resp, cardio Flashcards

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1
Q

what is asthma?

A

chronic inflammatory disease of airways caused by bronchial hyperresponsiveness & airway obstruction

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2
Q

what is the cause of asthma?

A

unknown; genetics

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3
Q

what are the risk factors of asthma?

A

environmental triggers eg allergens, dust particles, low birth weight

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4
Q

pathology of asthma?

A

environmental stimulus travels down to the bronchioles, comprising cartilage, smooth muscle & mucosal lining. immune cells eg mast cells, basophils are stimulated to release histamine & leukotrienes, causing an inflammatory response & smooth muscle to spasm (bronchospasm). this causes goblet cells to secrete mucus, causing an airway obstruction. over time, chronic inflammation results in scarring & fibrosis, permanently reduces airway diameter.

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5
Q

what are the symptoms of asthma?

A

wheezing, non-productive cough for 2 months, tachycardia, trouble breathing, SOB, chest tightness, dyspnea, decreased O2 saturation

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6
Q

diagnosis for asthma?

A
  1. PFT (FEV1/ FVC < 70% - airway obstruction
  2. PFR using peak flow meter
  3. ABG - alkalosis due to hyperventilation, which will later develop into acidosis due to dyspnea
  4. CBC shows elevated eosinophils
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7
Q

treatment for asthma?

A
  • supplemental O2
  • meds
    1. bronchodilators
  • SABA eg albuterol, salbutamol - quickly relieve asthma symptoms
  • LABA eg formoterol - taken daily to maintain asthma ctrl
  • anticholinergics eg ipratropium - inhibit AcH effect, inhibiting the parasympathetic syst
    2. corticosteroids eg budesonide, prednisone help with inflammation
    3. mast cells stabilisers eg cromolyn
    4. leukotriene R antagonists eg montelukast
    5. Ab omalizumab lower IgE levels
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8
Q

what are bronchodilators?

A
  • SABA eg albuterol, salbutamol - quickly relieve asthma symptoms
  • LABA eg formoterol - taken daily to maintain asthma ctrl
  • anticholinergics eg ipratropium - inhibit AcH effect, stimulating the parasympathetic syst
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9
Q

what are corticosteroids?

A

corticosteroids eg budesonide, prednisone help with inflammation

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10
Q

what are mast cells stabilisers?

A

cromolyn

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11
Q

what are leukotriene R antagonists?

A

montelukast

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12
Q

what is the last pharmaco treatment for asthma?

A

monoclonal Ab omalizumab lowers IgE levels, reducing chemical mediators from immune cells

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13
Q

what is bronchitis?

A

inflammation of bronchioles caused by dead epithelial cells & mucus

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14
Q

cause of bronchitis?

A

RSV, adenovirus, parainfuenza virus, (rarely) bacteria mycoplasma pneumoniae

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15
Q

risk factors of bronchitis?

A

young age, premature birth, crowded places, underlying conditions eg chronic lung disease, congenital heart disease or immunocompromised

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16
Q

mode of transmission of bronchitis?

A

resp droplets which can last on surfaces for a few hrs

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17
Q

pathology of bronchitis?

A

virus travels down the airway tract to the bronchioles, killing epithelial cells. immune cells are stimulated, narrowing the airway and stimulating goblet cells to secrete mucus. mucus and dead epithelial cells create a plug, obstructing the airway. this results in atelectasis and air-trapping (inhaled air remains; more inflated every inhalation).

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18
Q

symptoms of bronchitis?

A

wheezing, intercostal retractions, flu-like symptoms. for severe cases, lethargy, irritable, poor feeding, dehydration, central apnea (sleep disorder that causes breathing to repeatedly stop & start during sleep)

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19
Q

what is the normal range of RR for adults & newborn?

A

adults: 12-20
newborn: 30-60

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20
Q

diagnosis for bronchitis?

A
  1. swabbing secretions from nasopharynx
  2. rapid antigen detection test RADT
  3. PCR
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21
Q

treatment for bronchitis?

A
  • can be treated at home eg cool-mist humidifier, head elevated while awake, saline nasal drops, nasal suction, adequate fluid intake
  • smoke-free envt
  • acetaminophen (pain reliever) & ibuprofen (fever)
  • for severe symptoms, hospital -> supplemental O2 & IV fluid therapy
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22
Q

what is croup/ laryngotracheobronchitis?

A

inflammation of upper resp tract

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23
Q

cause of croup?

A

parainfluenza, adenovirus, influenza A or B, RSV

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24
Q

risk factors of croup?

A

seasonal, young age, boy, fam hx

25
Q

transmission of croup?

A

resp droplets, saliva, contact with infected person or surface

26
Q

pathology of croup?

A

virus enters airway through the pharynx, larynx, trachea, bronchioles, cause inflammation, swelling & mucus secretion, narrowing the subglottic area. this compromises the lower vocal cords & upper trachea, resulting to hoarseness during inspiration (inspiratory stridor) & croupy cough

27
Q

symptoms of croup?

