomy
and cause Hyperchloremic Metabolic Acidosis

Front 63

amiloride, triamterine, spironolactone, B-blockers

Back 63

Drugs
and cause Hyperchloremic Metabolic Acidosis

Front 64

What is a buffer solution?

Back 64

A solution that resists change in pH. The body has all kinds of buffers present to help prevent a life threatening change in total body pH with acid base disorders

Front 65

The most abundant and most important buffer

Back 65

is the bicarbonate (HCO3/CO2) buffer

Front 66

Other than bicarb buffers systems in the body are___

Back 66

Others include phosphate (HPO4/H2PO4), hemoglobin, and plasma proteins like albumin

Front 67

How buffers work?

Back 67

Buffers work instantaneously to control the acid base status. When there is a shift in the amount of acid the buffer systems in place will immediately buffer the change in H+ to help reduce the swing in total body pH.

Front 68

Name some instantenous rate buffer systems:

Back 68

Bicarb
Hb
P
Plasma protein

Front 69

Organs that play a role in the buffer system

Back 69

lungs- regulates elemination of Co2, rate from min to hours
ionic shift- exchange of intracellural K and Na for H, rate 2-4 hours
kidneys- Excretion of acid, reabsorption of bicarbonate and ammonia formation, rate from hrs to days
Bone- Exchanges of calcium, phosphate, and release of carbonate, rate from hours to days

Front 70

The kidneys work to remove acid by two ways

Back 70

They reabsorb bicarbonate (HCO3-)
They secrete acid in the urine (H+) alone or combined with NH3 to form NH4.

Front 71

Metabolic alkalosis is divided into

Back 71

into chloride-resistant or chloride-responsive.
Chloride-responsive are those in which the urinary chloride levels are < 15 mEq/L.
Chloride-resistant are those in which the urinary chloride levels are > 15 mEq/L.

Front 72

Respiratory acidosis is primarily caused

Back 72

by increased PaCO2.
The disorder is caused by a defect in the respiratory pump/mechanism or an increase in the opposing load.
The body compensates by retaining bicarbonate at the kidney.

Front 73

Disorders of the Respiratory Mechanism

Back 73

Depressed respiratory drive (medications, anatomical lesions, inflammatory conditions, infectious conditions, and metabolic derangements)
Abnormal neuromuscular transmission and lesions of the nervous systems (Guillain Barre syn.,multiple sclerosis, ALS)
Muscle dysfunction (fatigue, myopathic dz.)

Front 74

Causes of Increased Respiratory Load

Back 74

Increased load (pneumonia, pulmonary edema, ARDS)
Chest wall stiffness (flail chest, pneumothorax)
increased ventilatory demand (pulmonary embolism, sepsis)
High airflow resistance (upper airway obstruction, COPD, aspiration, laryngospasm)

Front 75

Respiratory alkalosis is primarily caused by

Back 75

decreased PaCO2.
Respiratory alkalosis is also called primary hypocapnia.
It is the result of increased minute ventilation or decreased CO2 production. It is also caused by anything that increases respiratory drive.
The body compensates with renal excretion of bicarbonate.

Front 76

also called primary hypocapnia.

Back 76

Respiratory alkalosis

Front 77

Causes of Respiratory Alkalosis

Back 77

Hypoxemia (PNA, cyanotic heart disease, pulmonary edema, pulmonary embolism, sever circulatory failure, and high altitude)
CNS stimulation (Fever, SAH, Tumor, Pain)
Drugs or hormones (Salicylates, Xanthines)
Stimulation of chest receptors (ARDS, Asthma)
Iatrogenic (Mechanical ventilation)

Front 78

compensation

Back 78

Compensations are the body’s response to abnormality in the pH.
The compensation will never completely normalize the pH or overshoot past the deficit.
The standard values are HCO3- = 24, and PCO2 = 40.

Front 79

1. Initial chemical change
2. compensatory response
3. compensatory mechanism
for metabolic acidosis

Back 79

1. decreased HCO3
2. decreased PCO2
3. hyperventilation

Front 80

1. Initial chemical change
2. compensatory response
3. compensatory mechanism
for metabolic alkalosis

Back 80

1. increased HCO3
2. increased PCO2
3. Hypoventilation

Front 81

1. Initial chemical change
2. compensatory response
3. compensatory mechanism
respiratory acidosis

Back 81

1. increased PCO2.
2. increased HCO3
3. NA

Front 82

1. Initial chemical change
2. compensatory response
3. compensatory mechanism
respiratory acidosis-acute

Back 82

1. increased PCO2.
2. increased HCO3
3. Intracellular Buffering (hemoglobin, intracellular proteins)

Front 83

1. Initial chemical change
2. compensatory response
3. compensatory mechanism
respiratory acidosis- chronic

Back 83

1. increased PCO2.
2. increased HCO3
3. Generation of new HCO3- due to the increased excretion of ammonium

Front 84

1. Initial chemical change
2. compensatory response
3. compensatory mechanism
respiratory alkalosis

Back 84

1. decreased PCO2.
2. decreased HCO3
3. NA

Front 85

1. Initial chemical change
2. compensatory response
3. compensatory mechanism
respiratory alkalosis-acute

Back 85

1. decreased PCO2.
2. decreased HCO3
3. Intracellular Buffering

Front 86

1. Initial chemical change
2. compensatory response
3. compensatory mechanism
respiratory alkalosis-chronic

Back 86

1. decreased PCO2.
2. decreased HCO3
3. Decreased reabsorption of HCO3-, decreased excretion of ammonium

Front 87

Pt present with low pH, high PaCO2 and high HCO3

Back 87

the bicarb is high because it tries to compensate

Front 88

extremely high PCO2, ph-normal, high HCO3

Back 88

calculate anion GAP, most likely triple disorder

Front 89

A mixed acid base disorder is one in which

Back 89

there are at least two primary disorders at one time.

Front 90

To determine if a mixed disorder is present

Back 90

adequate compensation should be tested. If the numbers did not match adequate compensation then a mixed disorder is likely

Front 91

Arterial blood gas values may be normal, but a high anion gap indicates a

Back 91

mixed disorder, metabolic acidosis and respiratory alkalosis. How?

With metabolic acidosis and respiratory alkalosis the PCO2 is lower than what would be predicted for acidotic state

Front 92

With metabolic alkalosis and respiratory acidosis the HCO3 is

Back 92

is higher than predicted for the acidotic state.

Front 93

When there is a metabolic and respiratory alkalosis the HCO3 and the PCO2 are

Back 93

lower than what would be expected in an alkalotic state caused by a primary disorder.

Front 94

It is possible to have a triple disorder
How?

Back 94

Have to have a HIGH ION GAP!
Either Hyperchloremic or a Metabolic Alkalosis. (not together)
And a Respiratory Disorder:
Either alkalosis or acidosis

Front 95

The calculation of the delta gap will allow the

Back 95

coexisting acid base derangements to be differentiated

Front 96

Delta ratio is used

Back 96

The delta ratio is used in the setting of a high anion gap acidosis.

Front 97

delta ratio is used to determine if there are

Back 97

are any other disorders present simultaneously with the high anion gap acidosis

Front 98

If a metabolic acid (HA) is added 1 H+ will be buffered by _____

Back 98

1 HCO3-

Front 99

Unmeasured anions will add to the gap and _____

Back 99

decrease the bicarbonate level by 1.

Front 100

A delta ratio below a 1:1 indicates

Back 100

a greater fall in HCO3- and this could be explained by a mixed metabolic acidosis.

Front 101

A value greater than 2:1 indicates

Back 101

a smaller fall in HCO3- and one would expect there to be a superimposed metabolic alkalosis or compensated chronic respiratory acidosis. There is more bicarb around than would be expected with just a high anion gap acidosis.

Front 102

The delta ratio should approach ___ to ____

Back 102

The ratio should approach 1:1 to 1.6:1

Front 103

Normal gap number

Back 103

12

Front 104

normal bicarb number

Back 104

24

Front 105

Delta anion gap calculation

Back 105

normal gap (12) - calc anion gap (Na-(Cl+HCO3)

Front 106

Delta bicarb calculation

Back 106

Normal bicarb (24)- bicarb level

Front 107

Delta ratio calculation=

Back 107

delta anion gap/delta bicarb calc

Front 108

Approach to Interpreting Acid Base Disorders

Back 108

1. GET A HISTORY. You need to perform a history and physical. Knowing what is going on makes all the difference.
2. Look at the pH. Normal is between 7.35 and 7.45.
3a. Look at PCO2 and HCO3-, and determine if values are normal or how they are abnormal.
3b. If the pH is abnormal the value (PCO2 or HCO3-) that matches the change in pH determines the primary disorder.
4a. Is there an Anion Gap?
Gap = Na - (Cl + CO2)
4b. If Gap, is there another disturbance? Use Delta Ratio.
DR= change in Gap/Change in Bicarb
4c. If metabolic Acidosis, check for respiratory disorder. Use the Winter’s formula.
PCO2 = (1.5 x HCO3) + 8 +/- 2
5. If metabolic alkalosis check for co-existing respiratory disorder.
PCO2 = (0.9 x HCO3) + 16 + 2
6. If respiratory disorder check for appropriate compensation.
Respiratory Acidosis
Acute ↑[HCO3-] = 1 mEq/L for every 10 mm Hg ∆PCO2
Chronic ↑[HCO3-] = 3.5 mEq/L for every 10 mm Hg ∆PCO2
Respiratory Alkalosis
Acute ↓[HCO3-] = 2 mEq/L for every 10 mm Hg ∆PCO2
Chronic ↓[HCO3-] =4 mEq/L for every 10 mm Hg ∆PCO2

Front 109

Winter’s formula

Back 109

for metabolic acidosis
PCO2 should be = HCO3
PCO2 = (1.5 x HCO3) + 8 +/- 2

Front 110

If metabolic alkalosis use formula

Back 110

PCO2 = (0.9 x HCO3) + 16 +/- 2

Front 111

. If respiratory disorder check for appropriate compensation.
if Respiratory Acidosis

Back 111

Acute ↑[HCO3-] = 1 mEq/L for every 10 mm Hg ∆PCO2
Chronic ↑[HCO3-] = 3.5 mEq/L for every 10 mm Hg ∆PCO2

Front 112

. If respiratory disorder check for appropriate compensation.
Respiratory Alkalosis

Back 112

Acute ↓[HCO3-] = 2 mEq/L for every 10 mm Hg ∆PCO2
Chronic ↓[HCO3-] =4 mEq/L for every 10 mm Hg ∆PCO2

Front 113

define Pneumothorax

Back 113

Pneumothorax is air in the pleural space

Front 114

Different types of Pneumothorax

Back 114

Primarily classified as Spontaneous or Traumatic

Primary spontaneous pneumothorax
Secondary spontaneous pneumothorax
Traumatic pneumothorax
Tension pneumothorax

Front 115

define Primary Spontaneous Pneumothorax

Back 115

Primary spontaneous pneumothorax is when air moves to the pleural space and is not caused by a traumatic event or is not in a patient with lung disease.
Usually in males less than 30

Front 116

Primary Spontaneous Pneumothorax Risk Factors

Back 116

Smoking (significant risk factor, the more you smoke the greater the risk)
Family history
Marfan’s syndrome
Homocystinuria
Thoracic endometriosis

Front 117

Initial Treatment Options of Primary Spontaneous Pneumothorax

Back 117

Observation
Supplemental oxygen
Needle aspiration of intrapleural air
Chest tube insertion
Thoracoscopy

Front 118

First primary spontaneous pneumothorax (PSP)

Back 118

Less than 2 to 3 cm on CXR
>3 cm, needle decompression
If needle decompression fails then place chest tube and perform thoracoscopy (pleurodesis through chest tube can be considered)

Front 119

Recurrent PSP tx

Back 119

Recurrent PSP or concomitant hemothorax
Chest Tube
Thoracoscopy, or chemical pleurodesis

Front 120

What does chest tube does in pneumothorax?

