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ADV. Human Phys > Test 5 Study Guide Part 4 > Flashcards

Test 5 Study Guide Part 4 Flashcards

1
Q

right shift in oxygen dissociation curve due to low pH is called:

A

A Bohr Effect

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2
Q

temperature effect on hemaglobin oxygen unloading:

A

High temperature right shift

Low temperature left shift

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3
Q

Sickle Cell Anemia:

  • Population at risk:
  • Alternative Hemoglobin:
A
  • Population at risk:
  • Alternative Hemoglobin:
    Hemoglobin S instead of hemoglobin A
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4
Q

Sickle Cell Anemia:

  • Hemoglobin S differs in what regard:
  • Physiological effect:
A
  • 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
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5
Q

Sickle Cell Anemia:

  • Impact of elongated cells:
  • Treatment:
A
  • 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
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6
Q

Thalassemia:

- Define:

A
  • Define:

Hemoglobinopathy (like sickle cell anemia), unusual shaped RBCs

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7
Q

Myoglobin:

  • Number of hemes:
  • Dissociation curve difference:
A
  • Number of hemes:
    1 heme (1 O2 molecule)
  • Dissociation curve difference:
    Very left shifted.
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8
Q

Myoglobin:

  • Function:
  • CO poisoning:
A
  • 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
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9
Q

CO2 composition in the blood stream:

A

10% dissolved in plasma
20% bound to hemaglobin (carbaminohemeglobin)
70% as bicarbonate ion (HCO3-)

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10
Q

Law of mass action:

A

Enzymes can drive the equation either way, increased reagents drive it one way, increased reactants drive it the other way

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11
Q

Why is the pH of deoxygenated blood lower than the pH of oxygenated blood?

A

Increased CO2 in deoxygenated, drives the enzyme carbonic anhydrase to make increase H2CO3 -> H+ + HCO3-

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12
Q

Where is carbonic anhydrase located?

A

In the RBCs

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13
Q

Chloride shift:

  • Story:
  • Where does it occur:
A
  • Story:
    carbonic anhydrase -> HCO3- -> diffuses out of cell -> Cl- replaces it
  • Where does it occur:
    Systemic capillaries (where CO2 is produced)
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14
Q

How is the bohr effect achieved?

A

H+ binds to Oxyhemaglobin, increasing the chance it will release O2

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15
Q

Deoxyhemaglobin and H+:

A

Binds with greater affinity then oxyhemaglobin. Slows loss of oxygen

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16
Q

Carbonic anhydrase, the lungs, and the law mass activation:

A

low Pco2 in lungs will cause HCO3- -> H20 + CO2

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17
Q

Reverse Cl- shift:

  • Define:
  • Occurs where:
A
  • Define:
    Low Pco2 in lungs -> HCO3- -> H20 + CO2 -> Cl- replaces HCO3- in RBC
  • Occurs where:
    The pulmonary capillaries
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18
Q

Blood pH:

A

7.4 (slightly alkaline)

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19
Q

Types of acids:
Can be converted to a gas (HCO3- -> CO2 + H20)
Cannot be converted to gas
Lactic acid, fatty acid, ketone bodies

A
  • Volatile Acid:

- Non-Volatile acid:

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20
Q

Why does non-volatile/metabolic acids not normally effect pH?

A

bicarbonate buffers pH changes

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21
Q

Respiratory acidosis:

Respiratory alkalosis:

A

Hypoventilation -> CO2 -> decreased pH

Hyperventilation -> CO2 -> increased pH

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22
Q

Metabolic acidosis:

- Causes:

A
  • Causes:
    Volatile fatty acid increase
    Lower levels of bicarbonate (diarhea, loss of bicarbonate from pancreatic juices)
23
Q

Vomiting and metabolic alkalosis:

A

Vomiting loses stomach acid, loss of acid produces metabolic alkalosis

24
Q

Kidney roll in acid regulation:

A

Regulates long term levels of various acids

25
Q

Respiratory compensation for metabolic acidosis:

Respiratory compensation for metabolic alkalosis:

A

Hyperventilate (breath off CO2, decrease acid levels)
Hypoventilate
(keep CO2, increase acid levels)

26
Q

During exercise what happens to arterial blood Po2 and Pco2 levels?

