Major Trends for Exam 4 Flashcards
Immunity: Immune Response
What happens to blood vessels during an immune response
mast cells secrete factors that mediate this
vasodilation = ↑ vascular permeability
vasocontriction = slow down immune response/ decrease vascular permeabil
Immunity
What leads to chronic systemic inflammation?
- inflamed synovium = no physical activity = accumulation of visceral fat = macrophage infiltration
- sarcopenia
- anaemia
- type 2 diabetes mellitus
- atherosclerosis
- alzhiemer disease
Immunity
What happens to the rate of immune response after second/reexposure?
faster and stronger
Kidneys
Amount of Excreted Solute Equation
Amount Filtered - Amount Reabsorbed + Amount Secreted
[F - R + S = E]
Kidney
Net Filtration Pressure
(Pressure Forcing Out) - (Pressure Pulling In)
(CHP + BCP) - (BHP + CCP)
(Capillary Hydrostatic Pressure + Bowman’s Colloid Pressure) - (Bownman’s Hydrostatic Pressure + Capillary Colloid Pressure)
(-) = movement into blood vessel
(+) = movement out of blood vessel
Kidney
Net Filtration Pressure and GFR
↑ NFP = ↑GFP
↓NFP = ↓GFP
Kidney
Koishikowr’s Protein Concetration Effects on Kidneys
↓ concentration of protein in capillary = water attracted to proteins = more materials fall into the kidneys and more proteins are excreted
Kidneys
ANP and GFR
Myogenic Mechanism for Autoregulation
Heart working too hard = ANP released = ↑GFR
Puts Na+ in urine = water follows = ↓BP
overstretch of the heart leads to release of ANP from atria
Kidney
Nitric Oxide and GFR
Tubuloglomerular Feedback for Autoregulation
When GFR is high = less NO release = no dilation = VASOCONSTRICTION
Kidney
Afferent Constriction
Neural Autoregulation: Norepinepherine = Vasoconstriction
Due to ↑BP = ↓GFR = ↓fluid into kidney
Result: ↓BP = ↓BV
Kidney
Efferent Constriction
Neural Autoregulation: Norepinepherine = Vasoconstriction
Due to ↓BP = ↑GFR = ↑Fluid in kidneys
Result: ↑BP = ↑BV
Kidney
Myogenic Mechanism in Response to ↑BP
↑BP = ↑stretch = ↑contraction = AFFERENT VASOCONSTRICTION = ↓GFR = ↓BP
Kidney
Myogenic Mechanism in Response to ↓BP
↓BP = ↓Stretch = ↓Contraction (relaxation) = AFFERENT VASODILATION = ↑GFR = ↑BP
Kidneys
Tubuloglomerular Feedback in Response to ↑BP
↑BP = ↑GFR = ↑NaCl excretion = ↑adenosine release onto Afferent = AFFERENT VASOCONSTRICTION = ↓GFR = ↓BP
also less NO release
more adenosine = X JGA cells secrete renin = ↓ BP
Tubuloglomerular Feedback in Response to ↓BP
↓BP = ↓GFR = ↑NO release onto Afferent = AFFERENT VASODILATION = ↑GFR = ↑BP
also less adenosine release = JGA cells secrete Renin = increases BP
Neural Regulation in Response to ↓BP
only occurs if BP is extremely low
AFFERENT VASOCONSTRICTION = to get more blood flow to other organs that are higher priority = ↓GFR = vasocontriction of systemic vessels = ↑BP
JGA cells release renin to ↑BP
Kidney
Renin-Angiotensin Aldosterone System in Response to ↓BP
↓BP = JGA cells release Renin = renin cleaves into angiotensinogen = angiotensinogen I = ACE converts ANG I to angiotensinogen II =
ANG II stimulates aldosterone release = ↑Na+ release = water follows (reabsorption) = ↑BP
ANG II also stimulates ADH release = opens aquaporins in collecting duct = ↑H2O reabsoprtion = ↑BP
ANG II does EFFERENT VASOCONSTRICTION = ↑GFR = ↑reabsorption of Na+ and H2O = ↑BP
Kidney
Renin-Angiotensin Aldosterone System in Response to ↑BP
↑BP = heart releases ANP = ANP blocks ANG II function
Kidney
Clearance of X < GFR
Net Reabsorption of X
Kidney
Clearance of X > GFR
Net secretion of X
Kidney
Clearance of X = GFR
X is niether reabsobed nor secreted
Kidney
Glucose Clearance
0 mL/min
No glucose excreted
Kidney
Inulin Clearance
100 mL/min
100% inulin excreted
Kidney
Urea Clearance
50 mL/min
50% urea excreted
Kidney
Penicillin Clearance
PAH effect on Penicillin also?
150 mL/min
More penicillin is excreted than was filtered
PAH increases penicillin’s half-life
Kidney
Vasopressin/ADH
causes insertion of aquaporins channels to increase water retention and BP
Kidney
What happens if you block aldosterone release?
↑Na+ in urine & ↑K+ in blood = hyperkalemia
↑K+ = cells more excitable because closer to threshold
Kidney
Acidosis
Intercalated A Cells
HCO3- = REABSORPTION
H+ = Excretion
retain bicarb, release H+
Kidneys
Alkalosis
Intercalated B Cells
HCO3- = CREATION + EXCRETION
(Cl- exchange)
retain H+, release bicarb
Kidney
Acidocis (Respiratory)
↑PCO2 = ↑H+ = ↓pH = ↑HCO3-
Kidney
Acidosis (Metabolic)
Normal or ↓PCO2 = ↑H+ = ↓pH = ↓HCO3-
Kidney
Alkalosis (Respiratory)
↓PCO2 = ↓H+ =↑pH = ↓HCO3-
Kidney
Alkalosis (Metabolic)
Normal or ↑ = ↓H+ = ↑pH = ↑HCO3-
Digestive
Alkaline Tide
during digestion of a meal, temporary increase ↑ blood pH as H+ is released into stomach and bicarb into interstitium
Digestive
What happens to pepsin and gastric lipase under neutral duodenum pH?
they stop working
Digestive
What does exocrine pancreas release
bicarb, pancreatic enzymes, pancreatic lipase, peptidase
Digestive
What does endocrine pancreas release?
insulin
Digestive
What pH is needed to convert pepsinogen to pepsin?
1.8 - 3.5
Digestive
What pH is needed to convert pepsin to pesinogen?
greater than 3.5
Digestive
What pH is needed to constantly convert pepsin back to pepsinogen or prevent pepsin formation?
neutral pH or above
at this point pepsinogen can’t be converted to pepsin = BAD!
Metabolism
Fed State
glucose → glycogen (glycogenesis)
Metabolism
Fasted State
glucose ← glycogen (glycogenolysis)
Metabolism
alpha cells
17% of pancreatic islet cells
secrete glucagon
Metabolism
beta cells
70% of pancreatic islet cells
secrete insulin
Metbolism
delta cells
7% of pancreatic islet cells
secrete somatostatin
Metabolism
f cells
6% of pancreatic islet cells
secrete pancreatic polypeptides
Metabolism
Fed State: Insulin Dominates
↑Glucose oxidation, ↑glycogen synthesis, ↑fat synthesis, ↑protein synthesis
Metabolism
Fasted State: Glucagon dominates
↑Glycogenolysis
↑Gluconeogenesis
↑Ketogenesis