Back 120

pull air or fluid out

Front 121

Chemical Pleurodesis define and drugs used

Back 121

Pleurodesis causes the pleurae to stick together, thereby eliminating the pleural space and preventing fluid accumulation.
Pleurodesis is a procedure that obliterates the pleural space to prevent recurrent pleural effusion or recurrent pneumothorax. It is most commonly performed by draining the effusion or intrapleural air and then inducing inflammation and fibrosis by either instilling a chemical irritant or performing mechanical abrasion.
Can be performed by placing one of the following agents in the tube;
Tetracycline
Doxycycline
Talc

Front 122

Secondary Spontaneous Pneumothorax

Back 122

Occur in patients with lung disease
Most common cause is COPD
others;
Pneumocystis jirovecii pneumonia(PCP)
Cystic Fibrosis
Tuberculosis (TB)

Front 123

Other Causes SSP

Back 123

Ankylosing Spondylitis
Asthma
Histiocytosis
Idiopathic Pulmonary Fibrosis
LAM
Lung Cancer
Marfan Syndrome
Necrotizing Syndrome
Rheumtoid Arthritis
Sacroidosis

Front 124

Tension Pneumothorax define

Back 124

When there is positive airway pressure in the pleural space

Front 125

Tension Pneumothorax findings

Back 125

compression of ipsilateral lung, contralateral shift of mediastinum, downward depression of the diaphragm

Front 126

pt sympt w Tension Pneumothorax

Back 126

Patients can be hypoxic and hypotensive
pt will be crushing

Front 127

Tension Pneumothorax tx

Back 127

If suspected you should perform needle decompression without waiting for radiograph.

Front 128

Unstable Patients w Tension Pneumothorax

Back 128

Chest tube if needle decompression is delayed
Needle decompression 14 - 20 gauge IV angiocatheter at midclavicular line and 2nd intercostal space.
The needle is place in the pleural space and the catheter is advanced and the needle is withdrawn.

Front 129

Chest Tube Placement
indications

Back 129

Tube Thoracostomy
Pneumothorax, Hemothroax, Hemopneumothorax, Hydrothorax, Chylothorax, Empyema, Pleural effusion.

Front 130

Tube Thoracostomy

Back 130

Chest Tube Placement

Front 131

Chest Tube Placement
Contraindications

Back 131

coagulopathy, pulmonary bullae, pulmonary, pleural, or thoracic adhesions, loculated pleural effusion or empyema, or skin infection over the chest tube insertion site

Front 132

Chest Tube placement

Back 132

Find site 4th to 6th intercostals space 
anterior to mid axillary line.
Clean
Anezthetize
Make incision
Open with Trochars and finger
Place tube
Sew tube in place

Front 133

Pleural Effusions

Back 133

An excess quantity of fluid in the pleural space. The pleural space is the space between the lung and the chest wall.
Categorized by the composition of the effusion.
Transudative
Exudative.
There are numerous mechanisms and causes

Front 134

Mechanisms that Cause Pleural Effusions***

Back 134

An increase in hydrostatic pressure in the microvascular circulation (CHF)
A decrease in oncotic pressure in the microvascular circulation (hypoalbuminemia)
A decrease in pressure in the pleural space (atelectasis)
Increased permeability of the microvascular circulation (Pneumonia)
Impaired lymphatic drainage from pleural space (Malignancy)
Movement of fluid from the abdomen into pleural space (cirrhosis)

Front 135

Transudative Causes****

Back 135

Congestive Heart Failure
Superior vena caval obstruction
Constrictive pericaditis
Cirrhosis with ascities
Hypoalbuminemia
Salt retaining syndromes
Peritoneal Dialysis
Hydronephrosis
Nephrotic Syndrome
Myxedema

Front 136

Exudative Causes****

Back 136

1. Infections; Paraneumonic effusions, Bacterial empyema, Tuberculosis, Fungi, Parasites, Viruses and Mycoplasma
2. Neoplasms; Primary and Metastatic lung tumors, Lymphomas, Leukemias, Tumors of the pleura, Intra-abdominal tumors with ascities
3. Vascular disease; Pulmonary embolism, Wegener granulomatosis
4. Intra-abdominal diseases; Pancreatitis and Pseudocysts, Subdiaphragmatic abscess
5. Trauma; Hemothorax, Chylothorax, Esophageal rupture, and Intrabdominal surgery
6. Miscellaneous; Drug-induced effusions, Uremic pleuritis, Yellow nail syndrome, Dressler syndrome, Familial Mediterranean fever

Front 137

Determining Transudative versus Exudative

Back 137

There are numerous markers that are used to help a clinician determine whether an effusion is transudative or exudative.
Light’s criteria was used extensively traditionally. There were some studies that demonstrated that it could be wrong a significant amount of the time.
Light’s criteria used primarily the following markers to determine exudate; ratio of pleural protein to serum protein > 0.5, pleural LDH to serum LDH > 0.6, and pleural LDH more than two-thirds the upper limit of normal for serum

Front 138

Light’s criteria

Back 138

To determining Transudative versus Exudative pleural effusion
Light’s criteria was used extensively traditionally. There were some studies that demonstrated that it could be wrong a significant amount of the time.
Light’s criteria used primarily the following markers to determine exudate; ratio of pleural protein to serum protein > 0.5, pleural LDH to serum LDH > 0.6, and pleural LDH more than two-thirds the upper limit of normal for serum.

Front 139

Metanalysis shows that Exudates have

Back 139

Pleural fluid protein > 2.9
Pleural Cholesterol > 45
Pleural Fluid LDH > 60% the upper limit for serum.

Front 140

Draw Transudative vs Exudative
table

Back 140

yonts- lung disease
31 slide

Front 141

Other studies for Transudative and Exudative

Back 141

Amylase
pH
glucose
Gram stain and culture
Cytology-malignancy
Lipids, fungal and viral cultures

Front 142

Thoracentesis

Back 142

A procedure in which a clinician places a catheter in the space between the parietal and visceral pleura and drains some fraction of the pleural effusion.
A thoracentesis can be diagnostic and therapeutic.
It is a procedure used to obtain a sample or remove the majority of a pleural effusion.

Front 143

Indications for Thoracentesis

Back 143

When there is an unexplained pleural effusion
When there is a need to remove the fluid to help remove cardiovascular or pulmonary dysfunction secondary to the effusion

Front 144

Contraindications for Thoracentesis

Back 144

Absolute contraindications are an uncooperative patient, and a coagulation disorder.
Relative contraindications are a site of insertion has bullous disease, the patient has PEEP or positive end expiratory pressure, only one functional lung.

Front 145

Possible Complications of Thoracentesis for pleural effusion

Back 145

Possible major complications are pneumothorax (3-30%), hemopneumothorax, hemorrhage, hypotension (low blood pressure due to a vasovagal response) and reexpansion pulmonary edema.
Possible minor complications are subcutaneous hematoma or seroma, anxiety, dyspnea and cough (after removing large volume of fluid).

Front 146

Drug Induced Lung Disease (DILD)

Back 146

Drugs can affect the complete respiratory system;
airways,
parenchyma,
pleura,
pulmonary vasculature,
respiratory muscles,
mediastinum.

Front 147

The major categories of DILD

Back 147

Bronchospasm and cough
Diffuse lung disease
Pulmonary edema
Pleural effusions
Pulmonary vascular disease
Hypoventilation

Front 148

Cough caused by what?

Back 148

The ACE inhibitor is the primary cause of cough in patients.

Front 149

Drugs that cause Bronchospasm

Back 149

Patients typically exhibit cough, dyspnea, and wheezing after exposure to the following drugs if they cause bronchospasm in the
Do not have to have asthma
Effects can be blunted if treated with bronchodilator before administration
Adenosine
Aspirin
Beta-Blockers
Contrast Media
Dipyridamole
Interlukin 2
Nitrofurantoin
Penicillamine
Pentamidine
Sulfonamides
Vinblastine

Front 150

Drugs That Can Cause Pulmonary Fibrosis

Back 150

Adalimumab (Humira) RA, Crohns, Psorias (TNF inhibitors)
Amiodarone (Pacerone) anti-arrthymic
Azathroprine (Imuran) Kidney transplant rejection Medicine
Carmustine (BiCNU) chemo drug for Multiple myeloma, Hodgkin & Non Hodgkin, and brain tumors
Bleomycin (Blenoxane) chemo drug for malignant pleural effusions, Hodgkin & Non Hodgkin, squamous cell tumors, and testicular CA
Busulfan (Myleran) for CML and Myelofibrosis
Chlorambucil (Leukaran) CLL and Lymphomas
Cyclophosphamide (Cytoxan) Chemotherapy, RA
Etanercept (Enbrel) RA, Psoriatic arthritis, ankylosis spondylitis
Fludarabine (Fludara) CLL
Gold (Myochrysine) RA
INF alpha 2b (Intron A) comdyloma acuminata, hairy cell leukemia
Infliximab (Remicade) RA, Psoriatic arthritis, ankylosis spondylitis, Crohns, and Ulcerative Colitis
Methotrexate (Trexall) RA, Psoriasis
Mitomycin (Mutamycin) Stomach CA, Pancreatic CA
Nitrofurantoin (Macrobid) (Macrodantin) Antibiotic for UTIs
Paclitaxil (Taxol) ovarian, breast, non-small lung CA, and Kaposi sarcoma
Penicillamine (Cuprimine) cystinuria, RA, Wilson Dz,
Phenytoin (Dilantin) Seizure disorders
Rituximab (Rituxan) Wegner, microscopic polyangitis, RA, CD20-pos CLL, non-Hodgkin lymphoma
Sirolimus (Rapamune) Kidney transplant rejection
Sulfasalazine (Azulfidine) RA, crohns, and ulcerative colitis

Front 151

Drugs That Can Cause Pulmonary Fibrosis

Back 151

Phenytoin (Dilantin) Seizure disorders
Nitrofurantoin (Macrobid) (Macrodantin) Antibiotic for UTIs
Methotrexate (Trexall) RA, Psoriasis
Amiodarone (Pacerone) anti-arrthymic

Front 152

Mortality due to drugs in Pulmonary Fibrosis

Back 152

Amiodarone pneumonitis causes death in 10% of cases.
bleomycin pulmonary toxicity occurs in 10% of cases, of those 1-2% are fatal
Cyclophosphamide-induced pulmonary fibrosis has a mortality rate arround 50%.
MTX-induced hypersensitivity reactions develop chronic fibrosis in about 7% of patients and 8% of those die of progressive respiratory failure.
Cytosine arabinoside, an antimetabolite used to treat acute leukemia, causes non cardiac pulmonary edema in 13-20% of patients, of those 2-50% can die.
Busulfan-induced pulmonary fibrosis occurs in about 4-5% of patients that use it, with mortality rates ranging from 50-80%.
BiCNU, or carmustine, causes pulmonary fibrosis with a mortality rate of nearly 90%.

Front 153

Drugs that Cause Bronchiolitis Obliterans Organizing Pneumonia(BOOP)Cryptogenic Organizing Pneumonia

Back 153

Symptoms include cough, dyspnea, patchy airspace infiltrates on imaging with possible air trapping, and a mixed obstructive and restrictive PFT pattern. Biopsy reveals polypoid, myxoid changes in the terminal bronchioles with organizing pneumonic change distal to the small airways. BOOP has a favorable outcome when treated with drug withdrawal and corticosteroids.

Front 154

Symptoms include cough, dyspnea, patchy airspace infiltrates on imaging with possible air trapping, and a mixed obstructive and restrictive PFT pattern. Biopsy reveals polypoid, myxoid changes in the terminal bronchioles with organizing pneumonic change distal to the small airways.

Back 154

Bronchiolitis Obliterans Organizing Pneumonia(BOOP) Cryptogenic Organizing Pneumonia

Front 155

Drugs that cause Cryptogenic Organizing Pneumonia

Back 155

Amiodarone
Amphoteracin
Bleomycin
Cyclophosphamide
INF alpha
Interferon beta
Nitrofurantoin
Penicillamine
Phenytoin

Front 156

Drug Induced Pulmonary Edema

Back 156

Drug-induced noncardiogenic pulmonary edema is characterized by acute dyspnea, alveolar opacities, and hypoxia in the absence of left heart failure. Pathologic findings can reveal bland edema with protein filling alveoli and occasionally diffuse alveolar damage. Treatment is judicious volume management and supportive care.

