Renal physiology - Exam 2 Flashcards
kidney functions
- excretion of metabolic waste products: urea, creatinine, bilirubin, hydrogen
- excretion of foreign chemicals: drugs, toxins, pesticides, food additives
- secretion, metabolism, and excretion of hormones and enzymes: EPO, Vit D, Renin
- regulation of acid-base balance
- gluconeogenesis: glucose synthesis from AA
- control of arterial pressure
- regulation of water & electrolyte excretion
afferent arteriole is going →
& becomes what →
toward the nephron
glomerulus or glomerular capillaries
JGA (juxtaglomerular apparatus) regulates:
blood pressure
when blood is filtered in the glomerulus in the __ __, this favors filtration and forms __
bowman’s capsule; filtrate
structures in the renal cortex:
- bowman’s capsule
- macula densa
- proximal tubule
- distal tubule
- connecting tubule
- cortical collecting tubule
structures in the renal medulla:
loop of Henle:
- thick segment of ascending limb
- thin segment of ascending limb
- descending limb
- medullary collecting tubule
- collecting duct
filtration (“glomerular filtration”)
movement of a substance from the glomerular capillaries into the bowman’s capsule
reabsorption
tubular reabsorption, the movement of substances from the renal tubules back into the peritubular capillaries
secretion
movement of substances from the peritubular capillaries into the tubular lumens
excretion equation
excretion = filtration - reabsorption + secretion
glomerular filtration
- substances move from the blood in the glomerulus into the glomerular capsule/BC
- ** fluids and small substances (ions/glucose/urea/creatinine/small proteins) to cross over into the tubules
- ** large molecules and cells remain in the blood
- glomerular capillaries are many times more permeable than other capillaries, d/t fenestrae, tiny openings in walls (filtrations slits/podocytes)
- glomerular filtrate is formed as substances filter from the glomerulus into the glomerular capsule
first step of urine formation
glomerular filtration
favors filtration
glomerular capillary blood pressure (Pgc)
oppose filtration
fluid pressure in bowman’s space (Pbs)
osmotic force d/t protein in plasma (pie
net glomerular filtration pressure
Pgc-Pbx- plasma oncotic pressure
glomerular filtration rate (GFR)
- rate of blood flow through the glomerulus
- directly proportional to the net filtration pressure
- can be estimated using renal clearance tests
- important clinically to assess kidney health, kidney dx, and kidney failure
average adult GFR
125 mL/min or 180 L/day
blood plasma is filtered __x/day
60
renal blood flow
- high blood flow (22% of CO)
- high blood flow needed for high GFR
- oxygen and nutrients delivered to kidneys normally greatly exceeds their metabolic needs
- a large fraction of renal oxygen consumption is related to renal tubular sodium reabosrption
alterations of GFR
- plasma protein concentration affects (plasma oncotic gc)
- hydration staus of the body affects Pgc & Pbs
- urinary tract obstruction affects Pbs
- MAP affects Pgc
mechanisms responsible for keeping the GFR constant:
- autoregulation
- sympathetic regulation
- hormonal regulation
autoregulation to keep GFR constant
- myogenic regulation causes vascular changes
- tubulo-glomerular feedback (by the action of renin and angiotensin II - locally)
sympathetic regulation to keep GFR constant
vasoconstriction of afferent arteriole
hormonal regulation to keep GFR constant
-the RAAS - systemically
- *** ANP: secreted by the heart, promotes Na secretion
increase in arterial BP will be autoregulated by
constricting afferent arteriole (AA)
decrease in arterial BP will be autoregulated by
dilating afferent arteriole (AA)
aldosterone
- hormone that promotes sodium re-absorption
- secreted by adrenal cortex
RAAS typically responds to
** a decrease in BP
effects of angiotensin II
- vasoconstriction
- increased aldosterone secretion
- increased ADH secretion
- increased thirst
ADH
- anti-diuretic hormone that promotes water re-absorption
- secreted by the posterior pituitary gland
tubulo-glomerular feedback mechanism mediated by renin
1.) decrease in GFR
2.) flow through the tubule decreases
3.) flow past macula densa decreases
