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Pathophysiology 2 > Final > Flashcards

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1
Q

Chest X-Ray

Croup vs. Epiglottitis

A

Croup- Steeple Sign; Subglottic narrowing lower in the airway. Linear narrowing of trachea (wedge shaped)

Epiglottitis- Thumb Sign; Swollen epiglottis higher in the airway

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2
Q

Bronchiectasis

A

Irreversible dilation and disortion of bronchial tree

Result of airway obstruction, chronic infection, and extensive inflammation

Dilation due to destruction of bronchial cartilage elastic fibres, blood vessels and smooth muscle

Congenital condition in a small number of patients

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3
Q

Bronchiectasis and Secretions

A

Leads to insufficient airway secretion clerance due to inadequate ciliary activity

Poro bronchial toliet will increase the risk of infection

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4
Q

Croup Treatment

A

Supportive Care-Humidity, Oxygen, Corticosteroids, Dexamethasone, Recemic Epinephrine (1:1000 mg- 5 ml)

Try to have minimal diagnositic and handling

May lead to intubation if obstruction become serious

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5
Q

Other Name for Croup

A

Laryngotracheobronchitis

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6
Q

Croup Clinical Manifestation

A

Barking, seal like cough

Hoarse voice and stridor

Low to moderate fever and dehydration

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7
Q

Pediatric Signs of Impending Respiratory Failure

A

Increased work of breathing at rest with intercostal and substernal retractions

Increasing O2 requirements and lethargy are signs of impending respiratory failure

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8
Q

Epiglottitis Pathophysiology

A

Acute bacterial infection

Inflammation of supraglottic structure producing an enlagred cherry red epiglottis which can partially or completely obstruct airway

Age on onset: < 6 years of age

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9
Q

Primary Cause of Epiglottitis

A

Haemophilusinfluenzae Type B

Rarer due to vaccinations*: 95% reduction in cases

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10
Q

Non-Infectious Causes of Epiglottitis

A

Aspiration of hot liquid

Multiple intubations

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11
Q

Pathology of Foreign Body Aspiration

A

Distal areas will become atelectatic and increased shunt

Can lead to infection

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12
Q

What are the 2 types of congenital diaphragmatic hernia

A
  • Bochdalek Hernia
    • Lateral and posterior defect
    • Usually will occur in the left hemidiaphragm
    • Most common
    • Occurs 90% of the time
  • Morgagni Hernia
    • Medial and anterior
    • Occurs on both sides
    • Liver will prevent some up the upwards movement
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13
Q

Congenital Diaphragmatic Hernia

Pathophysiology

A

Lung Hypoplasia because it does not have enough room to properly develop

Decreased pulmonary vasculature (Pulmonary hypertension and decreased alveolar count)

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14
Q

Congenital Diaphragmatic Hernia

Chest X Ray

A

Loop and air in the thoracic cavity

Mediastinum will be pushed to the right

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15
Q

Congenital Diaphragmatic Hernia

Clinical Manifestations

A
  • Significant respiratory distress at birth with severe hypoxia and acidosis
  • Scaphoid Abdomen (Depressed Triagular shape)
  • Barrel Chest
  • Heart displaced to the opposite side of the hernia
  • Increased PVR with a persistent shunt
    • Worsening right to left shunt
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16
Q

Angioplasty

A

Can be done at the same time as a angiography if needed

A catheter will be floated through the artery and then the balloon is repeated inflated and deflated to flatten the plauqe againt the artery wall

If this is the only treament given then renstenosis may be needed later on

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17
Q

Coronary Artery Disease

Coronary Angiography

A

Gold standard for diagnosis CAD will evaluate the extent and location of blockages

Only test that indicate which treatment to use

A catheter is inserted into an artery (usually femoral) which is threaded up into coronary artery

Dye is injected at this point and fluoroscopy captures the image of the blood flow

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18
Q

B Blockers

A

HR and contraction of the heart will decrease = Decrease BP

Will block the effects of epinephrine causing vasodilation

These drugs will end in -olol

Not used for people with asthma

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19
Q

ACE Inhibitor

A

Will inhibit ACE enzyme = decrease production of angiotensin II

As a result, blood vessels enlarge or dilate, and blood pressure is reduced.

Ends in -pril

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20
Q

Coronary Artery Disease

Stenting

A

Will commonly be done at same time as angiography

The goal is to help prevent restenosis, or at least lengthen the time before restenosis occurs

Use of drug-impregnated stents reduces risk of restenosis.

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21
Q

What Are Most Myocardial Infarctions Caused by

A

Most MI’s are caused through a ruptured atherosclerotic plaque

The risk factors for the development of CAD are also risk factors for an MI

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22
Q

Myocardial Infarction

Pathophysiology

A

Myocardium is deprived of oxygen which leads to ischemia ► Areas of Injury ►Infarction

Reperfusion injury is also an important component of the pathophysiology.