Front 157

Drugs that can cause Pulmonary Edema

Back 157

Aspirin
Carbamazepine
Contrast Media
Cyclophosphamide
Hydorchlorothiazide
Methotrexate
Muromonab-CD3
Retinoic Acid
Sulfonamides
Terbutaline

Front 158

Diagnosis of DILD

Back 158

Take a very good drug history
Chest radiograph
Pulmonary function tests
High resolution chest CT (HRCT)
Bronchoscopy with BAL; can help check for infections or lymphoma or predict

Front 159

Bronchoalveolar lavage findings in DILD:
Hemosiderin-laden macrophages
Progressive bloody lavage return

Back 159

Diffuse Alvolar Hemorrhage

Front 160

Bronchoalveolar lavage findings in DILD:
BAL lymphocytosis
Decreased CD4 to CD8 ratio

Back 160

Hypersensitivity Pneumonitis

Front 161

Bronchoalveolar lavage findings in DILD
Eosinophils > 25%

Back 161

Eosinophilic Pneumonia

Front 162

Bronchoalveolar lavage findings in DILD
Alveolar Macrophages with empty vacuoles
Positive result from Oil Red O stain

Back 162

Lipoid Pneumonia

Front 163

Bronchoalveolar lavage findings in DILD
Foamy Macrophages******

Back 163

Amiodarone use

Front 164

Bronchoalveolar lavage findings in DILD
Atypical Type II pneumocyte
BAL Neutrophils

Back 164

Cytotoxic reaction

Front 165

Classes of biological agents with reported pulmonary toxicity include

Back 165

tumor necrosis factor (TNF)-α blockers, anti-CD20 antibodies, recombinant interferon (INF) alfa, and T-cell antiproliferative agents

Front 166

Anti-TNF medications increase the risk of ____
and
Anti-TNF medications can also cause __________

Back 166

infection, including opportunistic infections, pneumonia, and TB.

cause infusion reactions, malignancy, and DILD.

Front 167

The most common type of DILD due to anti-TNF agents is

Back 167

diffuse interstitial lung disease or pulmonary fibrosis

Front 168

What drug is a chimeric monoclonal IgG directed against β-cell-specific CD20 antigen. It is commonly used for treatment of non-Hodgkin lymphoma and RA. cases of acute hypoxic respiratory failure within hours after its infusion has been observed. One such patient had a lung biopsy demonstrating diffuse alveolar damage and hemorrhage. The most common finding on biopsy is organizing pneumonia

Back 168

Rituximab

Front 169

They are often given in conjunction with ribavirin for the treatment of hepatitis C viral infection. Pulmonary toxicity due to INF use includes interstitial pneumonitis, sarcoid-like noncaseating granulomas, asthma exacerbation, pleural effusion, and BOOP

Back 169

INF alfa-2a and INF alfa-2b are commercially available recombinant alfa INFs that are pegylated in order to prolong drug half-life and achieve higher blood levels.

Front 170

Radiation Induced Lung Injury

Back 170

Are present today in people who undergo thoracic irradiation for lung, breast, and hematologic malignancy

Front 171

Radiation insults the lung by causing ________

Back 171

Radiation insults the lung by causing direct damage to the DNA, and fibrosis is caused by the number of cytokines that are generated by damaged chemical bonds. The chemical bonds are broken by the direct radiation.

Front 172

Risk Factors of Radiation Induced Lung Injury

Back 172

There is a direct relation to the volume of lung that is irradiated.
The higher the dose the more likely the patient is to receive radiation induced lung injury.
Spreading the dose out in the same day reduces the likelihood of radiation pneumonitis over giving the dose in treatment.
If the patient receives concurrent chemotherapy has an increased risk of radiation pneumonitis
There is some evidence that administration of paclitaxel with radiation therapy reduces the chance of radiation pneumonitis.

Front 173

Radiation Pneumonitis acute vs chronic

Back 173

Acute radiation pneumonitis occurs approximately 4 to 12 weeks following irradiation
Late or fibrotic radiation pneumonitis occurs 6 to 12 months after exposure

Front 174

Clinical Manifestations of Radiation Pneumonitis*****

Back 174

A nonproductive cough, which may occur during therapy as a manifestation of bronchial mucosal injury or later as a manifestation of fibrosis.
Dyspnea may only occur with exertion, or may be described as an inability to take a deep breath.
Fever is usually low grade, but can be more pronounced in severe cases.
Chest pain may be pleuritic or substernal and can represent pleuritis, esophageal pathology, or rib fracture.
Malaise and weight loss may be observed.

Front 175

A nonproductive cough, which may occur during therapy as a manifestation of bronchial mucosal injury or later as a manifestation of fibrosis.
Dyspnea may only occur with exertion, or may be described as an inability to take a deep breath.
Fever is usually low grade, but can be more pronounced in severe cases.
Chest pain may be pleuritic or substernal and can represent pleuritis, esophageal pathology, or rib fracture.
Malaise and weight loss may be observed.

Back 175

Clinical Manifestations of Radiation Pneumonitis

Front 176

Physical exam findings with Radiation Pneumonitis***

Back 176

Crackles or a pleural rub may be heard; in some cases auscultation is normal.
Dullness to percussion may be detected as a result of a small pleural effusion;
Skin erythema may outline the radiation port but is not predictive of the occurrence or the severity of radiation pneumonitis.
Tachypnea, cyanosis, or signs of pulmonary hypertension may be seen in more advanced cases.

Front 177

Crackles or a pleural rub may be heard; in some cases auscultation is normal.
Dullness to percussion may be detected as a result of a small pleural effusion;
Skin erythema may outline the radiation port but is not predictive of the occurrence or the severity of the disease.Tachypnea, cyanosis, or signs of pulmonary hypertension may be seen in more advanced cases.

Back 177

Physical exam findings with Radiation Pneumonitis***

Front 178

Chest Radiograph Findings of Radiation Pneumonitis

Back 178

Chest radiographs may be normal in symptomatic subjects during the subacute phase of radiation pneumonitis.
Perivascular haziness is an early radiation-induced abnormality on chest radiograph, often progressing to patchy alveolar filling densities.
Radiographs taken during the chronic phase of radiation pneumonitis may show volume loss with coarse reticular or dense opacities.
A straight line effect, which does not conform to anatomical units but rather to the confines of the radiation port, is often seen and is virtually diagnostic of radiation-induced lung injury.
Small pleural effusions and rib fractures may be seen, but lymphadenopathy does not occur.

Front 179

Treatment Of Radiation Pneumonitis

Back 179

Often Prednisone is used to treat, it works well in BOOP caused by radiation exposure, usually symptoms return with the radiographic findings after discontinuation of therapy.
Pentoxifylline has been used to try to prevent radiation pneumonitis and some studies have demonstrated some efficacy.
Improvements are noted in perfusion and ventilation of radiated lung from about 3 to 18 months after the injury. After 18 months very little change has been documented.

Front 180

Non infectious Complications following Lung transplant

Back 180

Malignancy
Recurrent primary disease
Graft vs Host disease
Phrenic nerve and diaphragmatic dysfunction
Cardiovascular
Pleural
Pulmonary Embolism
Other

Front 181

Malignancy following Lung transplant

Back 181

Solid organ transplant recipients are at an increased risk of developing cancer.
The most common malignancies are lymphomas, skin, lip, and perineal carcinomas, cervical cancer and Kaposi’s sarcomas.
The most common cancer like lung, breast, colon, and prostate are not increased.

Front 182

The most common malignancies are following Lung transplant

Back 182

The most common malignancies are lymphomas, skin, lip, and perineal carcinomas, cervical cancer and Kaposi’s sarcomas.

Front 183

The most common cancers after lung transplant

Back 183

like lung, breast, colon, and prostate are not increased

Front 184

What transplant recipients are at an increased risk of developing cancer?

Back 184

Solid organ

Front 185

Posttransplantation Lymphoproliferative Disorder (PTLD)

Back 185

A collection of lymphoproliferative disorders like lymphomas.
They are closely associated with the Ebstein-Barr virus.
The two year survival has been reported to be as low as 19%.

Front 186

Recurrent Primary Disease

Back 186

Sarcoidosis
Lymphangioleiomyomatosis
Diffuse panbronchiolitis
Pulmonary alveolar proteinosis
Desquamative interstitial pneumonia
Pulmonary Langerhans cell histiocytosis
Bronchioloalveolar carcinoma
Idiopathic pulmonary hemosiderosis
Giant cell interstitial pneumonitis
Alpha-1-antitrypsin deficiency
Pulmonary veno-occlusive disease

Front 187

Graft vs Host Disease

Back 187

Graft-versus-host disease (GVHD) results from an attack by viable donor lymphocytes on lymphoid tissues in an immunosuppressed recipient. This immunologic assault is manifested clinically by dysfunction of the skin, liver, gastrointestinal tract, and bone marrow.”
This is very rare in lung transplant and common following stem cell transplant.

Front 188

Phrenic Nerve and Diaphragmatic Dysfunction after lung transplant

Back 188

Occurs about 3 - 9% of the time
More common in heart and lung transplants
Causes longer stays, but did not cause serious long term complications

Front 189

Cardiovascular Complications after lung transplant

Back 189

Often there can be hemodynamic instability in the first 24 hours.
dysrhythmias are common and atrial fibrillation and atrial flutter are commonly the culprits.
Risk factors for cardiovascular disease will increase secondary to the use of immunosuppressive medications

Front 190

Pleural Complications after lung transplant

Back 190

Pleural effusions are common after lung transplant.
They generally resolve without chronic sequelae.

Front 191

Pulmonary Embolism after lung transplant

Back 191

Lung transplant recipients are at risk like other patients that undergo similar major surgeries.
The problem with PEs in these patients is that the symptoms are non-specific.

Front 192

Situations that alter the brain’s control of the respiratory drive.

Back 192

Disorders of Ventilatory Control

Front 193

Ventilatory Control Can be altered by numerous factors like

Back 193

hypoxia or hypocapnia

Front 194

COPD and ventilation problems.
“Blue Bloaters” are likely to have _____ and ____and ___________compared to the “Pink Puffers” that are _____ and generally_____O2 levels

Back 194

“Blue Bloaters” are likely to have CO2 retention and hypoxia and decreased respiratory drive compared to the “Pink Puffers” that are eucapnic and generally normal O2 levels

Front 195

“Blue Bloaters” are likely to have CO2 retention and hypoxia and decreased respiratory drive.
How this happens?

Back 195

1. low tidal volume and high frequency
2. Haldane Effect
As hemoglobin oxygen level increases the hemoglobins ability to carry CO2 will be decreased
3. Supplemental O2 will increase CO2 retention
suppresses hypoxic drive
Increasing CO2 will cause sedation and suppress hypercapnic drives

Front 196

Supplemental O2 will increase CO2 retention
in COPD pts and cause

Back 196

suppresses hypoxic drive
Increasing CO2 will cause sedation and suppress hypercapnic drives

Front 197

Haldane Effect
in COPD

Back 197

As hemoglobin oxygen level increases the hemoglobins ability to carry CO2 will be decreased

Front 198

Asthma and venitllatory drive

Back 198

Some patients have a weakened hypoxic and hypercapnic drive.
These patients are at risk of fatal exacerbations

Front 199

Some patients have a weakened hypoxic and hypercapnic drive.
These patients are at risk of fatal exacerbations
in what pts?

Back 199

Asthma

Front 200

Nearly absent respiratory response to hypoxia and hypercapnia
Is often associated with Hirschsprung’s disease

Back 200

Congenital Central Hypoventilation Syndrome

Front 201

Hirschsprung’s disease

Back 201

Congenital Central Hypoventilation Syndrome

Front 202

What is Hirschsprung’s disease?