4.) paracrine from macular densa to afferent arteriole, and renin release causes angiontensin II formation
5.) dilation in afferent arteriole, constriction in the efferent arteriole **
6.) hydrostatic pressure in glomerulus increases
7.) GFR increases back to normal
tubular reabsorption: at PCT
- 65% of Na, H₂O, and other solute reabsorption occurs
- aldosterone (or ANP) and ADH DO NOT control Na and H₂O reabsorption respectivley
tubular reabsorption: loop of Henle
- descending limb: only permeable to water, so water reabsorption occurs
- ascending limb: only permeable to Na, so sodium reabsorption occurs
- aldosterone (or ANP) and ADH DO NOT control Na and water reabsorption respectively
tubular reabsorption: DCT and collecting duct
hormones such as aldosterone (or ANP) and ADH control Na and water reabsorption
all
*** glucose has __ reabsorption
complete
- no glucose is excreted or in the urine
- important to have glucose transporters
- this transport maximum is why untreated diabetic patients have glucose in the urine
vasa recta AKA
peritubular capillaries
- a loop-like structure similar to the loop of Henle
- helps concentrate the urine
filtrate enters the descending limb, the osmolarity of the filtrate is the __ as the osmolarity of the blood
same
that leaves the vasa recta, so they go in opposite directions
osmolarity of the filtrate __ as it goes down the descending limb
increases
b/c the descending limb only reabsorbs water
as the loop goes deeper into the medulla it becomes more
salty
b/c it is more concentrated, and this will help with the reabsorption of water
the filtrate becomes more __ in the ascneding limb
dilute
b/c the ascending limb is only permeable to Na
tubular secretion
substances move from the peritubular capillaries into the tubular lumen
tubular secretion is an important mechanism for:
- disposing of drugs and drug metabolites
- eliminating undesired substances or end products that have been reabsorbed by a passive process (urea or ureic acid)
- remove excess K
- controlling blood pH
hormonal regulation of blood (plasma) volume: Increase water intake
- increase in water intake
- decrease in plasma osmolarity (sensed by osmoreceptors in the hypothalamus)
- posterior pituitary, decreases ADH
- decrease in water reabsorption from the DCT
- increased water excreted by the kidneys
- increase in water intake
- increase in VR
- increase in atrial stretch
- increase in ANP secretion
- increase Na secretion/ decrease Na reabsorption from the DCT
- decrease water reabsorption from the DCT
- increase water excreted by the kidneys
assessing kidney function
- plasma concentration of waste products (exp. BUN & creatinine)
- urine specific gravity, urine concentration ability
- urinalysis test reagent strips (protein, glucose, etc.)
- biopsy
- albumin excretion (microalbuminuria)
- isotope renal scans
- imaging methods ( exp. MRI, PET, arteriograms, IV pyelography, US, etc.)
- clearance methods (exp. 24 hr- creatinine clearance)
clearance
- “Clearance” describes the rate at which substances are removed (cleared) from the plasma
- renal clearance of a substance is the volume of plasma completely cleared of a substance per minute by the kidneys
clearance technique
- renal clearance (Cs) of a substance is the volume of plasma completely cleared of a substance per minute
Cs = Us x V / Ps = urine exertion rate/plasma rate
Cs = clearance of substance S
Ps = plasma concentration of substance S
Us = urine conc. of substance S
V = urine flow rate
use of clearance to measure GFR
for a substance that is freely filtered, but not reabsorbed or secreted (insulin, creatinine, I-iothalamate), renal clearance is equal to GFR
use of clearance to estimate renal plasma flow
- theoretically, if a substance is completely cleared from the plasma, its clearance rate would equal renal plasma flow
- paraminohippuric acid (PAH) is freely filtered and secreted and is almost completely cleared from the renal plasma
effects of severe kyperkalemia
- > 7.0
- partial depolarization of cell membranes
- cardiac toxicity (vfib or asystole)
effects of severe hypokalemia
- < 3.0
- hyperpolarization of cell membranes
- fatigue, muscle weakness
- hypoventilation
- delayed ventricular repolarization
factors that cause Intracellular K to go outside the cell
