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A&P Renal RBF
| Question | Answer |
|---|---|
| ***T/F - oxygen demand in the kidneys determines blood flow | false - makes it unique; |
| Contraction and relaxation of vascular smooth muscle cells (VSMC) in the kidneys is under what controls | intrinsic and extrinsic |
| Renal blood flow estimation | 1000 ml/min |
| renal fraction equation | RF = RBF/CO |
| approximate renal fraction | 20% |
| Renal plasma flow equation (RPF) | RPF = RBF * (1-hematocrit) |
| Normal value of renal plasma flow (RPF) | 1000 * (1 - 0.4) = 600 ml/min |
| The ratio between renal blood flow with respect to total cardiac output | Renal Fraction (RF) |
| This expresses how much of the plasma that enters the kidney per minute is actually filtered into the bowmens space | Filtration fraction (FF) |
| Equation for Filtration fraction (FF) | glomerular filtration rate / renal plasma flow (GFR/RPF) |
| Normal value for FF | 20% |
| Urine flow normal value | 1ml/min |
| how much fluid is reabsorbed in the kidney | >99% |
| ***T/F - Fluid filtration is slightly greater than urine ouput | false - far greater than urine output - lots of resorption |
| T/F - oxygen consumption is greatest in the kidneys | false - only one outdoes it - the heart |
| ***T/F - the arterial-venous oxygen difference is one of the lowest | true (theres a plethora of oxygen - venous blood is only slightly lower after passing through the kidneys) |
| Oxygen consumption relative to renal blood flow is _____ | not very high |
| O2 consumption in the kidneys parallels ________ | Na resorption |
| The two big pressure drops seen in hydrostatic pressure are due to what? | the afferent and efferent arterioles |
| reducing the radius of a blood vessel (in this case the renal vessels) will do what | increase resistance, reduce flow, DIVERT TO OTHER ORGANS |
| increase in the resistance in the efferent arteriole will result in what | increased glomerular capillary pressure, increased filtration rate, decreased renal blood flow |
| dilating the efferent arteriole will result in what | decrease in glomerular capillary pressure, decrease in glomerular filtration rate, and increase in renal blood flow |
| dilating the afferent arteriol will result in what | increase in glomerular capillary pressure, increase in glomerular filtration rate, and increase in renal blood flow |
| glomerular filtration rate is primarily driven by | glomerular capillary pressure |
| Two intrinsic mechanisms that allow your kidneys to work at the same function during sleep in spite of lowered SBP | Myogenic mechanism, Tubuloglomerular feedback mechanism |
| The kidney is able to maintain blood flow in spite of the changes in MABP - what is the broad term used to describe this | autoregulation |
| the goal of autoregulation in the kidneys | keep RBF and GFR constant |
| ***autoregulation is entirely an ________ process | intrinsic (requires no metabolic component, no renal nerves, no circulating hormones) |
| autoregulation occurs within what pressures | wide range - 90 - 180 mmHg |
| ***autoregulation is exclusive to ______ (mechanism) | as a result of changes in afferent arteriole resistance |
| When autoregulation occurs, what happens to GFR and RBF | remains constant |
| With autoregulation, when arterial pressures rise, resistance _______, whereas when arterial pressure drops, resistance ______ | rises, drops |
| which patients can lose the efficiency of autoregulation | pts with cardiovascular disease |
| An intrinsic mechanism that senses stretch in smooth muscle | myogenic mechanism |
| with the myogenic mechanism, what does stretching of the muscles do | cause the smooth muscles to contract - leading to greater resistance |
| T/F - the myogenic mechanism alone is sufficient to maintain renal blood flow in a normal healthy individual | false - the other mechanism (tubuloglomerular feedback system)is needed for precise control |
| How does the tubuloglomerular feedback system work | increased flow is sensed in the macula densa cells - which then send paracrine substances - ATP and adenosine. Both of these substances bind to receptors which cause the nephron to contract - increasing resistance. Also works in reverse |
| T/F - the kidneys have sympathetic and parasympathetic innervation | false - only sympathetic |
| How does the sympathetic NS do its thing to regulate RBF and GFR | dehydration, fear, pain, etc activate -> afferent vasoconstriction? -> decreases RBF & GFR |
| T/F - sympathetic innervation can override autoregulation | true |
| AVP/ADH is a ______ factor and does what | extrinsic; causes vasoconstriction in both afferent and efferent, resulting in decreased RBF and GFR and decreased BF to renal medulla; increases water reabsorption |
| Atrial Natiuretic Peptide does what | released from atria -> target kidneys -> kidneys drop more Na -> water follows; Also causes vasodilation of the afferent arteriol & constriction of efferent -> increasing GFR & increasing or maintaining RBF |
| How is the RAS system intrinsic? | It has everything it needs to make angiotensin II by itself |
| ______ is the rate limiting step in angiotensin II formation | renin |
| RAS pathway | Angiotensinogen (liver) -> Angiotensin I (renin) -> angiotensin II (ACE from lungs) -> AT1 receptor in adrenal gland (aldosterone), kidney, brain, heart, vessels |
| what does angiotensin II do | Na retention & fibrosis (kidney), aldosterone release (adrenal gland), inotropy, chronotropy, hypertrophy, and fibrosis (heart), constriction & hypertrophy (vessels), thirst, salt appetite, vasopressin release, sympathetic activation (brain) |
| What has no effect by itself in the RAS pathway | renin, angiotensin I |
| Angiotensin II does what to the kidneys | constriction of afferent and efferent arteriols - decreased RBF, GFR; and Kf (surface area filtration), increases sensitivity to tubuloglomerular feedback |
| which is the most powerful and longest lasting vasoconstrictor in the body | endothelin (also called death peptide) |
| endothelin has what effect | constriction of afferent and efferent arteriole, leading to decrease in GFR and RBF |
| this buffers excessive vasoconstriction by angiotensin II, endothelin, and NE | Nitric Oxide, Renal Prostaglandins |
| Nitric oxide has what effect | decreases TPR (and Im guessing increased GFR & RBF?) |
| Renal prostaglandins have what effect | cause vasodilation of both AA and AE -> increases RBF & GFR |
| What inhibits renal prostaglandins | NSAIDS |
| Effects of dopamine | Vasodilation (increases RBF & GFR) |
| Vasoconstrictors (reducing RBF & GFR) | AREA - Angiotensin II, RSNA, Endothelin, AVP |
| Vasodilators (increasing RBF & GFR) | PBnND - Prostaglandins, Bradykinin, NO, Natiuretic Peptides, Dopamine (low dose) |
| Extrinsic controllers of RBF & GFR | Sympathetic NS, AVP, ANP, Dopamine |
| Intrinsic controllers of RBF & GFR | Myogenic mechanism, Tubuloglomerular feedback mechanism |
| Intrinsic and Extrinsic controllers of RBF & GFR | RAS system, Endothelin, NO2, Renal Prostaglandins, |
| why wouldnt you want to have a patient taking NSAIDS prior to sx | They inhibit prostaglandins (which counteract vasoconstrictors) - allowing stress hormones to vasoconstrict the arteriols of the kidney causing acute kidney injury |
Created by:
mmw562