Sweep 1.1 Flashcards
Resting O2 consumption is
~250 ml/min, and the amount of dissolved O2 in the blood is less than 10% of what is needed to support basal metabolism.
Respiratory alkalosis
Respiratory rate faster
than normal or hyperventilation results in decreases in
[H+] and PCO2
Respiratory acidosis
Respiratory rate
lower than normal or hypoventilation results in increases in
PCO2 and [H+]
breath-holding is extreme hypoventilation
Effects of Hb on blood pH
Hb buffers
most of the H+ produced by the CA reaction
arterial pH = 7.4
venous pH = 7.36
H+ binds to —— residues on Hb, but affinity depends on ——
histidine
PO2
then in the lung, Hb releases
H+ to combine with HCO3- and CA reaction runs in reverse
CO2 + H2O ⇐ H2CO3 ⇐ HCO-3 + H+
CO2 is more —– in plasma than O2
soluble
increase Hb affinity for O2
à shift curve to left and Hb is saturated at a lower PO2
decrease Hb affinity for O2
à shift curve to right and Hb is less saturated for a given PO2
according to Vander, CO also shifts Hb-O2 dissociation curve to the
left (binding of CO will increase Hb’s affinity for whatever O2 is has).
peripheral chemoreceptors are stimulated by
↑ [H+] or ↓ PO2
central chemoreceptors are stimulated by
↑ [H+] in extracellular fluid in brain
ventilation rate increases below PO2 of about
60 mm Hg
central chemoreceptor response to
decrease in brain pH is primary regulator
Ventilation rate can be modified by
non-respiratory sources of H+
Immediate responses T
stimulate
ventilation –
increased dependence on anaerobic glycolysis –
hypoxic hypoxia or hypoxemia -
decreased arterial PO2
anemic hypoxia –
normal arterial PO2; decreased hemoglobin and O2 content of blood
ischemic hypoxia–
blood flow to tissues is too low
histotoxic hypoxia -
cells unable to utilize O2
renin – part of renin-angiotensin-aldosterone cascade to regulate
blood pressure
ESRD patients have a reduced ability to
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.
Contraindications for ESRD patients:
nephrotoxic drugs such as
tetracycline, acyclovir, aspirin, NSAIDs
Contraindications for ESRD patients:
increased susceptibility to bleeding due to
destruction of platelets
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
Inulin and creatinine are substances that can be used to
measure renal clearance
inulin –
small polysaccharide; freely filtered and not secreted or absorbed
creatinine –
product of muscle metabolism; freely filtered, not reasbsorbed, almost no secretion; normal creatinine levels < 1+ 0.5 mg/dl; if > 10 → requires dialysis
Autoregulation involves
intrinsic mechanisms that adjust bloodflow through the glomerulus; it is achieved by two primary mechanisms
- 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
- tubuloglomerular feedback –
feedback from the JGA adjusts afferent arteriole diameter and, thus, GFR
CA inhibitors – reduce
Na+ reabsorption; proximal tubule is major site of action
Loop diuretics – act in thick ascending limb to
inhibit Na+ reabsorption via the Na+ K+ 2Cl- symporter
Thiazides – block
Na+Cl- symporter in early distal tubule
K+ - sparing – two classes that both act in
late distal tubule and cortical collecting duct to inhibit sodium reabsorption AND potassium secretion
K+- sparing
- aldosterone antagonists
2. ENaC blockers
Aquaretics –
ADH receptor antagonists
Osmotic diuretics increase the osmotic pressure in the
tubular fluid, and, thus, impair Na+ reabsorption.
Osmotic diuretics Examples include
mannitol and pathologically elevated glucose.
Acetazolamide is an example of a
CA inhibitor.
CA inhibitors gain access to the proximal tubule via
secretion
Most of the diuretic effect is in the proximal tubule where ~1/3 of Na+ reabsorption relies on the
Na+/H+ antiporter
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
Loop diuretics are the most powerful of all diuretics; they inhibit
Na+ reabsorption in the ascending limb of the loop of Henle.
Loop diuretics
Inhibit ———- in the thick ascending limb which inhibits ————-
Na+K+2Cl- symporter
Na+ reabsorption
Loop diuretics
urine leaving loop is
not dilute
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)
Can increase Na+ excretion to as much as
25% of filtered load, because Na+ reabsorption capacities downstream of their site of action are limited.
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
Using EPO to treat anemia in
dialysis patients
Treatment of anemia typically uses Procrit ® to stimulate erythropoiesis (rather than rely on transfusions).
Side effects of Procrit ® treatment include
flu-like symptoms, headaches, high BP, and cardiovascular problems
