Path Exam 2 - Pathology Of The Respiratory System

Front 1

chronic bronchitis

Back 1

productive cough for 3 months of the year for 2 consecutive years

Front 2

chronic bronchitis pathogenesis

Back 2

mucus hypersecretion, hyperplasia of submucosal glands (bronchi), proteases stimulate mucus hypersecretion, increase in goblet cells

Front 3

chronic bronchitis clinical findings

Back 3

increased bronchial mucus secreting apparatus, reid index more than 0.5, cyanosis and edema. cor pulmonale, heart failure, cancerous transformations

Front 4

reid index

Back 4

measures the size of the mucous glands

Front 5

emphysema

Back 5

enlargement of airspaces distal to the terminal bronchioles with destruction of their walls without fibrosis

Front 6

emphysema pathogenesis

Back 6

smoke causes irritation and mucus secretion, neutrophils contain serine elastase causes destruction of elastic tissue in walls of airspace, inactivation of α-1-antitrypsin (by smoke) which inhibits many proteases including elastase

Front 7

centriacinar (centrilobular) emphysema

Back 7

most common, usually associated with cigarette smoking, characterized by destruction of the proximal acinus

Front 8

panacinar (panlobular) emphysema

Back 8

acini are uniformly involved, patients with hereditary α-1antitrypsin deficiency

Front 9

localized emphysema

Back 9

large area of destruction termed a bulla which may rupture and produce spontaneous pneumothorax

Front 10

emphysema clinical findings

Back 10

exertional dyspnea, tachypnea, barrel chest, ping puffers, use of accessory muscles of respiration to breathe

Front 11

asthma types

Back 11

1. atopic - allergen sensitization
2. nonatopic - frequently triggered by respiratory tract infection
3. drug induced asthma - aspirin
4. occupational asthma

Front 12

asthma pathogenesis

Back 12

allergen interacts with TH2 cells and IgE antibody bound to the surface of mast cells, type 1 hypersensitivity, inflammatory mediators lead to smooth muscle contraction, mucous secretion, increased vascular permeability

Front 13

asthma clinical findings

Back 13

tightness in chest and non productive cough, wheezing, ↑respiratory rate, dyspnea, status asthmaticus is severe bronchoconstriction

Front 14

pulmonary hypertension

Back 14

elevated pulmonary arterial pressure, mean pressure over 24 mm Hg at rest

Front 15

primary pulmonary hypertension

Back 15

most common in young women, insidious onset of dyspnea, cor pulmonale, heart-lung transplant often required

Front 16

secondary pulmonary hypertension

Back 16

1. after chronic pulmonary diseases - COPD, pulmonary embolism, tuberculosis
2. after heart disease - left-to-right cardiac shunts
3. thromboembolic pulmonary hypertension - multiple thromboemboli, gradual restriction of pulmonary circulation

Front 17

hypoxemia

Back 17

COPD, lung disease, kyphoscoliosis

Front 18

obesity-hypoventilation syndrome

Back 18

↓ventilatory responsiveness to hypercapnia/hypoxia

Front 19

picwikian syndrome

Back 19

extreme obesity, cyanosis, irregular breathing, secondary polycythemia, right ventricular hypertrophy, pulmonary hypertension

Front 20

pulmonary edema

Back 20

increased fluid in the alveolar spaces and lung interstitium

leads to ↓decreased gas exchange, hypoxia, hypertension

Front 21

protective mechanisms of lung against edema (3)

Back 21

1. ↓perfusion pressure in lung capillaries 2° ↓right centricular pressure
2. effective drainage of the intersitial space by lymphatics
3. tight cellular junctions between endothelial cells

Front 22

hemodynamic edema

Back 22

increased hydrostatic pressure (increased pulmonary venous pressure), decreased oncotic pressure

Front 23

cardiogenic pulmonary edema

Back 23

↑transmural pressure, ↑hydrostatic pressure, ↑alveolar surface tension,

ultrafiltration rate exceeds capacity, interstitial fluid build up exceeding clearance, alveolar flooding

Front 24

noncardiogenic pulmonary edema

Back 24

loss of integrity of alceolar epithelium and capillary endothelium, ↑permeability, disrupted epithelial barrier

Front 25

Acute Respiratory Distress Syndrome (ARDS)

Back 25

decreased lung compliance, hypoxemia, "white out" on xrays, caused by a large variety of lung insults

Front 26

ARDS pathogenesis

Back 26

endothelial cells injury causes alveolar fluid build up into interstitial spaces, loss of type 1 pneumocytes causes formation of Hyaline membrane, inflammation, proliferation of pneuomocytes II, fibroblasts deposit collagen in alveolar wall if patient survives acute phase

Front 27

ARDS pathology

Back 27

acute phase - diffuse alveolar damage, alveolar septa, hyaline membranes
later phase - proliferation of pneuomocytes type II and fribroblasts in interstitial space

Front 28

neonatal respiratory distress syndrome (RDS)

Back 28

results from immaturity of the surfactant system at birth, leading cause of morbidity/mortality in infants, very common in premature babies

Front 29

RDS pathogenesis

Back 29

lack of surfactant causes alveolar collapse during exhalation, inhalation is more difficult and damages alveolar lining

Front 30

RDS pathology

Back 30

lungs are dark red and airless, alveoli are collapsed, hyaline membranes

Front 31

RDS clinical findings

Back 31

within an hour of birth: ↑increased respiratory effort with forceful intercostal retraction, ↑respiratory rate, cyanosis, "ground glass" granularity in chest radiographs/"white out" of lungs, long periods of apnea leads to asphyxiation