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Respiratory Block Concept Map - Coggle Diagram

- - - - thromboxanes initiate thrombus formation hence the name thromboxane. since they are derived from prostaglandins resemble thromboxane structure except that a six membered ring includes an oxygen atom and understanding the role of thromboxane (TXA2) in clot formation it makes sense that low dose aspirin is used in prevention of secondary acute MI
    - - cox-1 is constitutively expressed in nearly all tissues while cox-2 is inducible in response to cytokines and growth factors from activated immune and inflammatory cells. both cox-1 and cox-2 block aspirin and other NSAIDs. Selective cox-2 inhibitors include Vioxx, Bextra, and Celebrex. Vioxx and Bextra have been removed from the market due to increased risk for heart attack and stroke
  - - - Ceramide + Phosphorylcholine ------ > Shingomyelin [When This Goes Wrong: Niemann-Pick Disease Type A and Type Build Up of Sphingomyelin ]
      - Ceramide + Galactose ----- > Galactocerbroside [When This Goes Wrong: Krabbe Disease or Globoid Cell Leukodystrophy]
      - Sphingosine + Fatty Acid ----- > Ceramide [Farber Disease]
      - Ceramide + Glucose ----- > Glucocerbroside [When This Goes Wrong = Gaucher Disease]
      - Ceramide + 2 or more sugars ------ > Globoside [When This Step Goes Wrong = Sandhoff's Disease and Fabry Disease]
      - Globoside and NANA ------ > Ganglioside [When This Step Goes Wrong =Tay Sachs Disease and GM1 Gangliiosidosis]
      - Sulfation of Galactocerbroside ----- > Sulfatide [When This Goes Wrong: Metachromatic Leukodystrophy]
      - Sphingolipid Degradation Below
    - - [Synthesis] The more common sites of synthesis of Phosphoglycerides include the liver, intestinal enterocytes, and type II cells in the lung. This makes intuitive sense as the liver produces bile and lipoprotein complexes. Intestinal enterocytes re-esterify biliary and dietary phospholipids during digestions and type II cells in the lung secrete pulmonary surfactant. All cells with the exception of Red Blood Cells are capable of synthesizing one or more phospholipids by using the G3P dehydrogenase enzyme. Why? Because all cells use glycolysis which produces DHAP. DHAP can be converted to Glycerol-3-Phosphate by G3P dehydrogenase. Glycerol-3-Phosphate can alternatively through multiple steps be converted to Phosphatidic Acid and then Glycerophospholipid
      - [degradation] Phospholipases break down phosphoglycerides and their name describes where they cleave the fatty acid. Phospholipase A1 cleaves the fatty acid on C1 of glycerol | phospholipase A2 cleaves the fatty acid on C2 of glycerol which is done in response to signals for the synthesis of eicosanoids | phospholipase C cleaves the phosphate group on C3 of glycerol thus hydrolyzing PIP2 to DAG and IP3
    - - Contain a vinyl ether double bound (-CH2-O-CH=CH-) which is present in higher level in the heart. This vinyl ether quenches free radicals and thus is protective against oxidative damage to lipids that sit on the plasma membrane of cells
  - - - Aspirin-Induced Asthma
      - Aspirin Preventing Myocardial Infarction
    - - Uncoupling of Phosphorylation from Electron Transfer --- FCCP, DNP, Valinomycin, Thermogenin
      - Inhibition of ATP-ADP exchange --- Atractyloside
      - Inhibition of ATP Synthase --- Aurovertin, Oligomycin, Venturicidin, DCCD
      - Inhibition of Electron Transfer --- Cyanide, Carbon Monoxide, Antimycin A, Myxothiazol, Rotenone, Amytal, Piercidin A, DCMU
- - - - Metabolic Alkalosis
      - Respiratory Acidosis
      - Respiratory Alkalosis
      - Metabolic Acidosis
- - - - Coelom extends from thoracic to pelvic cavity
      - Somatic mesoderm will form a mesothelial lining forming layers of serous membranes
      - Intra-embryonic coelom (body cavity) is lined by somatic & splanchnic mesoderm
    - - ..
        
