Test 5 Study Guide Part 4 Flashcards
right shift in oxygen dissociation curve due to low pH is called:
A Bohr Effect
temperature effect on hemaglobin oxygen unloading:
High temperature right shift
Low temperature left shift
Sickle Cell Anemia:
- Population at risk:
- Alternative Hemoglobin:
- Population at risk:
- Alternative Hemoglobin:
Hemoglobin S instead of hemoglobin A
Sickle Cell Anemia:
- Hemoglobin S differs in what regard:
- Physiological effect:
- Hemoglobin S differs in what regard:
Single amino acid shift within beta chains - Physiological effect:
in low Po2 hemaglobin S polymerizes, causing extended, sickle shaped cells
Sickle Cell Anemia:
- Impact of elongated cells:
- Treatment:
- Impact of elongated cells:
Reduced flexibility causes infarcts
Damaged plasma membrane = hemolysis
damaged RBCs injure vascular endothelium - Treatment:
Hydroxyurea -> gamma chains instead of beta chains -> fetal hemaglobin is used
Bone marrow transplant
Thalassemia:
- Define:
- Define:
Hemoglobinopathy (like sickle cell anemia), unusual shaped RBCs
Myoglobin:
- Number of hemes:
- Dissociation curve difference:
- Number of hemes:
1 heme (1 O2 molecule) - Dissociation curve difference:
Very left shifted.
Myoglobin:
- Function:
- CO poisoning:
- Function:
Oxygen storage
Oxygen release during oxygen deprivation (left shifted curve) - CO poisoning:
CO binds to myoglobin with more affinity then it binds to hemaglobin
CO2 composition in the blood stream:
10% dissolved in plasma
20% bound to hemaglobin (carbaminohemeglobin)
70% as bicarbonate ion (HCO3-)
Law of mass action:
Enzymes can drive the equation either way, increased reagents drive it one way, increased reactants drive it the other way
Why is the pH of deoxygenated blood lower than the pH of oxygenated blood?
Increased CO2 in deoxygenated, drives the enzyme carbonic anhydrase to make increase H2CO3 -> H+ + HCO3-
Where is carbonic anhydrase located?
In the RBCs
Chloride shift:
- Story:
- Where does it occur:
- Story:
carbonic anhydrase -> HCO3- -> diffuses out of cell -> Cl- replaces it - Where does it occur:
Systemic capillaries (where CO2 is produced)
How is the bohr effect achieved?
H+ binds to Oxyhemaglobin, increasing the chance it will release O2
Deoxyhemaglobin and H+:
Binds with greater affinity then oxyhemaglobin. Slows loss of oxygen
Carbonic anhydrase, the lungs, and the law mass activation:
low Pco2 in lungs will cause HCO3- -> H20 + CO2
Reverse Cl- shift:
- Define:
- Occurs where:
- Define:
Low Pco2 in lungs -> HCO3- -> H20 + CO2 -> Cl- replaces HCO3- in RBC - Occurs where:
The pulmonary capillaries
Blood pH:
7.4 (slightly alkaline)
Types of acids:
Can be converted to a gas (HCO3- -> CO2 + H20)
Cannot be converted to gas
Lactic acid, fatty acid, ketone bodies
- Volatile Acid:
- Non-Volatile acid:
Why does non-volatile/metabolic acids not normally effect pH?
bicarbonate buffers pH changes
Respiratory acidosis:
Respiratory alkalosis:
Hypoventilation -> CO2 -> decreased pH
Hyperventilation -> CO2 -> increased pH
Metabolic acidosis:
- Causes:
- Causes:
Volatile fatty acid increase
Lower levels of bicarbonate (diarhea, loss of bicarbonate from pancreatic juices)
Vomiting and metabolic alkalosis:
Vomiting loses stomach acid, loss of acid produces metabolic alkalosis
Kidney roll in acid regulation:
Regulates long term levels of various acids
Respiratory compensation for metabolic acidosis:
Respiratory compensation for metabolic alkalosis:
Hyperventilate (breath off CO2, decrease acid levels)
Hypoventilate
(keep CO2, increase acid levels)
During exercise what happens to arterial blood Po2 and Pco2 levels?