Back 202

Hirschsprung's disease is a blockage of the large intestine due to improper muscle movement in the bowel. It is a congenital condition, which means it is present from birth.
This is a congenital central hypoventilating syndrome

Front 203

A blockage of the large intestine due to improper muscle movement in the bowel. It is a congenital condition, which means it is present from birth

Back 203

Hirschsprung's disease

Front 204

Cheyne-Stokes Respirations (CSR)

Back 204

Graded increased cyclic breathing divided by periods of apnea
Respirations are driven by PaCO2 levels

Front 205

Graded increased cyclic breathing divided by periods of apnea
Respirations are driven by PaCO2 levels

Back 205

Cheyne-Stokes Respirations (CSR)

Front 206

Diseases or States with possible Cheyne-Stokes Respirations (CSR)

Back 206

Cardiac disease
Neurologic disease
Sedation
Acid-base disturbances
Prematurity
Altitude acclimation

Front 207

TX for Cheyne-Stokes Respirations

Back 207

Treat underlying disorders
O2
CPAP helpful
BiPAP should not be used (It can lower PaCO2 below apneic threshold)

Front 208

Those that weaken the respiratory drive are

Back 208

Myxedema
Starvation
Neuromuscular disease

Front 209

Myxedema

Back 209

bad hypothyroidsm (affect all organ systems)
weakens respiratory drive in (CSR) Cheyne-Stokes Respirations

Front 210

Medicines that alter Respiratory Drive

Back 210

Central nervous system depressants like benzodiazepines, barbiturates, and opiates can reduce the drive.
Medroxyprogesterones can increase the respiratory drive.
Acetazolamide can increase the drive
Antioxidants can increase the sensitivity of ventilatory response to the PaCO2 level

Front 211

Obstructive Sleep Apnea
Cardinal features***

Back 211

Irregular respiratory patterns, like apneas, hypopneas, and arousals
Snoring, restlessness, and snorts
Fatigue, sleepiness, or poor concentration during the day.

Front 212

Irregular respiratory patterns, like apneas, hypopneas, and arousals
Snoring, restlessness, and snorts
Fatigue, sleepiness, or poor concentration during the day.
****

Back 212

Obstructive Sleep Apnea

Front 213

Epidemiology of Obstructive Sleep Apnea

Back 213

Up to 1/4 of all patients will have sleep apnea
Usually increases in incidence in patienta 18-45 and is 2 to 3 times higher for patients over 65.
Risk greater in African Americans over caucasians that are less than 35 years of age.

Front 214

Risk Factors for Obstructive Sleep Apnea

Back 214

Obesity
Craniofacial or upper airway abnormality
Family history
Smokers
Nasal congestion

Front 215

Clinical Features of Obstructive Sleep Apnea

Back 215

Snoring and daytime sleepiness are the most common recognized features of OSA
Additional S/S; restless sleep, silence terminated by loud snoring, poor concentration, nocturnal angina, awakening with the sense of choking, gasping, or smothering

Front 216

Snoring and daytime sleepiness are the most common recognized features Additional S/S; restless sleep, silence terminated by loud snoring, poor concentration, nocturnal angina, awakening with the sense of choking, gasping, or smothering

Back 216

Obstructive Sleep Apnea

Front 217

Diagnosis of Obstructive Sleep Apnea

Back 217

Polysomnography is the first line disgnosic study.

Front 218

Polysomnography is the first line disgnosic study.

Back 218

Obstructive Sleep Apnea

Front 219

have passive or sedentary daytime sleepiness. it is often unapparent to the patient.

Back 219

Mild OSA

Front 220

patients are aware of daytime sleepiness and it often alters daily activities

Back 220

Moderate OSA

Front 221

have severe daytime symptoms that completely interferes with daily activities

Back 221

Severe OSA

Front 222

Severe OSA

Back 222

have severe daytime symptoms that completely interferes with daily activities.

Can have problems like hypertension, polycythemia, and cor pulmonale

Front 223

Moderate OSA

Back 223

patients are aware of daytime sleepiness and it often alters daily activities

Front 224

Mild OSA

Back 224

have passive or sedentary daytime sleepiness. it is often unapparent to the patient.

Front 225

Treatment OSA

Back 225

Oral appliance
CPAP
Oral surgery

Front 226

Negative Pressure Ventilation

Back 226

When the body creates a negative pressure in the chest and causes air to rush in the lungs by the difference in pressure, from high pressure to low pressure, gas exchange in the alveoli occur.

Front 227

Positive Pressure Ventilation

Back 227

The process of forcing air into the lungs. It is a completely artificial act of delivering breaths to the patient.
There is no pressure change in the thorax to increase air movement in the lungs with these artificial breaths.

Front 228

Concerns with Positive Pressure Ventilation through endotracheal intubation

Back 228

Peak Pressures:
You would like to keep these under 35 if at all possible. If they start climbing into the 40's to 50's you should consider changing to Pressure control ventilation. While there are several other manipulations that could also be tried, the implication is that the patient either has very restrictive lung disease and non-compliant lungs or a very severe obstructive lung pattern, in which case the pause pressure should be evaluated and attempts to improve bronchodilation should be increased

Front 229

the implication is that the patient either has very restrictive lung disease and non-compliant lungs or a very severe obstructive lung pattern, in which case the _______should be evaluated

Back 229

pause pressure

Front 230

Indications for mechanical ventilation

Back 230

Apnea
Acute Lung Injury/ARDS
Minute ventilation > 10 L/min
Arterial PaO2 with supplemental O2 < 55 mmHg
A-a gradient with 100% O2 > 450 mmHg
Clinical deterioration/Fatigue
Coma/GCS <8
Hypotension
PaCO2 > 50 mmHg with pH < 7.25
Neuromuscular disease

Front 231

Modes of Mechanical ventilation

Back 231

Control modes (CMV, IMV, VC, PC, PRVC)
Support modes (VS, PS, CPAP, BiPAP)
Hybrid modes; (SIMV, SIMV + PS)

Front 232

Assist control or Volume Control
Characteristics:

Back 232

preset rate and tidal volume (sometimes PIP), either on the patient's initiative or at the set interval a full mechanical breath is delivered.

Front 233

Assist control or Volume Control
Uses

Back 233

: for patients who have a very weak respiratory effort, allows synchrony with the patient but maximal support. Not a weaning mode, as at any rate they are getting complete mechanical support.

Front 234

Assist control or Volume Control
Contraindications:

Back 234

none

Front 235

Assist control or Volume Control
Advantages:

Back 235

fairly comfortable mode, providing a lot of support •

Front 236

Assist control or Volume Control
Disadvantages

Back 236

can lead to hyperventilation if not closely monitored, not able to wean in this mode.

Front 237

Pressure Control
Characteristics:

Back 237

basically IMV, where the breath is controlled by the Pmax or Swing pressure (∆P)\ and not the set tidal volume

Front 238

Pressure Control
Uses:

Back 238

in neonates, or in patients with high airway pressures(such as ARDS) to avoid barotrauma

Front 239

Pressure Control
Contraindications:

Back 239

none in particular, not a friendly mode in an awake patient

Front 240

Pressure Control
Advantages:

Back 240

Pressure limited, decreases the risk of barotrauma

Front 241

Pressure Control
Disadvantages:

Back 241

no guaranteed tidal volume

Front 242

Pressure Related Volume Control
Characteristics:

Back 242

a volume control assist control mode that adjusts the flow rate of the delivered air to deliver the set tidal volume at or below the set maximum pressure.

Front 243

Pressure Related Volume Control
Uses:

Back 243

in patients with high airway pressures, although it can be used in any patient.

Front 244

Pressure Related Volume Control
Contraindications:

Back 244

none in particular

Front 245

Pressure Related Volume Control
Advantages

Back 245

gives you a guaranteed tidal volume but minimizes barotrauma.

Front 246

Pressure Related Volume Control
Disadvantages:

Back 246

new, no particular disadvantages.

Front 247

Intermittent Mandatory Ventilation (IMV)
Characteristics

Back 247

set breath delivered at a fixed interval. No patient interaction, pressure or volume modes

Front 248

Intermittent Mandatory Ventilation (IMV)
Uses:

Back 248

commonly in neonates on the Sechrist, can be a weaning mode.

Front 249

Intermittent Mandatory Ventilation (IMV)
Contraindications:

Back 249

none really, unfriendly to older patients.

Front 250

Intermittent Mandatory Ventilation (IMV)
Advantages:

Back 250

regular guaranteed breath.

Front 251

Intermittent Mandatory Ventilation (IMV)
Disadvantages:

Back 251

does not allow patient to breath with the ventilator except by chance. Does not work with the patient

Front 252

Synchronous IMV (SIMV)
Characteristics

Back 252

: set breath delivered within an interval based on the set respiratory rate. Ventilator spends part of the interval waiting for spontaneous breath from the patient, which it will use as a trigger to deliver a full breath. If not sensed it will automatically give a breath at the end of the period. Any other breaths during the cycle are not supplemented.

Front 253

Synchronous IMV (SIMV)
Uses

Back 253

commonly used in many settings. Can be a weaning mode (see also with PS).

Front 254

Synchronous IMV (SIMV)
Contraindications:

Back 254

none in particular.

Front 255

Synchronous IMV (SIMV)
Advantages:

Back 255

allows work with the patient, somewhat friendlier.

Front 256

Set breath delivered within an interval based on the set respiratory rate. Ventilator spends part of the interval waiting for spontaneous breath from the patient, which it will use as a trigger to deliver a full breath. If not sensed it will automatically give a breath at the end of the period. Any other breaths during the cycle are not supplemented.

Back 256

Synchronous IMV (SIMV)

Front 257

Synchronous IMV (SIMV)
Disadvantages:

Back 257

Any other breaths during the cycle are not supplemented

Front 258

set breath delivered at a fixed interval. No patient interaction, pressure or volume modes

Back 258

Intermittent Mandatory Ventilation (IMV)

Front 259

a volume control assist control mode that adjusts the flow rate of the delivered air to deliver the set tidal volume at or below the set maximum pressure.

Back 259

Pressure Related Volume Control

Front 260

where the breath is controlled by the Pmax or Swing pressure (∆P)\ and not the set tidal volume

Back 260

Pressure Control

Front 261

preset rate and tidal volume (sometimes PIP), either on the patient's initiative or at the set interval a full mechanical breath is delivered.

Back 261

Assist control or Volume Control

Front 262

Synchronous IMV + Pressure Support (SIMV + PS)
Characteristics:

Back 262

combination of the previous two modes. Extra breaths in the cycle are supplemented with pressure support.

Front 263

combination of two modes. Extra breaths in the cycle are supplemented with pressure support.

Back 263

Synchronous IMV + Pressure Support (SIMV + PS)

Front 264

Synchronous IMV + Pressure Support (SIMV + PS)
Uses

Back 264

useful in most circumstances, including weaning

Front 265

Synchronous IMV + Pressure Support (SIMV + PS)
Contraindications:

Back 265

none in particular.

Front 266

Synchronous IMV + Pressure Support (SIMV + PS)
Advantages:

Back 266

allows both synchrony with the patient and help in overcoming the resistance in the endotracheal tube, to allow easier spontaneous breathing

Front 267

Synchronous IMV + Pressure Support (SIMV + PS)
Disadvantages:

Back 267

none in particular. PS does not add anything in the patient who is not spontaneously breathing. Sometimes patients will have difficulty with the pressure support on some ventilators.

Front 268

Pressure Support
Uses

Back 268

In the spontaneously breathing patient this helps overcome the airway resistance of the endotracheal tube. Usually use 5 for older patients and 10 for smaller (smaller ETT has higher resistance, more impediment to flow). Can be very helpful for weaning.

Front 269

Pressure Support
Characteristics:

Back 269

supports each spontaneous breath with supplemental flow to achieve a preset pressure. Gives a little push to get the air in, so to speak.

Front 270

supports each spontaneous breath with supplemental flow to achieve a preset pressure. Gives a little push to get the air in, so to speak.

