Pul. HTN + RDS Flashcards
How does pulmonary hypertension the lead to Cor pulmonale
Pulmonary hypertension – >severe resp distress – >cyanosis + RVH – >cor pulmonale
Explain how we get to pulmonary hypertension
Increased pressure on endothelium – >
Arteriosclerosis/atherosclerosis
SM medial hypertrophy
Intimal fibrosis
OF PUL. ARTERIES
Explain primary hypertension
- BMPR2 inactivated mutated gene
- Idiopathic
- Pulmonary venous occlusive disease PVOD
- Persistent pulmonary hypertension @newborn
– >Can’t inhibit the vascular SM proliferation – >
XS SM– >SM medial hypertrophy + intimal fibrosis + arterio/atherosclerosis – >Primary hypertension
Explain what causes secondary pulmonary hypertension
L – >R Shunt Hypoxaemia Acidosis respiratory Valve disease – Mitral stenosis Vasculature loss @ pulmonary Bed Drugs
Causes of respiratory distress syndrome?
G – sepsis 40%
Gastric aspiration 30%
Trauma 20%
Explain how the causes cause respiratory distress syndrome
The alveolar macrophages’s release cytokinins – >side can’t attract neutrophils – >neutrophils enter the area via diapedesis therefore increase permeability of capillaries – >release exudates into the interstitium– > oedema + necrotic epi cells
(sticky hyalin membranes= Thick diffusion barrier +sticky = increase surface tension) + coag casc
(neutrophils release proteases and FR’s – >Damage type one and type to numerous sites – >decrease surfactant – >increase surface tension = atelectasis
– >Cyanosis hypoxaemia resp distress dyspnoea
What are the clinical symptoms of RDS
Dyspnoea crackles cyanosis hypoxaemia
Later why do we get interstitial fibrosis in RDS ?
Type 2 pneumocytes = down
Progressive interstitial fibrosis Repair >regen
Explain atelectasis
Collapsed as space – >inadequate air space expansion – > Lose lung volume
Explain the resorption atelectasis
Six secretions/4 materials/bronchogenic carcinoma – >
Every instruction – >
Air cannot reach alveoli – >
Pulmonary capillaries absorb pre-existing air + alveoli – >
Airless state within a few hours due to time taken for diffusion+ Tactile fremitus D crease + dyspnoea decreased breath sound
Explain compression atelectasis
Tension pneumothorax/pleural effusion – >
Air/fluid respectively@Plural cavity – >
Increased pressure – >
Collapse small airway underneath pleura
Explain atelectasis due to surfactants loss
Decreases the fact – >increase surface tension – >
alveoli collapsing at expiration when expression pressure increases
What’s three reasons cause neonatal respiratory distress syndrome
C section, maternal diabetes, prematurity
What causes an increase in surfactant production
Increased cortisol
Increased thyroxine
Decreased insulin
Explain how C-section leads to neonatal RDS
See section – >decreased stress-induced cortisol compared to vaginal delivery– >
Decreased surfactants production + release from pneumocyte type 2
Explain how maternal diabetes leads to neonatal RDS
Maternal diabetes – >hypoglycaemia + baby – >increased insulin @baby – >D creased surfactants
After delivery there is XS insulin as baby is not connected to mother anymore all no glucose I s coming from the mother– >Hypoglycaemia – >seizures
Neuron Damage
Explain how prematurity leads to the neonatal RDS
Surfactants = start made @28 weeks
Adequate levels reach at @34 weeks
As time progresses the ratio of Lecithin:sphingomyelin increases
L:S>2= Adequate level
Give woman G.corticoids – >increase surfactant – >reduce p(RDS)
Explain how hypoxaemia can be damaging to neonate when born .
Persistent PDA
Decreased oxygen to gut – >intestinal ischaemia – >entry of gut bacteria into intestinal wall
Explain the problems of giving supplemental oxygen to neonate
Super oxide/free radicals – >
Retinopathy/blindness
Bronchopulmonary dysplasia – permanent small airway damage
