However, this is not what they will ask you – they will ask what is first step in management?
Echocardiogram – shows that they have fluid (proves it – b/c need to call surgeon to do pericardiocentesis).
What is it MC due to? Pericarditis. What is the MCC pericarditis? Coxsackie.
What if woman has this and a “+” serum ANA? Lupus.
Any young woman that has an unexplained pericardial or pleural effusion is lupus until proven otherwise.
Why? Serositis = inflame serosal membranes – its gonna leak fluid, leading to effusions. And is a feature of Lupus.
E. Constrictive pericarditis
In third world countries, TB is MC. In USA, due to previous cardiac surgery b/c have to go through pericardium.
Slide of a heart and thickened pericardium, no fluid, so when you breathe in blood goes to right heart, fills up and hits wall – called pericardial knock – therefore to differentiate pericardial effusion from constrictive pericarditis, have muffled heart sounds in effusion with no knock in pericardial effusion, and in have some filling up with a pericardial knock in constrictive pericarditis.
White stuff in pericardium is dystrophic calcification, and can see it on x-ray.
Pt goes to Russia and gets diarrhea = giardiasis)
81. Heart and Pericardium: constrictive pericarditis secondary to TB
CHAPTER 8: RESPIRATORY
I. A-a gradient – know how to calculate:
Alveolar O2 and arterial pO2 are never the same. The difference between the two is called alveolar arterial gradient.
Reasons for it:
(1) Ventilation and perfusion are not evenly matched in the lungs.
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When standing up the ventilation is better than perfusion in the apex, whereas perfusion is better than ventilation at lower lobes.
This explains why almost all pulmonary infarctions are in the lower lobes – perfusion is greater there.
Also, this explains why reactivation TB is in the apex – TB is a strict aerobe and needs as more O2, and there is more ventilation in the upper lobes (higher O2 content).
Normally, alveolar O2 is 100 and the arterial pO2 is 95.
So, normally, the gradient is 5 mmHg.
As you get older, the gradient expands, but not that much. Most people use their upper limit of normal – in other words, have a very very high specificity of 30 mmHg.
If you have an A-a gradient of 30 mmHg or higher there is a problem. It is very high specificity (aka PPV – truly have something wrong).
The concept is easy – you would expect the gradient btwn the alveolar O2 and the arterial O2 to be greater if you have primary lung dz. What will do this? Ventilation defects (produces hypoxemia, and therefore prolongs the gradient – dropping the PO2 and subtracting, and therefore a greater difference btwn the two), perfusion defect (ie pul embolus), and diffusion defect.
But the depression of the medullary resp center by barbiturates does not cause a difference in A-a gradient.
So, prolonged A-a gradient tells you the hypoxemia is due to a problem in the lungs (vent perfusion/diffusion defect).
A normal A-a gradient tells you that something outside the lungs that is causing hypoxemia (resp acidosis – in resp acidosis, PO2 will go down).
Causes of resp acidosis: pulmonary probs (COPD), depression of resp center (obstruct upper airway from epiglottitis, larygiotracheobronchitis, café coronary (paralyzed muscles of resp), Guillain Barre syndrome, amyotrophic lateral sclerosis, and paralysis of diaphragm.
These all produce resp acidosis and hypoxemia, but the A-a gradient will be NORMAL).
So, prolonged A-a gradient, something is wrong with the lungs.
If A-a gradient is normal, there is something OUTSIDE of the lungs that is causing a resp problem.
Few things must always be calculated: anion gap (with electrolytes) and A-a gradient for blood gases – all you need to do is calc alveolar O2.
We can calculate the A-a gradient = 0.21 x 713 = 150 (0.21 is the atmospheric O2; and 760 minus the water vapor=713). So, 150 minus the pCO2 (given in the blood gas) divided by 0.8 (resp quotient).
So, normal pCO2 = 40, and 40/.8=50 and 150-50 = 100; so, now that I have calc the alveolar O2, just subtract the measured arterial pO2 and you have the A-a gradient.
This is very simple and gives a lot of info when working up hypoxemia.
II. Upper Respiratory Disease:
A. Nasal Polyps:
3 diff types of nasal polyps – MC is an allergic polyp.
Never think of a polyp in the nose of kid that is allergic as an allergic polyp. Allergic polyps develop in adults after a long term allergies such as allergic rhinitis
– Example: 5 y/o child with nasal polyp and resp defects, what is the first step in
management? Sweat test – b/c if you have a polyp in the nose of the kid, you have cystic fibrosis; it’s not an allergic polyp.