Back 270

Pressure Support

Front 271

Pressure Support
Contraindications:

Back 271

patient who is not spontaneously breathing, i.e. on muscle relaxants

Front 272

Pressure Support
Advantages:

Back 272

helps overcome resistance of tube, making spontaneous breathing easier

Front 273

Volume Support
Characteristics:

Back 273

variable level of pressure support is delivered on each breath in order to maintain a minimum set goal minute ventilation. Note: because the goal the ventilator works from is a minute ventilation goal the patient's respiratory rate can fall below the 'set' rate as long as their breaths are large enough to maintain the goal minute ventilation

Front 274

variable level of pressure support is delivered on each breath in order to maintain a minimum set goal minute ventilation. Note: because the goal the ventilator works from is a minute ventilation goal the patient's respiratory rate can fall below the 'set' rate as long as their breaths are large enough to maintain the goal minute ventilation

Back 274

Volume Support

Front 275

Volume Support
Uses

Back 275

a weaning mode. The concept is that as the patient becomes stronger, or more awake they will make more respiratory effort on their own. The more effort they make the less support they will need from the ventilator and hence the level of pressure delivered will get smaller, often into the single digits

Front 276

Volume Support
Contraindications

Back 276

patient who is not spontaneously breathing, as there is no back-up rate

Front 277

Volume Support
Advantages:

Back 277

greatly decreases the number of interventions needed to wean patient from a ventilator versus traditional weaning

Front 278

Volume Support
Disadvantages:

Back 278

can be tricky on chronically ventilated patients. Takes some experience to understand when a patient is ready to be extubated when in this mode

Front 279

Continuous Positive Airway Pressure (CPAP)
Characteristics:

Back 279

: just as it says. This is very similar to PEEP, except that the inspiratory pressure is also maintained at the CPAP level, leading to support on inspiration and resistance on exhalation.

Front 280

Continuous Positive Airway Pressure (CPAP)
Uses:

Back 280

for patients with upper airway soft tissue obstruction or tendency for airway collapse. As a final mode prior to extubation in some patients

Front 281

Continuous Positive Airway Pressure (CPAP)
Contraindications:

Back 281

any patient without spontaneous respiratory effort. Not a good idea in a patient with obstructive pulmonary disease (like asthma, COPD)

Front 282

Continuous Positive Airway Pressure (CPAP)
Advantages

Back 282

simple, easy to use

Front 283

This is very similar to PEEP, except that the inspiratory pressure is also maintained at the level, leading to support on inspiration and resistance on exhalation.

Back 283

Continuous Positive Airway Pressure (CPAP)

Front 284

Continuous Positive Airway Pressure (CPAP)
Disadvantages

Back 284

provides no supportive ventilation.

Front 285

Settings for mechnical ventilation

Back 285

Rate-10
Tidal Volume-10
FiO2-100
Peak Inspiratory Pressure (PIP)

Front 286

Rate of mechnical ventilation

Back 286

Respiratory rates are usually 8-14 b/min
High rates are usually avoided because they may
Increase mean airway pressure
Allow less time for exhalation
Could cause breath stacking, by not giving the patient time to completely exhale the inspired tidal volume

Front 287

Tidal Volume of mechnical ventilation

Back 287

Due to the risk of barotrauma and volutrauma, lower tidal volumes are recommended.
Initial volumes of 5-10 ml/kg
With pulmonary diseases like COPD, or ARDS a lower initial setting would be appropriate.
Initial volumes of 5-8 ml/kg

Front 288

Fraction of Inspired Oxygen (FiO2)

Back 288

FIO2 is expressed in percentages.
Room air is 21%, and the addition of supplemental oxygen will increase this percentage all the way to 100% or pure oxygen only.
Keeping the FiO2 above 60% for long periods of time can cause oxygen toxicity.
Oxygen toxicity is the result of a supersaturation of oxygen causing an increase in free radicals that cause cellular injury.

Front 289

Peak Inspiratory Pressures

Back 289

Peak Inspiratory pressures need to be below 40 cm H2O
There is chance of barotrauma above 40 cm H2O

Front 290

Other mechanical ventillation Settings

Back 290

Positive End Expiratory Pressure(PEEP)
Inspiratory Time
I:E Ratio
Trigger sensitivity

Front 291

(PEEP) Positive End Expiratory Pressure

Back 291

A setting that maintains some pressure in the airway after expiration
Increases gas exchange by increasing usable surface volume.
Indications;
ARDS
Pneumonia
Pulmonary edema
Atelectasis

Front 292

A setting that maintains some pressure in the airway after expiration
Increases gas exchange by increasing usable surface volume.

Back 292

(PEEP) Positive End Expiratory Pressure

Front 293

(PEEP) Positive End Expiratory Pressure
indications

Back 293

Indications;
ARDS
Pneumonia
Pulmonary edema
Atelectasis

Front 294

Inspiratory Time in mechanical ventilation

Back 294

The time over which the volume is delivered or the pressure is supported
Settings can vary, but average Inspiratory times range from 1.5-2 sec.

Front 295

I:E ratio in mechanical ventilation

Back 295

Inspiratory to expiratory ratio
Some vent settings adjust Inspiratory to Expiratory ratio (I:E) and these also can vary from 1:1 to 1:5 in conventional ratios, or they can be reversed in inverse ratios (5:1, 3:1)

Front 296

Flow Pattern in mechanical ventilation

Back 296

Often called rise time the setting looks at how the volume of air is delivered.
Constant;
Decelerating;
Sinusoidal;

Front 297

Trigger Sensitivity in mechanical ventilation

Back 297

The measure of the trigger of patient activity (inspiratory effort) when the ventilator will deliver a breath.
There are two types;
Flow; as patient pulls air the change in flow is detected. when the flow is above the variable setting
Pressure; detects a pressure change and delivers a breath when the pressure change is above the variable setting
The smaller the value of the above settings the more sensitive the trigger

Front 298

Improving CO2 Elimination in mechanical ventilation*****

Back 298

Because CO2 rapidly diffuses across the alveolar space, the more air you can move into and out of the lungs the more rapidly the CO2 can be removed
The greatest determinant of CO2 elimination is minute ventilation (VE):
VE = Tidal volume (Vt) x Resp.rate (R)

Front 299

Improving Oxygenation in mechanical ventilation*******
The greatest determinants of O2:

Back 299

The greatest determinants of O2:
The inspired fraction of oxygen (FIO2)
Positive end expiratory pressure (PEEP)
I:E ratio

Front 300

Complications of mechanical ventilation

Back 300

Barotrauma
Breath stacking
Volutrauma
Ventilator associated pneumonia
Oxygen toxicity

Front 301

Barotrauma

Back 301

Barotrauma: not only due to high pressures, but also due to high volumes and shear injury (due to repetitive collapse and re-expansion of alveoli and due to tension at the interface between open and collapsed alveoli
pneumothorax
pneumomediastinum
pneumopericardium
surgical emphysema
acute lung injury

Front 302

not only due to high pressures, but also due to high volumes and shear injury (due to repetitive collapse and re-expansion of alveoli and due to tension at the interface between open and collapsed alveoli

Back 302

Barotrauma in mechanicla ventilations

Front 303

Gas trapping in mechanical ventilation

Back 303

Gas trapping often called breath stacking: occurs if there is insufficient time for alveoli to empty before the next breath. More likely to occur:
in patients with asthma or COPD
when inspiratory time is long (and therefore expiratory time short)
when respiratory rate is high (absolute expiratory time is short)

Front 304

often called breath stacking: occurs if there is insufficient time for alveoli to empty before the next breath.

Back 304

Gas trapping

Front 305

Gas trapping likely to occur :

Back 305

in patients with asthma or COPD
when inspiratory time is long (and therefore expiratory time short)
when respiratory rate is high (absolute expiratory time is short)

Front 306

Croup

Back 306

A inflammation of the larynx and subglottic airway.
Patients present with inspiratory stridor, cough, and hoarseness.
Infants and young children; a barking cough is more common.
Older children and Adults; hoarseness predominates
The most common cause is viruses

Front 307

A inflammation of the larynx and subglottic airway.

Back 307

Croup

Front 308

Patients present with inspiratory stridor, cough, and hoarseness.
Infants and young children; a barking cough is more common.

Back 308

Croup

Front 309

MC cause of Croup & others causes

Back 309

is viruses
Parainfluenza type 1
Parainfluenza type 2
Parainfluenza type 3
RSV
Adenoviruses
Human coronavirus NL63
Measles
Rhinoviruses
Metapneumoviruses

Front 310

is inflammation of the larynx and the primary manifestation is hoarseness.

Back 310

Laryngitis

Front 311

is inflammation of the larynx and trachea. Typical barking cough.

Back 311

Laryngotracheitis (croup) is

Front 312

when the inflammation moves down into the bronchi. You may appreciate Wheezing, rhonchi, or rales on exam.

Back 312

Laryngotracheobronchitis

Front 313

Laryngotracheobronchitis (LTB)

Back 313

Laryngotracheobronchitis (LTB) when the inflammation moves down into the bronchi. You may appreciate Wheezing, rhonchi, or rales on exam.

Front 314

when the inflammation moves down into the bronchi. You may appreciate Wheezing, rhonchi, or rales on exam. The infection can move further and cause a pneumonia and be called a

Back 314

laryngotracheobronchopneumonitis.

Front 315

laryngotracheobronchopneumonitis.

Back 315

when the inflammation moves down into the bronchi. You may appreciate Wheezing, rhonchi, or rales on exam. The infection can move further and cause a pneumonia

Front 316

is when there are sudden episodes of stridor that occur at night and then suddenly stop.

Back 316

Spasmodic croup

It is sometimes called allergic croup.

Front 317

It is sometimes called allergic croup.

Back 317

Spasmodic croup is when there are sudden episodes of stridor that occur at night and then suddenly stop. It is sometimes called allergic croup.

Front 318

Laryngomalacia

Back 318

Malacia- softening, floppiness;
Laryngomalacia is just that…of the epiglottis, arytenoid cartilages (larynx) + redundant tissue

Stridor- sound produced by turbulent flow of air through the upper resp tract.
*”Noisy breathing”
“Always Congested”

Front 319

softening, floppiness of the epiglottis, arytenoid cartilages (larynx) + redundant tissue
and sound produced by turbulent flow of air through the upper resp tract.
*”Noisy breathing”
“Always Congested”

Back 319

Laryngomalacia

Front 320

sound produced by turbulent flow of air through the upper resp tract.
*”Noisy breathing”
“Always Congested”

Back 320

Stridor

Front 321

Stridor

Back 321

sound produced by turbulent flow of air through the upper resp tract.
*”Noisy breathing”
“Always Congested”

Front 322

is just that…of the epiglottis, arytenoid cartilages (larynx) + redundant tissue

Back 322

Laryngomalacia

Front 323

Malacia

Back 323

softening, floppiness;

Front 324

softening, floppiness;

Back 324

Malacia

Front 325

MC cauuse of LARYNGOMALACIA

Back 325

The MOST common cause of noisy breathing in infants and children (up to 85% of stridor- varies)

Front 326

The most common congenital abnormality of the larynx

Back 326

LARYNGOMALACIA

Front 327

Symptoms can be ABSENT at birth and progress in days to weeks after– worsen in first 2-3 months
MOST resolve in 12-18 months of age, some until 3-4 years old

Back 327

LARYNGOMALACIA

Front 328

GERD HYPOTHESIS

Back 328

Studies have found that there is an association between GERD and laryngomalacia.
There are many that believe that there is more GERD in lga, (chicken/egg?)
Bottom line is, that even if it doesn’t cause it there is an exacerbation/inflammation to the floppy tissues that occurs. (video)
Some recommend pH probe in workup

Front 329

Stridor/ noisy breathing worse in SUPINE position, better in prone in sniffing
Worse when crying or agitated
Normal voice or hoarse voice
Louder on INSPthe harder they suck in, the louder the noise (airways collapse/prolapse and obstruction)

