Renal / Urology - Anatomy/Physiology (pre-clinical) Flashcards
(48 cards)
Function of afferent arteriole, efferent arteriole, and glomerulus
Blood enters glomerulus via afferent arteriole, gets filtered by yhe glomerulus, then filtrate-depleted blood exits glomerulus and goes back into circulation (via efferent arteriole)
3 main holistic functions of the renal system
- Filtration - removal of metabolic products and toxins from the blood for excretion
- Regulation - of fluid balance (BP), electrolyte imbalance, and acid-base balance (pH)
- Production/Activation - of hormones involved in erythrogenesis, Ca2+ metabolism, and the regulation of blood pressure (RAAS)
Functions of kidney
- Maintains blood volume (through excretion or retention of fluid)
- maintains concentration of ions within blood
- maintains pH of blood (acid-base balance) - modulation of hydrogen ions and bicarbonate
- produces glucose by gluconeogenesis - usually minimal contribution to glucose production, except when fasting where glucose production increases
- activates vitamin D –> controls calcium and phosphorus metabolism
- excretes metabolic waste (urea + creatinine, water-soluble drugs, toxins)
- renin production (RAAS system)
- new RBC production (EPO)
Describe this graph
- GFR is determined by the net filtration pressure across the glomerular capillaries
- blood flow is proportional to changes in pressure - ie. increased blood flow = increased pressure
How is renal blood flow controlled?
- Increased/Decreased afferent/efferent arteriolar resistance has effects on renal blood flow and net ultrafiltration pressure
Glomerular haemodynamics
Name 2 mediators of renal blood flow that cause vasoconstriction + how they work
- Sympathetic nerves (‘fight or flight’)
- norepinephrine released –> causes increased resistance of both afferent/efferent arterioles
- this causes a decreased in renal blood flow and GFR
- this prevents fluid loss
. - RAAS (angiotensin II)
- ANG II constricts both afferent/efferent arterioles, but works with prostaglandins to constrict efferent > afferent
- this maintains GFR when renal perfusion is low
Name 2 mediators of renal blood flow that cause vasodilation + how they work
- Prostaglandins
- dampen renal vasoconstrictor effects (esp. on afferent arterioles)
- therefore, prevents severe/harmful vasoconstriction and renal ischaemia
. - Natriuretic peptides (ANP and BNP)
- ANP and BNP released by heart in response to increased blood pressure
- causes vasodilation of afferent > efferent arterioles
- this increases renal blood flow and GFR
- (ANP also inhibits secretion of renin, therefore decreases ANG II lvls)
Why is autoregulation of renal blood flow in response to systemic BP important and what are the 2 processes involved?
- to maintain renal blood flow and GFR within narrow limits, despite changes in mean material pressure (BP)
.
1. Myogenic response - afferent arterioles can constrict/relax in response to BP –> helps prevent excessive increases in RBF and GFR when systemic BP increases/decreases
-
eg. BP increases –> afferent arteriole constricts –> increased afferent arteriolar resistance –> decreased RBF –> decreased GFR –> maintained RBF/GFR (no excessive increase)
.
2. Tubulo-glomerular feedback mechanism - increase in arterial pressure (BP) increases filtration (GFR) and therefore Na+ and Cl- in proximal tubule
- increase in Na+ ions is sensed by macula densa cells of the JGA
- macula densa cells then release paracrine agents which triggers contraction of nearby vascular smooth-muscle cells in afferent arteriole
- this increases afferent arteriolar resistance, which decreases GFR, counteracting the initial increase in GFR
Glomerular filtration VIDEO
https://www.youtube.com/watch?v=9A2dAyWyK6o
Which of the following would cause the greatest decrease in GFR in a person with otherwise normal kidneys?