B. Triad Asthma – take an aspirin or NSAID, have nasal polyps and of course have asthma.
They don’t tell you the pt took aspirin and that the pt has a polyp.
The aspirin or NSAID is the answer but this is how they will ask the question: 35 y/o woman with chronic headaches or fibromyalgia.
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Pt has some type of chronic pain syndrome and will not tell you that the pt is on medication, and she develops occasional bouts of asthma – what is the mech of the pt’s asthma? B/c she is taking an NSAID.
What they won’t tell you that she has a polyp and that she is on an NSAID; however, if a pt is in pain or has chronic pain, it is safe to assume the pt is on pain medication (ie an NSAID, Motrin or aspirin).
Mech of asthma from pain medication: what do aspirin/NSAIDs block? COX, therefore arachidonic acid cannot forms PGs but the Lipoxygenase pathway is left open.
Some people are very sensitive to this and LT C4, D4, and E4 are formed, which are potent bronchoconstrictors, leading to asthma.
It is NOT a type I HPY rxn.
It is a chemical mediated non type I HPY rxn.
So, chronic pain can lead to asthma b/c of aspirin sensitivity.
Another assumption you have to make: any well built male on anabolic steroids (ie football player, wrestler) with intraperitoneal hemorrhage – produce benign liver cell adenomas which have the tendency of rupturing.
C. Laryngeal carcinoma (a squamous cell carcinoma) Concept of synergism: MCC = Smoking; 2nd MCC = alcohol
Alcohol and smoking have a SYNERGISTIC effect which leads to laryngeal carcinoma.
Example: lesion in this slide is a laryngeal specimen – which of the following have the greatest risk factor? Answer – alcohol AND smoking (this is true for any squamous cancer from the esophagus to the mouth to the larynx).
Smoking = MCC cancer in mouth, upper esophagus and larynx.
Alcohol can do the same thing, so if you are smoker and alcohol consumer, you can double your risk.
MC symptom assoc = hoarseness of the throat.
3. Laryngectomy: squamous cell carcinoma
Example: epiglottis; what can infect it? H. influenza – what is the symptom? Inspiratory strider.
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12. X-ray of lateral neck: thumbprint sign of acute epiglottitis due to Hemophilus influenzae
Example: 3 month old child died with inspiratory strider – dx? Croup – parainfluenza; this is a TRACHEAL inflammation.
Whereas epiglottitis is elsewhere. Both produce upper airway obstruction.
III. Respiratory Distress Syndromes:
A. Hyaline membrane dz (Neonatal Resp distress syndrome) If something has a lot of pink in it, what is it? Hyaline
Key to understanding this dz is massive atelectasis
4. Newborn lungs with hyaline membrane disease (respiratory distress syndrome)
1. What is atelectasis? Collapse of airways.
- Why did these airway collapse? No surfactant (aka lecithin/phosphotidyl choline/phosphotidyl glycerol – they are all surfactant).
- So, deficient of surfactant causes atelectasis b/c:
Collapsing pressure in the airways = surface tension/radius of airway.
So, on expiration, normally the airway will be smaller b/c there is a postive intrathoracic pressure.
If you decrease the radius, you will increase the collapsing pressure in the airways.
Therefore, on expiration (in all of us), we have to decrease surface tension (which is what surfactant does) – by doing this, it keeps the airways open on expiration, preventing atelectasis.
2. Three causes of RDS:
a. Prematurity: surfactant begins syn early, but it peaks at 32-35 week, so if you are born prematurely, you will not have enough surfactant, and baby will develop increased risk of developing RDS.
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b. Sometimes mother has no choice and must deliver baby, or else it will die, and there is something you can do to the mom so the baby has more surfactant: give mother glucocorticoids b/c they stimulate surfactant synthesis.
c. Example: what can you do to increase surfactant (but glucocorticoids wasn’t one of the answer choices) – thyroxine (thyroid hormone) (as does prolactin); does that mean you give thyroxine b4 delivering the baby? No, will give mom and baby hyperthyroidism.
d. Diabetes: gestational diabetes = woman who wasn’t pregnant, becomes pregnant, and then obtains glucose intolerance after delivery – so if a diabetic gets pregnant, this is not called gestational diabetes, but a diabetic that got pregnant.