        Mesentery of Esophagus
        
        Pleuroperitoneal Folds and Membranes
        
        Septum Transversum [Mesoderm] -------- > Central Tendon of the Diaphragm
        
        Muscular Ingrowth From Body Wall
    - - Week 16 - Week 25 [Canalicular Phase] ---- Lumina of bronchi and terminal bronchioles enlarge, increased vascularity, formation of respiratory bronchioles and a few terminal sacs
      - Late Fetal Period to Childhood ---- Mature alveoli have well-developed epithelial endothelial contacts, maximum production 2 weeks before birth
      - Week 6 --- Branching yields tertiary bronchial buds (ten on right; eight on left); these represent future bronchopulmonary segments
      - Week 36 --- Terminal sacs begin to differentiate into mature alveoli; alveoli continue to form through the 8th year
      - Week 5 --- Branching yields secondary bronchial buds (three on right; two on left); these will be future lung lobes
      - Week 4 --- Respiratory Diverticulum forms and begins to branch into left and right bronchial buds while the stem of the diverticulum begins to differentiate into trachea and larynx
      - Week 26 - birth [Terminal Sac Period | think the terminal sac phase terminates with birth] ---- Number of terminal sacs increase with thin epithelium and abundant capillaries blood air barrier, development of alveolar epithelial cells type I and II (surfactant cells. Terminal bronchioles have formed respiratory bronchioles; the surrounding mesenchyme becomes highly vascular; first terminal sacs (primitive alveoli) form | Type I Alveolar Epithelial Cells [gas exchange between blood and air possible in primitive alveoli] and Type II Alveolar Epithelial Cells [produces surfactant beginning at the end of the 6th month with the maximum production being 2 weeks before birth. For Type I think the first order of business is to make sure gas is exchanged between the blood. So Type I Alveolar Epithelial Cells take care of gas exchange. Think second order of business is to create surfactant. So Type II Alveolar Epithelial Cells produce surfactant.
      - Week 5 - Week 17 --- Pseudoglandular Phase similar to development of an exocrine gland HOW?
      - Pseudoglandular Phase [Week 5-17] -- > Canicular Phase [Week 16-25] --> Terminal Sac [Week 26 -birth] Phase --> Alveolar Phase
    - - When This Goes Wrong ---- Esophageal atresia with tracheoesophageal fistula (TEF) can occur whereby the esophageal opening is abnormal in one part of the esophagus while simultaneously the trachea and the other part of the esophagus is attached to the trachea. When only atresia of the esophagus exists this is called Pure Esophageal Atresia but when only a fistula connecting the esophagus and trachea exists this is called tracheoesophageal fistula.
        Tracheoesophageal Fistula is associated with other anomalies such a vertebral defect, anal atresia, cardiac anomalies, tracheoesophageal fistula, renal anomalies, esophageal atresia, and limb deformities
    - - Ectopic lung lobes
      - Congenital lung cysts due to dilation of terminal bronchi
      - Hypoplasia of lungs
      - Agenesis of lungs
      - Accessory lung additional respiratory buds (most common the left side) think the side with the lowest number of buds is more likley to have an abnormal addition of lung buds
      - Unilateral hypoplasia may results from posterolateral diaphragmatic herniation
  - - - Surfactant
        
        Alveolar Epithelium
        
        Basement Membrane
        
        Interstitial Space
        
        Basement Membrane
        
        Capillary Endothelium
        
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- - - - Emphysema
      - Asthma
      - Chronic Bronchitis
      - Bronchiectasis
    - - Pneumoconioses
      - Sarcoidosis
      - Idiopathic Pulmonary Fibrosis
      - Hypersensitivity Pneumonitis
      - Pulmonary Edema and ARDS make the lungs less compliant
- - - - GLUCOSE 6 PHOSPHATE
        
        GLUCOSE 1 PHOSPHATE
        
        UDP-GLUCOSE (glycogen synthase)
        
        GLYCOGEN (glycogen phosphorylase |this enzyme is present in the muscle and the liver | think Muscle for McArdle's DIsease and Hepatic for Her's | McArle's = muscle cramps on exertion, myoblobinuria, hypoglycemia on exertion [glycogen is stuck in the muscle cell] | Her's Disease = hepatomegaly and hypoglycemia [when exercising and cannot break down glycogen you have McArdle's but when fasting and cannot break down glycogen you have Her's disease NOTE glycogen can also be branched with branching enzyme and when branching enzyme is deficient then we have Andersen's Disease *think Anderson Cooper looking straight into the CNN camera when there is no branching enzyme the long straight form of glycogen is stored in the liver resulting in Cirrhosis (fatal) also remember in an analogous way
        
        GLUCOSE 1 PHOSPHATE (debranching enzyme | Cori Disease | same symptoms as von Gierke Disease since only one reaction upstream but abnormal accumulation of branched structure).| think coral reef and visualize how branched a coral reef is HOWEVER do not confuse this with Pompe Disease [named after Dr. J.C. Pompe a Dutch pathologist who discovered that this condition was due to genetic mutation resulting in glucosidase dysfunction) which is also due to a dysfunction of de-branching enzyme but specifically in lysosomes | cardiomegaly is present in the infantile-form [the infantile form simply means there is little or no enzyme] while late-onset or juvenile simply means reduced enzyme and is associated with proximal limb weakness (shoulders and hips) and progressive diaphragm weakness (the heart is not involved in late onset or juvenile) NOTE Pompe Diseasae can be categorized simultaneously as a lysosomal disease and a glycogen storage disease
        
        GLUCOSE-6-PHOSPHATE (glucose 6 phosphatase | von Gierke Disease | Accumulation G6P in liver | Hepatomegaly | Hypoglycemia | Hyperlipidemia (limited available glucose for energy lipids spill into blood stream | Hyperuricemia (limited available glucose for energy use proteins uric acid in urine)
        
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