Back 329

LARYNGOMALACIA

Front 330

Diagnosis/Evaluation
of LARYNGOMALACIA

Back 330

XR’s (A/P and lateral) can suggest the diagnosis
Can identify other stuff--epiglottitis, tracheitis, subglottic stenosis
Mainstay of diagnosis is flexible nasopharyngoscopy
What we do… best performed in an unaesthetized child in upright position—keepem breathing!
Scope passed through nasal passage
Classically, you have a collapse on supraglottic larynx on inspiration
Look at cords to make sure they are mobile

Front 331

LARYNGOMALACIA
CONTRIBUTING FACTORS

Back 331

Multiple factor are likely

1. ANATOMIC
- shortening of the aryepiglottic folds, anterior prolapse of cuneiform cartilages
2. NEUROLOGIC
-immature neurological control
3. INFLAMMATORY
- Known association GERD

Front 332

Bronchiolitis

Back 332

A lower respiratory tract infection of the bronchioles (small airways)

Front 333

A lower respiratory tract infection of the bronchioles (small airways)
Patients present with wheezing and airway obstruction.
Nasal congestion and/or discharge
Mild cough
Fever
Cough
Possible respiratory distress
Nasal flaring
Retractions
Grunting

Back 333

Bronchiolitis

Front 334

A lower respiratory tract infection of the bronchioles (small airways)

Back 334

Bronchiolitis

Front 335

Patients present with wheezing and airway obstruction.
Nasal congestion and/or discharge
Mild cough
Fever
Cough
Possible respiratory distress
Nasal flaring
Retractions
Grunting

Back 335

Bronchiolitis

Front 336

Risk Factors for Bronchiolitis

Back 336

Prematurity (gestational age <37 weeks)
Low birth weight
Age less than 6 to 12 weeks
Chronic pulmonary disease (bronchopulmonary dysplasia, cystic fibrosis, congenital anomaly)
Hemodynamically significant congenital heart disease (eg, moderate to severe pulmonary hypertension, cyanotic heart disease, or congenital heart disease that requires medication to control heart failure)
Immunodeficiency
Neurologic disease
Congenital or anatomical defects of the airways

Front 337

Environmental Risk Factors for Bronchiolitis

Back 337

Having older siblings
Concurrent birth siblings
Native American heritage
Passive smoke
Household crowding
Child care attendance
High altitude

Front 338

Causes of Bronchiolitis

Back 338

RSV *
Rhinovirus
Parainfluenza
Human metapneumovirus
Influenza
Coronavirus
Human bocavirus
Human polyomaviruses

Front 339

Congenital Lobar Emphysema

Back 339

Marked hyperinflation of a lobe of the lung, usually an upper lobe.
Compression of remaining normal lung.
Symptoms present in the newborn period.
Etiology: Segmental bronchomalacia.
Floppy cartilage collapses airway during exhalation with resulting hyperinflation-
Ball/valve effect
Airway growth gradually improves airway obstruction and hyperinflation

Front 340

Marked hyperinflation of a lobe of the lung, usually an upper lobe.
Compression of remaining normal lung.
Symptoms present in the newborn period.
Etiology: Segmental bronchomalacia.
Floppy cartilage collapses airway during exhalation with resulting hyperinflation-
Ball/valve effect
Airway growth gradually improves airway obstruction and hyperinflation

Back 340

Congenital Lobar Emphysema

Front 341

Pulmonary Sequestrations

Back 341

“Pulmonary sequestration is a cystic or solid mass composed of nonfunctioning primitive tissue that does not communicate with the tracheobronchial tree and has anomalous systemic blood supply. It is a type of congenital thoracic malformation. It may present as a lung infection on physical examination and chest imaging. Its blood supply is from systemic circulation rather than the pulmonary circulation.”
A mass of pulmonary tissue that:
Lacks normal connection to the tracheobronchial tree.
Has an anomalous vascular supply.
May be intralobar or extralobar.
Most occur on the left.
Treatment is surgical resection.
Identify vascular supply prior to surgery.

Front 342

cystic or solid mass composed of nonfunctioning primitive tissue that does not communicate with the tracheobronchial tree and has anomalous systemic blood supply. It is a type of congenital thoracic malformation. It may present as a lung infection on physical examination and chest imaging. Its blood supply is from systemic circulation rather than the pulmonary circulation.”

Back 342

Pulmonary Sequestrations

Front 343

A mass of pulmonary tissue that:
Lacks normal connection to the tracheobronchial tree.
Has an anomalous vascular supply.
May be intralobar or extralobar.
Most occur on the left.
Treatment is surgical resection.
Identify vascular supply prior to surgery.

Back 343

Pulmonary Sequestrations

Front 344

Pulmonary Hypoplasia

Back 344

Primary pulmonary hypoplasia is rare, and the cause is unknown.
Pulmonary hypoplasia is usually secondary to events occurring during gestation which restrict lung growth and development.
Degree of hypoplasia is related to the duration of the insult, timing, and presence and/or severity of other anatomic abnormalities.

Front 345

Degree of hypoplasia is related to the___

Back 345

duration of the insult, timing, and presence and/or severity of other anatomic abnormalities.

Front 346

Pulmonary hypoplasia is usually secondary to events occurring during____

Back 346

gestation which restrict lung growth and development.

Front 347

In Pulmonary Hypoplasia
Restriction of Fetal Thoracic Volume by

Back 347

Congenital diaphragmatic hernia.
Pleural effusions with fetal hydrops.
Restrictive chest wall defects (skeletal dysplasias).
Abdominal masses.
Giant omphalocele.
Prune Belly syndrome.

Front 348

Oligohydramnios

Back 348

In Pulmonary Hypoplasia
Fetal Compression Syndrome).
Conditions reducing amniotic fluid production.
Renal agenesis (Potter’s syndrome).
Urinary tract obstruction.
Chronic amniotic fluid leakage.
Prolonged premature rupture of membranes.

Front 349

Decreased Fetal Breathing.
In Pulmonary Hypoplasia

Back 349

Inadequate flow of lung fluid due to decreased or altered breathing may affect lung growth.
Brainstem malformations.
Cervical spinal cord malformations.
Phrenic nerve damage.
Neuromuscular disorders.

Front 350

Congenital Diaphragmatic Hernia

Back 350

Neonatal respiratory distress, decreased breath sounds, and scaphoid abdomen.
Pulmonary hypoplasia and pulmonary hypertension can be life-threatening.
Chronic lung disease common in survivors.
Bochdalek hernia: left posterior.
Hernia of Morgagni: anterior, less severe.

Front 351

Neonatal respiratory distress, decreased breath sounds, and scaphoid abdomen.
Pulmonary hypoplasia and pulmonary hypertension can be life-threatening.
Chronic lung disease common in survivors.

Back 351

Congenital Diaphragmatic Hernia

Front 352

Bochdalek hernia:

Back 352

left posterior in Congenital Diaphragmatic Hernia

Front 353

Hernia of Morgagni:

Back 353

anterior, less severe.
in Congenital Diaphragmatic Hernia

Front 354

Hydrocarbon Pneumonitis

Back 354

Most serious complication of petroleum product ingestion is pneumonia.
Most cases occur in children <2-years of age.
Causes lung disease by aspiration.
Hydrocarbons affect surfactant function, so restrictive disease results.
If death occurs, nearly always from pneumonia.
Long-term airway hyperreactivity.

Front 355

What is life-threatening in pt w Congenital Diaphragmatic Hernia?

Back 355

Pulmonary hypoplasia and pulmonary hypertension can be life-threatening.

Front 356

Interstitial Pneumonitis

Back 356

Final common pathway for many types of lung injury.
Shortness of breath, tachypnea, hypoxia, activity limitation, digital clubbing and growth failure.
Fine crackles, occasionally wheezing.
Chest X-ray: Fine reticular pattern.
-FLU! Random Viruses? Mycoplasma? Genetic Predisposotion?

Front 357

Final common pathway for many types of lung injury.
Shortness of breath, tachypnea, hypoxia, activity limitation, digital clubbing and growth failure.
Fine crackles, occasionally wheezing.
Chest X-ray: Fine reticular pattern.
-FLU! Random Viruses? Mycoplasma? Genetic Predisposotion?

Back 357

Interstitial Pneumonitis

Front 358

Shortness of breath, tachypnea, hypoxia, activity limitation, digital clubbing and growth failure.

Back 358

Interstitial Pneumonitis

Front 359

Diagnostic Evaluation.
of Interstitial Pneumonitis

Back 359

High-resolution thin-cut CT of the lungs.
Bronchoalveolar lavage.
Open lung biopsy.

Front 360

Interstitial Pneumonitis TX

Back 360

Depends on etiology.
High dose corticosteroids.
Other immunosuppressant medications.

Front 361

Pulmonary Hemorrhage and Hemoptysis

Back 361

Bleeding in the conducting airways is rare in children.
May be focal or diffuse.
Most common cause is bronchiectasis:
Cystic Fibrosis.
Retained foreign body.
Lung Abscess.
Tuberculosis.
UPPER AIRWAY!

Front 362

In Pulmonary Hemorrhage and Hemoptysis the most common cause is bronchiectasis which lead to what other disorders?

Back 362

Cystic Fibrosis.
Retained foreign body.
Lung Abscess.
Tuberculosis.
UPPER AIRWAY!

Front 363

Bleeding in the conducting airways is rare in children.
May be focal or diffuse.

Back 363

Pulmonary Hemorrhage and Hemoptysis

Front 364

Goodpasture’s Syndrome

Back 364

Diffuse alveolar hemorrhage associated with glomerulonephritis.
Usually both pulmonary and renal symptoms present, but may present with isolated lung or kidney signs.
Diagnosis: elevated circulating anti-glomerular basement antibody (anti-GBM).
Outcome depends primarily on renal disease.

Front 365

Diffuse alveolar hemorrhage associated with glomerulonephritis.
Usually both pulmonary and renal symptoms present, but may present with isolated lung or kidney signs.
Diagnosis: elevated circulating anti-glomerular basement antibody (anti-GBM).
Outcome depends primarily on renal disease.

Back 365

Goodpasture’s Syndrome

Front 366

Bronchopulmonary Dysplasia(BPD)*Chronic Lung Disease of Infancy (CLDi)****

Back 366

Chronic lung disease sequelae of neonatal lung injury.
Classically in preterm infants with RDS treated with supplemental oxygen and assisted ventilation.
Suspect BPD in any infant born prematurely or with neonatal lung injury.
Decreased pulmonary reserve: may be asymptomatic when well, but deteriorate with respiratory infections.
May see spongelike appearnance on CXR.

Front 367

Chronic lung disease sequelae of neonatal lung injury.
Classically in preterm infants with RDS treated with supplemental oxygen and assisted ventilation.

Back 367

Bronchopulmonary Dysplasia(BPD)*Chronic Lung Disease of Infancy (CLDi)

Front 368

May see spongelike appearnance on CXR.

Back 368

Bronchopulmonary Dysplasia(BPD)*Chronic Lung Disease of Infancy (CLDi)

Front 369

Treatment ofBronchopulmonary Dysplasia

Back 369

Aerosolized B2 Agonists.
Aerosolized cromolyn or corticosteroids (budesonide) are sometimes used, but efficacy not proven, but clinically they do!
Supplemental oxygen to maintain Spo2 >95%.
Diuretics with potassium sparing diuretic (spironolactone) or KCl supplementation.

Front 370

Bronchopulmonary Dysplasia Improvement depends on

Back 370

initial lung injury, prematurity, and avoiding pneumonias.

Front 371

Long-term sequelae of Bronchopulmonary Dysplasia

Back 371

airway obstruction and hypereactivity.

Front 372

RSV Prophylaxis

Back 372

Palivizumab (Synagis).
Monoclonal antibody against RSV, given IM.
Given monthly from November-April.

Front 373

Palivizumab (Synagis).