Its imp that a woman in pregnancy has good glucose control b/c if she is hyperglycemic, baby will be, too.
B/c baby is hyperglycemic, it will stimulate insulin synthesis, and insulin has a negative effect on surfactant syn and will decrease its synthesis.
e. C section – b/c the baby is not delivered vaginally, there is no stress.
B/c the baby has not been stressed, the ACTH and cortisol are not released, and surfactant is not made.
Whereas a child that is delivered vaginally has a lot of stress and therefore a lot of ACTH and cortisol is being released, which stimulates surfactant release.
So, C section predisposes to RDS.
So, these are the three main causes (prematurity, diabetes, and C section).
3. Complications and associated conditions:
a. Example: why are the babies of poor glycemic control big (macrosomial)? The baby’s insulin is increased to keep the glucose down.
Insulin will increase storage of triglyceride in adipose (it increases fat storage). Where is most of the adipose located? Centrally.
So, one of the reasons why they have macrosomia is b/c insulin stimulates synthesis of TG and deposition of fat.
Also, insulin increases uptake of aa’s in muscle (like growth hormone). So, it will increase muscle mass.
So, the reason for macrosomia is increased adipose and muscle mass, both due to insulin.
This also explains why they get hypoglycemia when they are born.
The mother’s hyperglycemia is coming into the baby, causing the baby to release insulin; the moment insulin is made and the cord is cut, and no more increase in glucose, glucose goes down, and leads to hypoglycemia.
b. Superoxide free radical damage seen in retinopathy of prematurity and blindness and bronchopulmonary dysplasia.
c. Why do babies with RDS commonly have PDA? B/c they have hypoxemia. When a normal baby takes a breath, it starts the process of functional closure of the ductus.
However, with hypoxemia after they are born, it remains open, and they have a machinery murmur.
d. Hyaline membranes are due to degeneration of type II pneumocytes and leakage of fibrinogen, and it congeals to form the membrane.
So, they will give a classic history for RDS, and then will ask for the pathogenesis of hypoxemia in the baby.
This is a massive ventilation defect b/c everything is collapsing.
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This is a SHUNT problem, which leads to a massive interpulmonary shunt.
Rx=PEEP therapy – positive end exp pressure b/c these airways are collapsed and you need to get O2 into them and surfactant.
So, give O2 and at the end of expiration, pump in pressure, which keeps airways open on expiration, so you can keep O2 in them & put little of surfactant that will give good recovery rate.
Example: pic with type II pneumocyte (with lamellar bodies – look like onion, and hyperplastic arteriolosclerosis b/c they are concentrically shaped).
These lamellar bodies contain surfactant.
This would ID it as a type II pneumocyte.
They commonly give EMs of the lung with an alveolar macrophage.
Macrophage has ‘junk’ in the cytoplasm.
The type II pneumocyte is the repair cell of the lung and synthesizes surfactant.
5. EM: type II pneumocyte with lamellar bodies
B. Adult Respiratory Distress Syndrome (ARDS)
In terms of ARDS, essentially it is the same as RDS in pathophys, but is NEUTROPHIL related injury.
In RDS you’re not making surfactant b/c you are too premature or have too much insulin and just have collapsed alveoli.
BUT in ARDS its b/c you have too much inflammation; there is no inflammation in RDS.
MCC ARDS = septic shock (MCC septic shock = E coli from sepsis from an indwelling catheter; MCC DIC = septic shock).
Example: In the ICU – if a pt come in with dyspnea and its within 24 hrs of having septic shock, pt has ARDS.
If pt is in septic shock and within 48 hrs of admission and is bleeding from every orifice, he has DIC.
So, first day = septic shock, second day = ARDS, third day = DIC.
Pathogenesis: Neutrophils get into the lung in septic shock and start destroying all the cells of the lung (type I and II pneumocytes).
So surfactant production decreases and result is massive atelectasis (collapse).
However, this is neutrophil related (the neutrophils are destroying the type II pneumocyte.
The reason why they get hyaline membranes in the ARDS is b/c the neutrophils have to get in the lungs by going through the pulmonary capillaries, so they put holes in them as they get out of the bloodstream and into the lungs (this is why it is called leaky capillary syndrome).
All the protein and fibrinogen get in and produce hyaline membranes.
Therefore, you can actually see hyaline membranes in ARDS.