- Source of fever in atelectasis
- 2 membranes, TCA cycle in inner matrix
- Has 2 membranes, the outer membrane continuous with Rough ER.
- Inside the nucleus; has no membrane; ribosomes are made here.
- Makes protein for export, (increased in pancreatic acinar cells)
- For cytoplasmic lipid/steroid synthesis, detoxify drugs (increased in liver and adrenal cortex)
- Is 60% protein, 40% lipids
- Cholesterol increases membrane fluidity
- Calcium is released from sarcoplasmic reticulum causing muscle excitation-contraction syndrome.
- Signs: Fever, tachycardia, rigidity, acidosis, hyperkalemia.
- First sign is high end tidal CO2
- Tx: Dantrolene, inhibits calcium release and decouples excitation complex, cooling blankets, HCO3, glucose, supportive care.
- Diaphragm is 1st muscle to recover
- Neck and face muscles are last
- No basement membrane, loose cell-to-cell jxn
- Not present in muscle, bone, tendon, brain
- Rate limiting step (in liver, steroid precursor) = HMG CoA Reductase
- Go to nucleus after binding in cytoplasm of target cell.
- 36 ATP from 1 glucose (eukaryote cells) (38 in prokaryote cells)
- Anaerobic glycolysis = 2 ATP and lactate
- ↑ Activity (ACT UP): Anticonvulsants, Coumadin, and Theophylline
- ↓ Activity (DIM C): Disulfiram, INH, MAO-I, Cimetidine.
- Senses low Na/Cl, produces Renin which converts angiotensinogen to angiotensin I, which is converted to angiotensin II in the lungs by the A.C.E.
- ATII is a (potent) vasoconstrictor and ⬆ aldosterone, which keeps Na, loses K/H in urine.
- Kidney loses Ca, keeps PO4; decrease vit D 1-hydroxylation; all leads to secondary HPT
- From muscle glucose to lactate → in liver lactate to glucose
- Intermediate product in liver and muscle: Pyruvate