A

Pco2 and Po2 stay constant.

Not mediated by normal H+ increase due to CO2 increase

27
Q

Despite high hemaglobin saturation levels what may reduce O2 transfer to tissues?

A

Linear decrease in plasma pO2, which dictates how much pO2 can be in the plasma at any given time

28
Q

Hypoxic ventilatory response:

  • Define:
  • Compensation mechanism:
A
  • 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
29
Q

How can ventilation directly try to compensate for high altitude?
What is the limit to this?

A
  • Increase tidal volume, breath out more air, removes dead air with lower O2
  • PO2 of arterial blood can never be greater then atmospheric P02
30
Q

Lung and NO in high altitude:

A

NO is produced by lungs.
Vasodilatation of pulmonary arteries
NO also binds to hemaglobin, and contributes to hypoxic drive in the medulla oblongata

31
Q

What happens to the affinity of oxygen at high altitudes:

A

it shifts right, increased oxygen unloading in tissues (but a small decrease in O2 loading in lungs)

32
Q

Acetazolamide:

A

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

33
Q

What is the ideal way to prepare for high altitude?

A

Acclimatize at progressively higher and higher base camps

34
Q

What stimuli causes increased EPO production in the kidneys?

A

Decreased O2 levels are detected

35
Q

Increased RBC counts have what downside?

A

Polycythemia produces increased vascular resistance (the blood is more viscous)
Can cause pulmonary hypertension -> ventricular hypertrophy -> heart failure

36
Q

Ideal hemaglobin level:

Level in those with chronic mountain sickness:

A

18g/dL

21 to 23 g/dl

37
Q

Change in chest associated with whole life spent at high altitude:

A

Larger chest, larger lungs

38
Q

Effect of chronic life at altitude on pulmonary capillaries:

A

More capillaries develop

39
Q

Renal pelvis:

A

All urine made enters the renal pelvis, which is a hollow cavity.
Flow from here to ureter

40
Q

Filtrate vs urine:

A

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.

41
Q

Renal Cortex:

A

Outermost layer of the kidney.

Granular in appearance due to many capillaries

42
Q

Renal Medulla:

A

Inner from the renal cortex
Striped appearance due to microscopic tubules
Composed of 8 - 15 renal pyramids separated by renal columns

43
Q

Renal Pyramid:

A

Located within the renal medulla

44
Q

Minor Calyces:

Major Calyces:

A

Renal pyramids drain into this hollow structure

It becomes this hollow structure, which leads to the renal pelvis

45
Q

Ureters, calyces and renal pelvis exhibit what type of movement?

A

Peristalsis

46
Q

Where are the pacemakers for the ureters peristalsis located?

A

Renal calyces and pelvis

47
Q

Flow of urine from minor calyces onward:

A

Minor calyces -> major calyces -> renal pelvis -> ureter -> bladder -> urethra -> outside

48
Q

Urethra:

  • Define:
  • Female:
  • Male:
A
  • 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
49
Q

Why does an enlarged prostate compress the urethra?

A

Because it flows through the prostate gland

50
Q

Muscular wall of the bladder:

  • Name:
  • Parasympathetic axons:
A
  • Name:
    Detrusor muscle
  • Parasympathetic axons:
    ACh parasympathetic innervation causes urination
51
Q 
bladder control:
Smooth muscle (not consciously controlled)
Skeletal muscle (consciously controlled)
A

Internal Urethral Sphincter:

External Urethral Sphincter:

52
Q

Exercises to strengthen external sphincter

A

Kegel exercises:

53
Q

CO2 bound to hemoglobin:

A

Carbaminohemeglobin

ADV. Human Phys (51 decks)

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