Pco2 and Po2 stay constant.
Not mediated by normal H+ increase due to CO2 increase
Despite high hemaglobin saturation levels what may reduce O2 transfer to tissues?
Linear decrease in plasma pO2, which dictates how much pO2 can be in the plasma at any given time
Hypoxic ventilatory response:
- Define:
- Compensation mechanism:
- Define:
entering higher altitudes lowers plasma Po2 causes hyperventilation.
Decreases Pco2 causing respiratory alkalosis. - Compensation mechanism:
Kidney’s excrete bicarbonate, causing more to be made, normalizing pH
How can ventilation directly try to compensate for high altitude?
What is the limit to this?
- Increase tidal volume, breath out more air, removes dead air with lower O2
- PO2 of arterial blood can never be greater then atmospheric P02
Lung and NO in high altitude:
NO is produced by lungs.
Vasodilatation of pulmonary arteries
NO also binds to hemaglobin, and contributes to hypoxic drive in the medulla oblongata
What happens to the affinity of oxygen at high altitudes:
it shifts right, increased oxygen unloading in tissues (but a small decrease in O2 loading in lungs)
Acetazolamide:
In the family of Carbonic anhydrase inhibitor
Causes excretion of HCO3- -> More to be made -> increases pH -> increases ventilation -> helps compensate for high altitude sickness
What is the ideal way to prepare for high altitude?
Acclimatize at progressively higher and higher base camps
What stimuli causes increased EPO production in the kidneys?
Decreased O2 levels are detected
Increased RBC counts have what downside?
Polycythemia produces increased vascular resistance (the blood is more viscous)
Can cause pulmonary hypertension -> ventricular hypertrophy -> heart failure
Ideal hemaglobin level:
Level in those with chronic mountain sickness:
18g/dL
21 to 23 g/dl
Change in chest associated with whole life spent at high altitude:
Larger chest, larger lungs
Effect of chronic life at altitude on pulmonary capillaries:
More capillaries develop
Renal pelvis:
All urine made enters the renal pelvis, which is a hollow cavity.
Flow from here to ureter
Filtrate vs urine:
Filtrate: exists in the renal cortex and renal medulla. This fluid is still being processed.
Urine: exists once the filtrate enters the renal pelvis, no more processing.
Renal Cortex:
Outermost layer of the kidney.
Granular in appearance due to many capillaries
Renal Medulla:
Inner from the renal cortex
Striped appearance due to microscopic tubules
Composed of 8 - 15 renal pyramids separated by renal columns
Renal Pyramid:
Located within the renal medulla
Minor Calyces:
Major Calyces:
Renal pyramids drain into this hollow structure
It becomes this hollow structure, which leads to the renal pelvis
Ureters, calyces and renal pelvis exhibit what type of movement?
Peristalsis
Where are the pacemakers for the ureters peristalsis located?
Renal calyces and pelvis
Flow of urine from minor calyces onward:
Minor calyces -> major calyces -> renal pelvis -> ureter -> bladder -> urethra -> outside
Urethra:
- Define:
- Female:
- Male:
- Define:
Where the urine exits the bladder - Female:
shorter, wider urethra. More likely to get urinary tract infections - Male:
Longer narrower, prostate gland enlargement can cause problems
Why does an enlarged prostate compress the urethra?
Because it flows through the prostate gland
Muscular wall of the bladder:
- Name:
- Parasympathetic axons:
- Name:
Detrusor muscle - Parasympathetic axons:
ACh parasympathetic innervation causes urination
bladder control: Smooth muscle (not consciously controlled) Skeletal muscle (consciously controlled)
Internal Urethral Sphincter:
External Urethral Sphincter:
Exercises to strengthen external sphincter
Kegel exercises:
CO2 bound to hemoglobin:
Carbaminohemeglobin