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23
Q

Myocardial Area of Injury

A

An area of injury can repair itself but 100% as there is extra fibrinogen, fat deposits, etc

24
Q

Area of Infarction

Transmural

A

Full thickness of myocardium

25
Area of Infarction Subendocardial
Partial thickness of myocardium
26
Myocardial Infarction Blood Markers-Myoglobin
Very sensitive and early marker of myocardial necrosis, but is not specific for MI Levels will begin to rise within 1 hour with peaks within 4-8 hours Will return to normal by 36 hours
27
Myocardial Infarction Blood Markers Troponin I
#1 test of choice Marker of damaged tissue after an MI Detectable at 3-6 hours and peaks at 26 hours Remains elevated for 14 days Highly sensitive test
28
Myocardial Infarction ECG-ST Segments
Depression (ischemia) Elevation (infarction) ST segment elevation is only considered pathologic if it occurs in two or more anatomically contiguous leads!
29
Meconium Aspiration Syndrome (MAS) Anatomic Alterations of the Lungs
Meconium can either fully or partially obstruct the airway and create a ball-valve effect - meaning that the air can enter the alveoli but not readily leave Chemical Pneumonitis Decreased Surfactant=RDS Hypoxia-induced vasoconstriction and vasospasm. The vasospasm can pulmonary hypertension - right to left shunt
30
Myocardial Infarction Time Frames
* 0-30 Minutes * Reversible injury * 1-2 Hours * Onset of irreversible injury * 4-12 Hours * Beginning of necrosis
31
How long does necrosis and scar tissue development after MI occur for
There will continue to be necrosis and development of scar tissues occurs up until 8th week post infarct The risk for myocardial rupture is greatest at days 4-7 post infarct As the tougher fibrotic scar tissue starts to form 7-10 days post infarct
32
Myocardial Infarction Blood Markers Total CK
Enzyme of cardiac damage
33
Vessels Commonly Used for CABG
saphenous vein, internal mammary artery or radial artery
34
Myocardial Infarction Blood Markers CK-MB
Levels will begin to rise within 4 hours and peak at 24 hours Levels will subside by 3 days Not specific to MI
35
Reperfusion therapy
Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a MI The goal is to reduce mortality and limit the infarct size
36
Methods for Reperfusion Therapy
* Thrombolytics * Dissolve blood and platelet clots * Best is used within 60-90 minutes of onset * Should be given by EMT * Risk of bleeding must be considered, because you will have a time period when there is no clotting factors avalible * Percutaneous Coronary Interventions (PCI) * CABG
37
Cor Pulmonale
Enlargement and failure of right ventircle due to increase resistance from lungs Chronic pulmonary heart disease will usually result in right ventricular hypertrophy
38
Left Sided Heart Failure
The left side of the heart is unable to properly pump blood=low systemic perfusion Low systemic perfusion will then lead to vasoconstriction (increased SVR) Blood may back into pulmonary system ►pulmonary congestion and right sided heart failure When the RH fails there is a decreased pulmonary congestion giving a false look of improvement
39
Right Sided Heart Failure Hemodynamic Profile
* Increased * CVP
40
Left Sided Heart Failure Hemodynamics
* Increased * PAWP * HR * Decreased * CO * Pulse pressure
41
Right Sided Heart Failure Forward Failure
Decreased RV output leading to venous congestion
42
Right Sided Heart Failure Backwards Failure
Decrease RV output -\> Decreased pulmonary perfusion -\>Decreased LV filling -\>Decreased LV output -\> systemic perfusion
43
Myocardial Infarction 12 Leads and Coronary Arteries-Anterior Injury
V3, V4
44
Myocardial Infarction 12 Leads and Coronary Arteries-Septal Injury
V1, V2
45
Pulmonary Interstitial Emphysema (PIE) Pathophysiology
The small airway rupture will compress the vasculature leading to **decreased pulmonary perfusion, increase PVR, and incresae R-L shunt** There will be an **increased airway resistance** due to the decrease in the lumen of the bronchioles
46
Neonatal Jaundice
Occurs in 50% normal births Can occur due to delayed feeding, hemolytic disease, liver/gut defects.
47
Kernicterus
Severe hyperbilirubinemia Will toxifie the baby and lead to CNS impairment, seizures, and motor dsyfunction
48
Treatment for Jaundice
Phototherapy (blue light) helps to form conjugated bilirubin to allow excretion, and exchange transfusion.
49
Necrotizing Enterocolitis (NEC)
Inflammatory destructive bowel disease that is charaterized by **necrosis of colon and ileum caused by intestinal ischemia** Necrosis will cause abdominal distension, sepsis, hypoxemia, respiratory failure, intestinal perforation Gangrene can also occur Related to asphyxia in utero
50
Periventricular Leukomalacia (PVL) Pathophysiology
Occurs in the white matter adjacent to the lateral ventricles Injury occurs in response to hypotension, ischemia, and necrosis due to asphyxia. Can also results from increased fluid or hemorrhage compressing arterioles in the white matter.
51
IVH- Intraventricular Hemorrhage Pathophysiology
Bleeding starts in the germinal matrix (a highly vascular network that matures and gets smaller with gestational age) Blood fills the ventricles and compresses brain parenchyma Any factor that increases or decreases cerebral blood flow will cause rupture
52
Acute epiglottitis Vs Laryngotracheobronchitis(croup) Cause
Croup- Viral (parainfluenza, RSV) Epiglottis-Bacterial (harmophilius influenze type B)
53
Bronchiolitis
Inflammatory disease of the bronchioles Most common lower respiratory infection in pediatrics Most common cause: RSV (Respiratory Syncytial Virus)
54
Sweat Chloride Test Infants Six Months or Younger
≤29 mmol/L: Normal (CF very unlikely) 30 to 59 mmol/L: Intermediate (Possible CF) ≥60 mmol/L: Abnormal (CF Diagnosis)
55
Sweat Chloride Test Infants Older than Six Months, Children and Adults
≤39 mmol/L: Normal (CF very unlikely) 40 to 59 mmol/L: Intermediate (Possible CF) ≥60 mmol/L: Abnormal (CF Diagnosis)
56
Sleep Apnea
Cessation of bretahing for 10 sec or longer until the brain over comes the problem Sleep apnea is diagnosed when there is more than 5 apneas per hour occurring over a 6 hour period
57
How Do Third Degree Burns Heal
The resultant damage heals with hypertrophic scars (keloids) and chronic granulation

Pathophysiology 2 (9 decks)

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