A

inspiratory stridor, croupy (seal-like bark), cough, intercostal retractions, fever, myalgia. for severe cases, fatigue (seen thru poor appetite), diminished breath sounds, hypoxia, cyanosis

28
Q

diagnosis for croup?

A

CXR (steeple sign/ inverted V below the vocal cord seen)
labs & radiology studies done for cases when pneumonia is suspected

29
Q

treatment for croup?

A

bronchodilators, corticosteroids, antipyretics, humidified supplemental O2. for severe cases, resp impending failure -> intubation & mechanical ventilation

30
Q

what are the 4 types of acyanotic CHD?

A
  1. VSD
  2. ASD
  3. patent ductus arteriosus
  4. coarctation of aorta
31
Q

what is the cause for ACHD?

A

unknown

32
Q

risk factors for ACHD?

A
  1. chromosomal abnormalities of fetus
  2. maternal infections
  3. exposure to teratogens
  4. chronic illnesses
33
Q

risk factors for PDA?

A
  1. premature birth
  2. rubella infection during pregnancy
  3. asphyxia during delivery
34
Q

explain eisenmenger syndrome

A

when pulmonary flow is higher since blood moves from L to R, resulting in higher pulmonary pressure. this leads to R to L shunting, moving deoxygenated blood from R to L.

35
Q

what is the treatment for PDA?

A

indomethacin

36
Q

what is treatment for coarctation of aorta?

A
  1. prostaglandin E1 infusion (opens ductus arteriosus, allowing blood to bypass the narrowing)
  2. antihypertensives
37
Q

what is the clinical manifestation of coarctation of aorta?

A

BP of upper limbs > lower limbs

38
Q

what is used to treat heart failure?

A

digoxin

39
Q

what is used to treat infective endocarditis?

A

prophylactic antibiotics

40
Q

what is used to treat pulmonary edema?

A

diuretics

41
Q

what are the 5 types of CCHD?

A
  1. tetralogy of fallot
  2. translocation of great arteries
  3. tricuspid atresia
  4. truncus arteriosus
  5. total anomalous pulmonary venous return
42
Q

what are the 4 features of ToF?

A

PROVe
1. Pulmonary stenosis
2. RV hypertrophy
3. Overriding aorta
4. VSD

43
Q

what are the complications of ToF?

A

tet spell (cyanotic episode) due to RV outflow tract obstruction, resulting in less blood flow to the lungs. occurs when infant is stressed eg crying, feeding as the infundibular septum spasms, worsening the narrowing

44
Q

what are the clinical manifestations of CCHD?

A

cyanosis, clubbing of fingers, tachycardia, tachypnea, tet spells & boot shape heart (ToF), squatting

45
Q

non-surgical treatments for CCHD?

A

placing infant in a knee-chest position, antihypertensives, phenylephrine (vasoconstrictor)

46
Q

what is kawasaki disease?

A

inflammation of medium-sized arteries eg coronary artery

47
Q

cause of KD?

A

unknown

48
Q

risk factors of KD?

A

young, male, asian or pacific islander ancestry

49
Q

pathology of KD?

A

immune cells activated attack the endothelial lining of the inner most layer of the artery - tunica intima

50
Q

what are the layers of coronary artery?

A
  1. tunica adventitia (loose connective tissue)
  2. tunica media (smooth muscle)
  3. tunica intima (loose connective tissue)
51
Q

complications of KD?

A

results in aneurysm (abnormal bulging of the artery) since damage to the endothelial lining causes it to become thin and blood clots are formed. the aneurysm can rupture, decreasing blood flow to the heart, causing ischemia, MI and/ or death.
the activated immune cells can move and attack other parts of the heart, causing valvulitis, myocarditis, pericarditis

52
Q

what are the clinical manifestations of KD?

A

CRASH
1. Conjunctiva hyperemia (photophobia due to increased sensitivity to light)
2. Rashes
3. Adenopathy (swollen cervical lymph nodes)
4. Strawberry tongue & dry lips
5. Hands & feet changes (edema and peeling of skin)
6. Burn (fever for > 5 days)

53
Q

what is the treatment for KD?

A
  1. aspirin therapy (to prevent thrombosis)
  2. IV immunoglobulin (delay live vaxx for > 11 mths)
54
Q

will hematocrit be low or high for KD?

A

low since anaemia occurs due to prolonged active inflammation of the arterial vessels

55
Q

will C-reactive protein CRP made in liver be low or high for KD?

A

high since high level of inflammation

56
Q

will erythrocyte sedimentation rate ESR be low or high for KD?

A

high since high level of inflammation

57
Q

will ALT & AST (serum transaminase) levels be low or high for KD?

A

high (measure the amt of e/z in blood to check for liver damage)

58
Q

why is aspirin used for KD?

A

the risk for thrombosis blocking blood flow is higher than risk for Reye disease (brain/ liver damage)
ibuprofen, paracetamol and other NSAIDS cannot be used