Back 373

Monoclonal antibody against RSV, given IM.
Given monthly from November-April.
RSV Prophylaxis

Front 374

Viral croup fails to resolve: high fever, toxicity, stridor, barking cough, retractions, leukocytosis.
***

Back 374

Bacterial Tracheitis****

Front 375

Potentially serious disorder due to severe airway obstruction.
Complication or superinfection of viral respiratory infection.

Back 375

Bacterial Tracheitis****

Front 376

Bacterial Tracheitis**** caused by what bug?

Back 376

Staphylococcus aureus.

Front 377

Bacterial Tracheitis****
Most common under ___-years of age.

Back 377

4

Front 378

Bacterial Tracheitis**
complication of

Back 378

Boop/COp

Front 379

Potentially serious disorder due to severe airway obstruction.
Complication or superinfection of viral respiratory infection.
Staphylococcus aureus.
Most common under 4-years of age.
Viral croup fails to resolve: high fever, toxicity, stridor, barking cough, retractions, leukocytosis
Bacterial disease is rapidly progressive.
Tracheal secretions are copious.
Necrotic tissue forms pseudomembranes, which worsen airway obstruction.
Most common complication is pneumonia.
Treatment: Intubation, mechanical assisted ventilation, and antibiotics.

Back 379

Bacterial Tracheitis**

Front 380

MC complication w Bacterial Tracheitis**

Back 380

pneumonia.

Front 381

Dilated and inflamed subsegmental airways.
May be localized or diffuse.
Airways are torturous, floppy, and partially obstructed with mucopurulent secretions.

Back 381

Bronchiectasis

Front 382

Focal Bronchiectasis cause and Tx

Back 382

Most common cause of focal bronchiectasis in children is a retained foreign body.
Foreign body interferes with normal mucociliary clearance, causing suppuration.
Over time, subsequent inflammation and destruction lead to bronchiectasis.
Treatment: antibiotics, chest physiotherapy, bronchodilators, and rarely lung resection.

Front 383

Foreign body interferes with normal mucociliary clearance, causing suppuration.
Over time, subsequent inflammation and destruction lead to bronchiectasis.

Back 383

Focal Bronchiectasis

Front 384

Most common cause of focal bronchiectasis

Back 384

in children is a retained foreign body.

Front 385

TX of Focal Bronchiectasis

Back 385

Treatment: antibiotics, chest physiotherapy, bronchodilators, and rarely lung resection.

Front 386

Diffuse Bronchiectasis causes

Back 386

TB
adenovirus, Influenze, Measules
pmeumo
CF
Immune def
PCK (primary ciliary dyskinesia

Front 387

Alpha-1-Anti-Trypsin Disease

Back 387

Autosomal recessive disorder.
Emphysema and liver disease.
Due to absence of protease inhibitor.
Emphysema rare before age 20-years.
Liver disease precedes lung disease.
Rarely a cause of chronic lung disease in children.
Much worse in SMOKERS!

Front 388

Repetitive episodes of complete inspiratory upper airway (extrathoracic) obstruction during sleep.

Back 388

Obstructive Sleep Apnea Syndrome

Front 389

Repetitive or persistent partial upper airway obstruction without apnea may result in ____.

Back 389

hypoxia and hypercapnia during sleep

Front 390

The most important cause of OSAS is a

Back 390

small upper airway.

Front 391

OSAS in infants almost always due to

Back 391

craniofacial anomalies

Front 392

OSAS Common in children ____ years due to adenotonsillar hypertrophy.

Back 392

age 2-6

Front 393

OSAS in Infants

Back 393

Infants with OSAS usually have some congenital anomaly of the upper airway.
Choanal atresia or stenosis.
Mid-face hypoplasia.
Microagnathia.
Pierre Robin syndrome.
Down syndrome.
Cleft palate.

Front 394

Snoring.
Agitated Arousals.
Respiratory distress during sleep.
History of obstructive apneas during sleep.
Unusual sleep postures.
Enuresis.

Back 394

Symptoms of OSAS

Front 395

Symptoms of OSAS

Back 395

Snoring.
Agitated Arousals.
Respiratory distress during sleep.
History of obstructive apneas during sleep.
Unusual sleep postures.
Enuresis.

Front 396

Repetitive episodes of complete inspiratory upper airway (extrathoracic) obstruction .Cessation of airflow at the nose and moth with continued respiratory effort.
Repetitive or persistent partial upper airway obstruction without apnea may result in hypoxia and hypercapnia during sleep.
Sleep relaxes upper airway skeletal muscle tone.
The most important cause is a small upper airway.
Common in children age 2-6 years due to adenotonsillar hypertrophy.
Almost always due to craniofacial anomalies in infants.

Back 396

OSAS

Front 397

Treatment of OSAS

Back 397

Adenotonsillectomy.
Nasal CPAP or BiPAP.
Positioning.
Supplemental oxygen.
Uvulopalatopharyngoplasty (UPPP).
Tracheostomy.

Front 398

Adenotonsillectomy is a TX for

Back 398

OSAS in children
Improves OSAS by increasing airway caliber.
Even normal sized tonsils and adenoids may cause disproportionate obstruction in a small upper airway.
May be useful in obesity and craniofacial anomalies.

Front 399

Positive Airway Pressure

Back 399

CPAP supplies a steady air pressure providing a pneumatic splint to hold open the airway.
B-PAP allows for separate inspiratory and expiratory pressures, may increase patient comfort.

Front 400

CPAP

Back 400

PAP
supplies a steady air pressure providing a pneumatic splint to hold open the airway.

Front 401

B-PAP

Back 401

+ airway P (PAP)
allows for separate inspiratory and expiratory pressures, may increase patient comfort.

Front 402

5-10% Weight Loss can improve what?

Back 402

severity of OSAS

Front 403

Sudden Infant Death Syndrome

Back 403

Most common cause of infant death between the ages of 1-month and 1-year.
Cause remains unknown.
Can not be predicted in infants prior to death.
Reduction in SIDS possible for populations.
Individual SIDS deaths can not be prevented.

Supine sleeping is better

Front 404

A higher incidence of SIDS is observed in infants who sleep _____

Back 404

Prone

Front 405

Prone Sleeping and SIDS

Back 405

A higher incidence of SIDS is observed in infants who sleep prone.
Mechanism unknown.
SIDS rates have decreased by over half in countries who reduce prone sleeping in infants.
Little or no risk to supine sleeping.
Healthy infants should sleep on their backs.

Front 406

"Back to Sleep"

Back 406

A higher incidence of SIDS is observed in infants who sleep prone.
Mechanism unknown.
SIDS rates have decreased by over half in countries who reduce prone sleeping in infants.
Little or no risk to supine sleeping.
Healthy infants should sleep on their backs.

Front 407

Causes of Pulmonary edema

Back 407

ARDS
High altitude
Neurogenic edema
Narcotic overdose
Pulmonary embolism
eclampsia

Front 408

How to discern from CHF from PE

Back 408

Pulmonary artery catheter (Swan-Ganz) catheter
Acute lung injury of wedge pressure is less than 18
BNP

Front 409

Things that mimic pulmonary edema

Back 409

Diffuse alveolar hemorrhage
Cancer disseminating throughout body
Lymphomas
Acute leukemia
Lymphangitic spread of solid tumors

Front 410

Re-perfusion & Re-expansion pulmonary edema

Back 410

After removal of thromboembolic obstructions
After re-expansion of a collapsed lung in a pneumothorax or removal of obstructing endobronchial tumor
Typically immediately after, but can be up to 24 hours after

Front 411

Opiate overdose in P embolism

Back 411

Can occur in heroin and methadone overdose
Cause is unknown

Front 412

Salicylate Toxicity

Back 412

Salicylate toxicity with pulmonary edema is an absolute indication for hemodialysis.

Front 413

Acute Respiratory Distress Syndrome (ARDS)

Back 413

Pulmonary edema secondary to non-cardiac causes.
There are two very similar entities often confused as the same thing.
Acute lung injury (ALI) is very similar with only minimal differences

Front 414

ARDS vs ALI

Back 414

Both have three characteristics in common
Acute Onset
Bilateral infiltrates
No evidence of elevated left atrial pressure (<18 mmHg)
The difference is in the final category
PaO2/FiO2 of 201 to 300 mmHg = ALI
PaO2/FiO2 < 200 mmHg = ARDS

Front 415

ARDS presentation

Back 415

Presentation
Dyspnea, tachypnea, hypoxemia
Physical exam
Tachycardia, cyanosis, tachycardia, & diffuse rales
ABG
Acute Respiratory Alkalosis, hypoxemia, & elevated A-a gradient

Front 416

Presentation
Dyspnea, tachypnea, hypoxemia
Physical exam
Tachycardia, cyanosis, tachycardia, & diffuse rales
ABG
Acute Respiratory Alkalosis, hypoxemia, & elevated A-a gradient

Back 416

ARDS

Front 417

Pulmonary Embolism

Back 417

An obstruction of the pulmonary artery or one of its terminal branches that originated elsewhere in the body.
Massive PE Bp < 90 mmHg, or drop in Bp of > 40 mmHg from baseline for greater than 15 minutes
Death usually occurs in 1 to 2 hours of the event
Saddle PE is a PE that lodges at the bifurcation of the right and left pulmonary arteries

Front 418

Saddle P Embolism

Back 418

is a PE that lodges at the bifurcation of the right and left pulmonary arteries

Front 419

Pulmonary Embolism Symptoms

Back 419

Dyspnea at rest or with exertion (73%)
Pleuritic pain (44%)
Cough (34%)
> 2 pillow orthopnea (28%)
Calf and thigh pain (44%)
Calf and thigh swelling (41%)
Wheezing (21%)
Onset with in seconds (44%)
Onset with in minutes (26%)

Front 420

Pulmonary Embolism Signs

Back 420

Tachypnea (54%)
Tachycardia (24%)
Rales (18%)
Decreased breath sounds (17%)
Accentuated pulmonic component of 2 heart sound (15%)
JVD (14%)

Front 421

Tachypnea (54%)
Tachycardia (24%)
Rales (18%)
Decreased breath sounds (17%)
Accentuated pulmonic component of 2 heart sound (15%)
JVD (14%)

Back 421

Pulmonary Embolism Signs

Front 422

Diagnosis of PE (other)

Back 422

ABG; Respiratory Alkalosis, hypocapnia, hypoxemia
Troponin; can be elevated in 30 to 50 % of patients who have a mod to large PE
CXR; only reported normal in about 12% of cases
Atelectasis or pulmonary parenchymal abnormality noted in 58 to 69% of patients
ECHO; not real helpful
D-dimer (clot breakdown) (degradation of cross-linked fibrin)
Sensitivity from 95 to 50%
Specificity 40 to 65%
V/Q scan
Normal approx 0%
Low 4% probability
Intermediate
High 95%

Front 423

ABG; Respiratory Alkalosis, hypocapnia, hypoxemia
Troponin; can be elevated in 30 to 50 % of patients who have a mod to large disease. CXR; only reported normal in about 12% of cases
Atelectasis or pulmonary parenchymal abnormality noted in 58 to 69% of patients
ECHO; not real helpful

Back 423

Diagnosis of P Embolism (other)

Front 424

Diagnosis of P Embolism (other) on ECG

Back 424

ECG (signs that demonstrate a poor prognosis)
Atrial arrhythmias
RBBB
Inferior Q waves
Precordial T wave inversion & ST segment elevation

Front 425

Wells Criteria for PE

Back 425

Clinical feature Points
Clinical symptoms of DVT 3
Other diagnosis less likely than PE 3
Heart rate greater than 100 beats per minute 1.5
Immobilization or surgery within past 4 weeks 1.5
Previous DVT or PE 1 Hemoptysis 1 Malignancy 1

Front 426

Interpretation of Well’s criteria for PE

Back 426

Risk score interpretation (probability of PE):
>6 points: high risk (78.4%);
2 to 6 points: moderate risk (27.8%);
<2 points: low risk (3.4%)

Front 427

Well’s Criteria for DVT

Back 427

In patients with symptoms in both legs, the most symptomatic leg is used.
score 0 or less- low risk  (3% probability DVT)
score 1 or 2- moderate risk  (17% probability DVT)
score 3 or more- high risk  (75% probability DVT)

Front 428

Diagnosis of P Embolism

Back 428

Angiography considered the “gold standard”
Spiral CT; 98% of PEs diagnosed by CT-PA/CT-PE study
CT scans are helpful in diagnosing other problems that caused the symptoms

Front 429

Risk Factors of P Embolism

Back 429

Immobilization
Travel of 4 hr or more in the past month
Surgery within the last 3 months
Malignancy, especially lung cancer
Current or past history of thrombophlebitis
Trauma to the lower extremities and pelvis during the past 3 months
Smoking
Central venous instrumentation within the past 3 months
Stroke, paresis, or paralysis
Prior pulmonary embolism
Heart failure
Chronic obstructive pulmonary disease
Obesity
Varicose veins
Inflammatory bowel disease

Front 430

Hypercoaguable state

Back 430

Antithrombin III deficiency (1965)
Protein C deficiency (1981)
Protein S deficiency (1984)
Activated Protein C resistance (Factor V Leiden) (1993)
Antiphospholipid syndrome (1970s-1980s)
Prothrombin 20210 defect (1996)
Dysfibrinolysis (1990s)

Front 431

TX of Pulmonary embolism

Back 431

Coumadin, but heparin for pregnant women
Anticoagulation
Thrombolysis
IVC filters
Embolectomy

Front 432

Anticoagulation

Back 432

Acute anticoagulation is with IV or subcutaneous treatment.
Low molecular weight heparin
Unfractionated heparin
Long term treatment is with warfarin. It takes about 5 days for warfarin to get into steady state. Heparin products serve as a means to keep the blood thin until the warfarin is at steady state.

