His tidal volume was 500 mL. End-expiratory was +5 cm and end-inspiratory was +25. We were supposed to use the difference in airway pressure, and not the end-inspiratory pleural pressure (+20).

Compliance = ΔV/ΔP = 500 / 20 = 25 mL/cm H2O

Basement membrane integrity is the determinant of full lung recovery following pulmonary insult.

Summary:

(1) loss of basement membrane integrity is critical in determining the “point of no return,” and contributes to the inability to reestablish normal lung architecture with promotion of fibrosis;

(2) loss of epithelial cells, endothelial cells, and basement membrane integrity in usual interstitial pneumonia associated with idiopathic pulmonary fibrosis leads to destroyed lung architecture and perpetual fibrosis;

(3) transforming growth factor-β is necessary, but not entirely sufficient, to promote permanent fibrosis;

(4) persistent injury/antigen/irritant is critical for the propagation of fibrosis;

(5) idiopathic pulmonary fibrosis is an example of a process related to the persistence of an “antigen(s),” chronic inflammation, and fibrosis; and

(6) unique cells are critical cellular players in the regulation of fibrosis.

citation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/

Basement membrane integrity is the determinant of full lung recovery following pulmonary insult.

Summary:

(1) loss of basement membrane integrity is critical in determining the “point of no return,” and contributes to the inability to reestablish normal lung architecture with promotion of fibrosis;

(2) loss of epithelial cells, endothelial cells, and basement membrane integrity in usual interstitial pneumonia associated with idiopathic pulmonary fibrosis leads to destroyed lung architecture and perpetual fibrosis;

(3) transforming growth factor-β is necessary, but not entirely sufficient, to promote permanent fibrosis;

(4) persistent injury/antigen/irritant is critical for the propagation of fibrosis;

(5) idiopathic pulmonary fibrosis is an example of a process related to the persistence of an “antigen(s),” chronic inflammation, and fibrosis; and

(6) unique cells are critical cellular players in the regulation of fibrosis.

citation: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2645241/

Here’s another very nice one that superimposes the pathway onto a simplified brainstem drawing (nice for the anatomical relations):

https://webeye.ophth.uiowa.edu/eyeforum/cases-i/case252/Fig2-INO-LRG.png

Source article:

https://webeye.ophth.uiowa.edu/eyeforum/cases/252-internuclear-ophthalmoplegia.htm

To see even more, try google image search on “medial longitudinal fasciculus”:

https://www.google.com/search?q=medial+longitudinal+fasciculus&tbm=isch

1) Superficial (first-degree) = Epidermis ~ presents as red skin without blisters

2) Superficial partial thickness (second-degree) = Extends into superficial (papillary) dermis ~ Presents with redness with clear blister & blanches with pressure

3) Deep partial thickness (second-degree) = Extends into deep (reticular) dermis ~ presents as yellow or white skin with less blanching. May be blistering.

4) Full thickness (third-degree) = Extends through entire dermis ~ presents as stiff and white/brown skin. No blanching.

5) Fourth-degree = Extends through entire skin, and into underlying fat, muscle and bone ~ presents as black skin; charred with eschar

1) Superficial (first-degree) = Epidermis ~ presents as red skin without blisters

2) Superficial partial thickness (second-degree) = Extends into superficial (papillary) dermis ~ Presents with redness with clear blister & blanches with pressure

3) Deep partial thickness (second-degree) = Extends into deep (reticular) dermis ~ presents as yellow or white skin with less blanching. May be blistering.

4) Full thickness (third-degree) = Extends through entire dermis ~ presents as stiff and white/brown skin. No blanching.

5) Fourth-degree = Extends through entire skin, and into underlying fat, muscle and bone ~ presents as black skin; charred with eschar

Tanner stages start at TEN years old

Stage I:

• I is flat, as in flat chest;
• I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

• 2 balls (testicular enlargement)
• 2 hairs (pubic hairs now appearing)
• 2 breast buds form

Stage III (3): starts at 13 y/o

• If you rotate 3, it looks like small breasts (Breast mounds form);
• If you squiggle the III they look like curly+coarse pubic hair
• Increased penis length and size can be represented by: II --> III
  (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

• First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
  MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
• The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

• V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
• 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

Tanner stages start at TEN years old

Stage I:

• I is flat, as in flat chest;
• I is alone, as in no sexual hairs.

Stage II (2): stage II starts at 11 y/o (II look like 11)

• 2 balls (testicular enlargement)
• 2 hairs (pubic hairs now appearing)
• 2 breast buds form

Stage III (3): starts at 13 y/o

• If you rotate 3, it looks like small breasts (Breast mounds form);
• If you squiggle the III they look like curly+coarse pubic hair
• Increased penis length and size can be represented by: II --> III
  (your penis was thin II but now its thicker III)

Stage IV (4): starts at 14 y/o

• First imagine: The I in IV represents the thigh, and the V in IV looks like the mons pubis between your legs:
  MEANING: you have hair in mons pubis (V) but you have a border detaining the hair from growing into thighs.
• The V is pointy, as in now the breasts are pointy (raised areola or mound on mound)

Stage V (5): 15 y/o

• V has no borders detaining hair from growing into thighs (pubic hair + thigh hair)
• 5 fingers(as in hands) flattening the areolas when grabbing them (areola flatten at this stage and no more "mound on mound")

This more likely to be diuretics rather than laxatives b/c

the lab study shows a renal dysfunction (BUN & Creatinine are elevated)

Most likely the patient abused loop diuretics; also knows to cause contraction alkaloids, along with renal problems such as interstitial nephritis

Premie has no surfactant

Angiotensin II - generated in hypovolemia

Dipalmitoyl lecithin aka dipalmitoylphosphatidylcholine lung surfactant

Phosphatidylinositol 4,5-bisphosphate aka PIP2 Gq receptor pathway

Phosphatidylserine -involved in intrinsic apoptosis when exposed on extracellular surfaces

Sphinogmyelin - composes myelin and also has roles in signal transduction, apoptosis. Lecithin: Sphingomyelin ratio >2 indicates mature fetal lungs.

The damage is in the L midbrain in the area affecting the corticospinal tract. Because it is in the midbrain, decussation in the pyramids (medulla) so it will show ipsilateral dysfunctional motor signs.

Photo of midbrain and important areas: shorturl.at/myHLR

Swelling of the cell (e.g., hydropic degeneration): tissue ischemia → decreased ATP production → decreased Na+/K+ ATPase and Ca2+pump activity → diffusion of Na+ and water into the cell → cellular swelling

Swelling of the cell (e.g., hydropic degeneration): tissue ischemia → decreased ATP production → decreased Na+/K+ ATPase and Ca2+pump activity → diffusion of Na+ and water into the cell → cellular swelling