Sweep 1.1 Flashcards

1
Q

Resting O2 consumption is

A

~250 ml/min, and the amount of dissolved O2 in the blood is less than 10% of what is needed to support basal metabolism.

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2
Q

Respiratory alkalosis

Respiratory rate faster

A

than normal or hyperventilation results in decreases in

[H+] and PCO2

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3
Q

Respiratory acidosis

Respiratory rate

A

lower than normal or hypoventilation results in increases in
PCO2 and [H+]

breath-holding is extreme hypoventilation

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4
Q

Effects of Hb on blood pH

Hb buffers

A

most of the H+ produced by the CA reaction
arterial pH = 7.4
venous pH = 7.36

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5
Q

H+ binds to —— residues on Hb, but affinity depends on ——

A

histidine

PO2

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6
Q

then in the lung, Hb releases

A

H+ to combine with HCO3- and CA reaction runs in reverse

CO2 + H2O ⇐ H2CO3 ⇐ HCO-3 + H+

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7
Q

CO2 is more —– in plasma than O2

A

soluble

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8
Q

increase Hb affinity for O2

A

à shift curve to left and Hb is saturated at a lower PO2

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9
Q

decrease Hb affinity for O2

A

à shift curve to right and Hb is less saturated for a given PO2

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10
Q

according to Vander, CO also shifts Hb-O2 dissociation curve to the

A

left (binding of CO will increase Hb’s affinity for whatever O2 is has).

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11
Q

peripheral chemoreceptors are stimulated by

A

↑ [H+] or ↓ PO2

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12
Q

central chemoreceptors are stimulated by

A

↑ [H+] in extracellular fluid in brain

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13
Q

ventilation rate increases below PO2 of about

A

60 mm Hg

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14
Q

central chemoreceptor response to

A

decrease in brain pH is primary regulator

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15
Q

Ventilation rate can be modified by

A

non-respiratory sources of H+

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16
Q

Immediate responses T

stimulate

A

ventilation –

increased dependence on anaerobic glycolysis –

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17
Q

hypoxic hypoxia or hypoxemia -

A

decreased arterial PO2

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18
Q

anemic hypoxia –

A

normal arterial PO2; decreased hemoglobin and O2 content of blood

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19
Q

ischemic hypoxia–

A

blood flow to tissues is too low

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20
Q

histotoxic hypoxia -

A

cells unable to utilize O2

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21
Q

renin – part of renin-angiotensin-aldosterone cascade to regulate

A

blood pressure

22
Q

ESRD patients have a reduced ability to

A

eliminate nitrogenous wastes (urea) and excess nitrogen is converted to ammonium. The excess ammonium has direct effects on health – the blood is alkalized which leads to an increased pH in the oral cavity.

23
Q

Contraindications for ESRD patients:

nephrotoxic drugs such as

A

tetracycline, acyclovir, aspirin, NSAIDs

24
Q

Contraindications for ESRD patients:

increased susceptibility to bleeding due to

A

destruction of platelets

25
response of the juxtaglomerular apparatus (JGA) located at the intersection of the
macula densa of distal tubule with afferent and efferent arterioles – the JGA secretes the hormone renin which regulates systemic blood pressure, and, therefore, glomerular blood flow
26
Inulin and creatinine are substances that can be used to
measure renal clearance
27
inulin –
small polysaccharide; freely filtered and not secreted or absorbed
28
creatinine –
product of muscle metabolism; freely filtered, not reasbsorbed, almost no secretion; normal creatinine levels < 1+ 0.5 mg/dl; if > 10 → requires dialysis
29
Autoregulation involves
intrinsic mechanisms that adjust bloodflow through the glomerulus; it is achieved by two primary mechanisms
30
1. myogenic mechanism –
vascular smooth muscle tends to contract when it is stretched, and relax when not stretched constriction or dilation of smooth muscle in afferent or efferent arterioles has contrasting effects on RBF
31
2. tubuloglomerular feedback –
feedback from the JGA adjusts afferent arteriole diameter and, thus, GFR
32
CA inhibitors – reduce
Na+ reabsorption; proximal tubule is major site of action
33
Loop diuretics – act in thick ascending limb to
inhibit Na+ reabsorption via the Na+ K+ 2Cl- symporter
34
Thiazides – block
Na+Cl- symporter in early distal tubule
35
K+ - sparing – two classes that both act in
late distal tubule and cortical collecting duct to inhibit sodium reabsorption AND potassium secretion
36
K+- sparing
1. aldosterone antagonists | 2. ENaC blockers
37
Aquaretics –
ADH receptor antagonists
38
Osmotic diuretics increase the osmotic pressure in the
tubular fluid, and, thus, impair Na+ reabsorption.
39
Osmotic diuretics Examples include
mannitol and pathologically elevated glucose.
40
Acetazolamide is an example of a
CA inhibitor.
41
CA inhibitors gain access to the proximal tubule via
secretion
42
Most of the diuretic effect is in the proximal tubule where ~1/3 of Na+ reabsorption relies on the
Na+/H+ antiporter
43
Diuretic effect is not large | downstream segments will increase
Na+ reabsorption when tubular Na+ increases typically increases Na+ excretion to 5-10% of filtered load
44
Loop diuretics are the most powerful of all diuretics; they inhibit
Na+ reabsorption in the ascending limb of the loop of Henle.
45
Loop diuretics | Inhibit ---------- in the thick ascending limb which inhibits -------------
Na+K+2Cl- symporter Na+ reabsorption
46
Loop diuretics | urine leaving loop is
not dilute
47
Loop diuretics | no osmotic gradient established in the
medulla interstitium so water is not reabsorbed along collecting duct → urine is dilute (500 mOsm instead of 1400 mOsm)
48
Can increase Na+ excretion to as much as
25% of filtered load, because Na+ reabsorption capacities downstream of their site of action are limited.
49
Thiazide diuretics | Thiazide diuretics like
chlorothiazide are secreted into the proximal tubules, and they act in the early distal tubule to block the Na+Cl- transporter
50
Using EPO to treat anemia in
dialysis patients | Treatment of anemia typically uses Procrit ® to stimulate erythropoiesis (rather than rely on transfusions).
51
Side effects of Procrit ® treatment include
flu-like symptoms, headaches, high BP, and cardiovascular problems