Front 433

Thrombolysis

Back 433

Destruction of an clot with a thrombolytic
Often indicated with a massive PE
most commonly used is
Recombinant tissue plasminogen activators
Alteplase (rtPA)
Reteplase
Tenecteplase
Streptokinase
Urokinase

Front 434

IVC filters

Back 434

Filters that keep clots from passing from the lower extremities to the lungs

Front 435

Indications for IVC filters

Back 435

Absolute contraindication to anticoagulation (eg, active bleeding)
Recurrent PE despite adequate anticoagulant therapy
Complication of anticoagulation (eg, severe bleeding)
Hemodynamic or respiratory compromise that is severe enough that another PE may be lethal

Front 436

Complications with IVC Filter Placement

Back 436

Complications related to the insertion process (eg, bleeding, venous thrombosis at the insertion site).
Filter misplacement.
Filter migration.
Filter erosion and perforation of the IVC wall.
IVC obstruction due to filter thrombosis.

Front 437

Embolectomy

Back 437

Removal of emboli with catheters or by surgery.
TX for P emboli

Front 438

Wegner’s Granulomatosis (WG) and Microscopic Polyangitis (MP)

Back 438

A small vessel vasculitis present in the upper airway or lower airways or both.
Can affect other parts of the body like joints, eyes, skin, and the nervous system.
Renal and pulmonary involvement is common.

Front 439

A small vessel vasculitis present in the upper airway or lower airways or both.
Can affect other parts of the body like joints, eyes, skin, and the nervous system.
Renal and pulmonary involvement is common.

Back 439

Wegner’s Granulomatosis (WG) and Microscopic Polyangitis (MP)

Front 440

Clinical Presentation of both WG and MP

Back 440

More common
Persistent rhinorrhea
Purulent/bloody nasal discharge
Oral or Nasal ulcers
Mayalgias or Sinus pain


Less Common
Horseness
Stridor
Earache
Otorrhea
Conductive and sensorineural hearing loss

Front 441

More common
Persistent rhinorrhea
Purulent/bloody nasal discharge
Oral or Nasal ulcers
Mayalgias or Sinus pain


Less Common
Horseness
Stridor
Earache
Otorrhea
Conductive and sensorineural hearing loss

Back 441

Clinical Presentation of both WG and MP

Front 442

Pulmonary Involvement

Back 442

Often just pulmonary involvement can be asymptomatic
MP pulmonary involvement can present with;
Hemoptysis
Pulmonary hemorrhage
Pleuritis

Front 443

Often just pulmonary involvement can be asymptomatic
MP pulmonary involvement can present with;
Hemoptysis
Pulmonary hemorrhage
Pleuritis

Back 443

Pulmonary Involvement

Front 444

Renal Involvement of WG and MP

Back 444

Patients can only have renal involvement
Acute renal failure
Hematuria, red cell and other casts
Proteinuria
Renal biopsy demonstrates Segmental necrotizing glomerulonephritis

Front 445

Organ Systems Involved w WG and MP

Back 445

Joints
Eyes
Skin
Breast
Heart
Liver
Thyroid
Parotid gland
Nervous system
Gastrointestinal tract
Genitourinary tract

Front 446

Clinical Criteria of WG and or MP

Back 446

Nasal or oral inlammation
Abnormal x-ray findings (nodules, cavities, and fixed infiltrates)
Abnormal urinary sediment
Granulomatous inflammation on biopsy of artery or perivascular area

Front 447

Laboratory findings of WG and or MP

Back 447

Common findings
leukocytosis
Thrombocytosis > 400,000
Elevated Erythrocyte sedimentation rate (ESR)
Elevated C-reactive protein (CRP)
A positive Antineutrophil cytoplasmic antibodies (ANCA)is found in 90 to 95 percent of active WG
There are two main types one or both can be positive in patients with WG and MP;
Cytoplasmic-ANCA (C-ANCA)
Perimuclear-ANCA (P-ANCA)

Front 448

Treatment of WG and MP

Back 448

Immunosuppression is the main mode of treatment.

Front 449

MP versus WG

Back 449

Absence of granulomatous inflammation in MP on biopsy
WG is associated with PR3-ANCA
MP is associated with MPA-ANCA
Lower rate of upper respiratory tract symptoms in MP
Lower rate of relapse in MP

Front 450

patients can develop saddle nose deformity

Back 450

WG

Front 451

Behcet Disease

Back 451

A vasculitis that has been known for a triad of
Recurrent oral aphthous ulceration
Genital ulceration
Uveitis

Front 452

A vasculitis that has been known for a triad of
Recurrent oral aphthous ulceration
Genital ulceration
Uveitis

Back 452

Behcet Disease

Front 453

Organs or systems involved w Behcet Disease

Back 453

Skin
Joints
large Vessels
Brain/Neurologic disease
Gastrointestinal
Genitourinary

Front 454

Pulmonary Manifestation of Behcet Disease

Back 454

Pulmonary manifestation of Behcet disease is rare
When pulmonary manifestation is present it can cause;
BOOP
Pulmonary vascular involvement

Front 455

Pulmonary Vascular involvement of Behcet Disease

Back 455

Pulmonary artery aneurysm
Thrombotic occlusion
Pulmonary infarction
Pulmonary hemorrhage

Front 456

Diagnosis of Behcet Disease

Back 456

Oral aphthae (3 times in 1 year), and
2 of the following
Recurrent genital aphthae
Eye lesions
Skin lesions
Positive pathergy test (2 mm or larger papule after oblique insertion of a 20 to 25 gauge needle into skin of forearm)

Front 457

Churg-Strauss Syndrome (CSS)******

Back 457

Also called allergic granulomatosis and angiitis
Characterized by three things;
Chronic rhinosinusitis
Asthma
Prominent eosinophilia

Front 458

Also called allergic granulomatosis and angiitis
Characterized by three things;
Chronic rhinosinusitis
Asthma
Prominent eosinophilia
**********

Back 458

Churg-Strauss Syndrome (CSS)

Front 459

Phases of the CSS******

Back 459

Prodromal phase occurs in 2nd to 3rd decade. Patients generally have asthma, allergic rhinitis, and atopic disease
Eosinphilic phase is when there is an elevation of peripheral eosinophils and they infiltrate diverse organs.
Vasculitic phase occurs in the 3rd to 4th decade of life and patient experience a systemic vasculitis. They may have symptoms like fever, weight loss and fatigue.

Front 460

Upper airway involvement w Churg-Strauss Syndrome (CSS)******

Back 460

Nasal obstruction
Recurrent sinusitis
Nasal polyposis
Chronic serous otitis
Sensorineural hearing loss

Front 461

Skin Manifestations with CSS

Back 461

Over half of the patients with CSS have skin lesions consisting of tender subcutaneous nodules on the extensor surfaces of the;
Arm
Elbows
Hands
Legs

Front 462

Cardiovascular Involvement w CSS

Back 462

About a half of the deaths related to CSS is secondary to cardiac involvement
Patients can have heart failure and or cardiac rhythm abnormalities
A mural thrombus can also be present

Front 463

About a half of the deaths related to CSS is secondary to cardiac involvement
Patients can have heart failure and or cardiac rhythm abnormalities
A mural thrombus can also be present

Back 463

Cardiovascular Involvement

Front 464

Neurologic Involvement w CSS

Back 464

Can cause peripheral neuropathy
Mononeuritis multiplex painful neuropathy that can damage motor and sensory in two different unrelated areas.

Front 465

Diagnosis of CSS

Back 465

Only 40 to 60 patients have a positive ANCA
Peripheral eosinophilia is usually present. (5,000 to 9,000 eosinophils/microL)

Front 466

Surgical lung biposy is the “Gold Standard”

Back 466

CSS
Churg-Strauss Syndrome

Front 467

What is the “Gold Standard”
in CSS?

Back 467

Surgical lung biposy

Front 468

Aspirin Exacerbated Respiratory Disease

Back 468

Do not confuse AERD with CSS
A combination of asthma
Chronic Rhinosinusitis
Nasal Polyps
Reaction to Aspirin or any other COX-1 NSAID

Front 469

Goodpasture’s Syndrome

Back 469

Anti-GBM antibody disease that primarily attacks the kidneys but can cause problems in the lungs.
Known to cause glomerulonephritis

Front 470

Anti-GBM antibody disease that primarily attacks the kidneys but can cause problems in the lungs.
Known to cause glomerulonephritis

Back 470

Goodpasture’s Syndrome

Front 471

Pulmonary Involvement w Goodpasture’s Syndrome

Back 471

Generally consists of pulmonary hemorrhage
Presentation; cough dyspnea, and sometimes hemoptysis.
CXR often demonstrates pulmonary infiltrates
The DLCO will be increased secondary to the pulmonary hemorrhage and hemoglobin in the alveoli

Front 472

Acute onset stridor in infancy due to

Back 472

viral croup, foriegn body

Front 473

Chronic stridor in infancy due to

Back 473

Laryngomalacia
Vocal cord paralysis
Subglottic Stenosis
larengyal cyst
Hemangioma
Epiglottic cyst

Front 474

Acute onset stridor in older child adolesence due to

Back 474

viral croup
epiglottitis********
peritonsillar abcess

Front 475

Chronic stridor in older child adolesence due to

Back 475

Subglottic Stenosis
Fireign body
papilloma

Front 476

Acute onset Wheezing in Infancy

Back 476

Bronchiolitis
Asthma
Foreign body

Front 477

Chronic Wheezing in Infancy

Back 477

Asthma
BPD
Recurrrent aspiration

Front 478

Acute Wheezing in Older Child or Adolescent

Back 478

Asthma
Foreign body
Allergic reaction

Front 479

Chronic Wheezing in Older Child or Adolescent

Back 479

Asthma
Foreign body
CF

Front 480

chronic cough in infancy

Back 480

Aspiration
Asthma
CF
Pulmonary infections
CHD

Front 481

chronic cough in early childhood

Back 481

Aspiration
Retained Forein Body
Asthma
CF
Bronchiectasis
Chronic otitis

Front 482

chronic cough in late childhood and adolesence

Back 482

asthma
Bronchiectasis
CF
Pulmonary infections
chronic otitis

Front 483

Hydrocarbons affect ____________ so restrictive disease results.

Back 483

surfactant function,

Front 484

Gold standerd in diagnosis of P Embolism

Back 484

Angiography