- Decrease in renal arterial pressure from 100 to 80 mmHg
- 50% increase in proximal tubular sodium reabsorption
- 50% decrease in afferent arteriolar resistance
- 50% decrease in efferent arteriolar resistance
- 5 mmHg decrease in Bowman’s capsule pressure
50% decrease in efferent arteriolar resistance
- causes a substantial decrease in GFR
(a decrease in renal arterial pressure from 100 to 80 mmHg would only cause a slight reduction in GFR because of autoregulation)
(the other options would tend to increase GFR)
Net contribution by the kidneys to whole-body glucose production is minimal (<10%) except under conditions of ________ , when they can contribute up to 30% to 40%.
fill in the blank
Net contribution by the kidneys to whole-body glucose production is minimal (<10%) except under conditions of prolonged fasting, when they can contribute up to 30% to 40%.
Which of the following, compared with normal, might you expect to find 3 weeks after a patient ingested a toxin that caused sustained impairment of proximal tubular NaCl reabsorption? Assuming no change in diet or ingestion of electrolytes.
- No change in GFR, no change in afferent arteriolar resistance
- Decreased GFR, increased afferent arteriolar resistance
- Increased GFR, increased afferent arteriolar resistance
- Increased GFR, decrease afferent arteriolar resistance
Decreased GFR, increased afferent arteriolar resistance
- impairment of proximal tubular NaCl reabsorption would increase NaCl delivery to the macula densa, which in turn would cause a tubuloglomerular feedback-mediated increase in afferent arteriolar resistance (the increased afferent arteriolar resistance would decrease GFR)
Which mediator acts to selectively modulate the sympathetic vasoconstrictive effects on the afferent arterioles to prevent sustained damage?
- Brain natriuretic peptide
- Prostaglandin
- Angiotensin II
Prostaglandin
A selective decrease in efferent arteriolar resistance would ______ glomerular hydrostatic pressure, ______ GFR, and ______ renal blood flow.
insert increase or decrease
A selective decrease in efferent arteriolar resistance would decrease glomerular hydrostatic pressure, decrease GFR, and increase renal blood flow.
What is an acid?
What is a base?
What is a weak acid?
What is a buffer?
- Acid –> H+ donor (fully dissociates into H+ ions in water
- Base –> H+ acceptor
- Weak acid –> only partially dissociates into hydrogen ions (H+) when dissolved in water
- Buffer (buffered solution) –> weak acids or weak bases (addition of acid or base does not affect pH of solution)
- Disturbances of HCO3 are primary _________ disorders.
- Disturbances of CO2 are primary __________ disorders.
- Disturbances of HCO3 are primary metabolic disorders.
- Disturbances of CO2 are primary respiratory disorders.
Arterial pH for:
- Acidemia
- Alkalemia
- Acidemia - arterial pH <7.35
- Alkalemia - arterial pH >7.45
Renin Angiotensin Aldosterone System - Video
Dr Matt and Dr Mike: https://www.youtube.com/watch?v=ibjodC7Ft7U
What cells in the afferent arteriole release renin?
Juxtaglomerular cells (granular cells) - baroreceptors
Name 3 ways in which renin is stimulated to be released (triggers)
- Drop in BP in afferent arteriole (renal perfusion) - detected by juxtaglomerular cells (baroreceptors)
- Drop in Na+ concentration in DCT - detected by macula densa cells (chemoreceptors)
- Increased sympathetic NS innervation - fight or flight response
.
(note: macula densa cells and juxtaglomerular cells are connected by connective tissue)
(sympathetic NS directly innervates the juxtoglomerular (granular) cells to release renin)
Where is the majority of sodium (Na+) reabsorbed back into the body?
Proximal tubule of the kidney - 65%
Describe the process of how angiotensin II is produced.
- Renin is released by kidney
- Angiotensinogen is released by liver into the bloodstream
- Renin converts angiotensinogen into angiotensin I
. - Lungs produce ACE
- ACE converts angiotensin I into angiotensin II
What are the functions of angiotensin II?
- Generalised vasoconstrictor - increases BP
- Constricts smooth muscle of efferent arteriole - increases filtration rate (GFR) which increases Na+ in DCT –> -ve feedback loop
- Stimulates adrenal cortex to release aldosterone - aldosterone increases Na+ reabsorption into the body –> wherever sodium goes, water follows –> increases BV –> increases BP
- Stimulates release of ADH from posterior pituitary gland (hypothalamus) - ADH travels to DCT and collecting ducts, and increases water reabsoprtion –> increases BV –> increases BP