- cell lysis
- strenuous exercise
- B-blockade
- acidosis
factors that cause extracellular K to go inside of the cell
- insulin
- aldosterone
- B- adrenergic
- alkalosis
control of cortical collecting tubule (principal cells) K⁺ secretion
- extracellular K concentration: increases secretion
- aldosterone: increases K secretion
- Na (volume) delivery: increases K secretion
acid-base status: K secretion
- acute acidosis: decreases K secretion
- chronic acidosis: increases K secretion
- alkalosis: increases K secretion
local renal mechanisms
- changes in GFR
- changes in tubular reabsorption
- changes in tubular secretion
systemic mechanisms (which can affect the whole body)
- changes in hormones
- changes in sympathetic activity
- changes in blood pressure
- changes in blood composition
buffer systems of the body
- bicarb: most important ECF buffer
- phosphate: important renal tubular buffer
- ammonia: important renal tubular buffer
- proteins: important intracellular buffers
(60-70% of buffering is in the cells)
mechanisms of hydrogen ion regulation
- body fluid chemical buffers (rapid but temporary): bicarb, proteins, ammonia, phosphate
- Lungs (rapid, eliminates CO₂)
- Kidneys (slow, powerful); eliminates non-volatile acids
- secretes hydrogen ions
- reabsorbs bicarb ions
- generates new bicarb ions
renal regulation of acid-base balance
- kidneys eliminate non-volatile acids
- filtrate of bicarb
- secretion of H
- reabsorption of bicarb
- production of new bicarb
- excretion of bicarb
kidneys conserve bicarb and excrete acidic or basic urine depending on the body’s needs
regulation of H⁺ secretion
- increased pCO₂ increases H⁺ secretion (exp. resp acidosis)
- increased extracellular H⁺ increases H⁺ secretion (metabolic or resp acidosis)
- increased tubular fluid buffers increase H⁺ secretion (exp. metabolic or respiratory acidosis)
renal compensations for acid-base disorders: acidosis
- increased H⁺ secretion
- increased bicarb reabosrption
- production of new bicarb
renal compensations for acid-base disorders: alkalosis
- decreased H⁺ secretion
- decreased bicarb reabsorption
- loss of bicarb in urine
thiazide diuretics
used to treat:
- hypertension
- edema
- renal stones (nephrolithiasis)
inhibit Na & Cl reabsorption in the tubular lumen
K sparring diuretics – mineralocorticoid receptor antagonists and Na channel inhibitors
used to treat:
- primary aldosteronism
- secondary aldosteronism
- “resistant HTN”
- HF
- HTN (na⁺ channel blockers)
loop diuretics
used to treat:
- pulmonary edema
- cirrhosis
- acute renal failure
inhibit the actions of Na, Cl, and K reabsorption and promote these to be part of the urine
can have an effect on causing K depletion
renal insufficiency
25-30% of normal GFR
renal failure
10-25% if normal GFR
- AKI, elevated BUN, creatinine, and oliguria (30mL/hr or 400mL/day); may be reversible
- chronic renal disease
- ESRD: < 10 -15% of GFR
AKI
kidney function abruptly decreases (GFR declines) over days to weeks, but may recover
CKD
kidney function (GFR) declines progressively over months to years, and is usually irreversible, but can be slowed or perhaps arrested with effective treatment
CKD: slowly developing viscous cycle
- primary kidney dx
- decrease in # of nephrons
- hypertrophy and vasodilation of surviving nephrons
- increase in glomerular pressure and/or filtration
- increase in arterial pressure
- leads to glomerular sclerosis
urinary obsruction
blockage of urine flow within the urinary tract
- obstruction can be caused by an anatomical or a functional defect: obstructive uropathy
severity of obstruction is based on
- location
- completeness
- involvement of one or both upper urinary tracts
- duration
- nature and/or cause
upper urinary tract obstruction: complications
- hydroureter: dilation of the ureters
- hydronephrosis: dilation of the renal pelvis and calyces
- ureterohydronephrosis: dilation of both the ureters and the renal pelvis and calyxes
- tubulointerstitial fibrosis: deposition of an excessive amount of extracellular matrix
- leads to excess cellular destruction and death of nephrons
compensatory hypertrophy and hyperfunction:
partially counteracts the negative consequences of unilateral obstruction
- obligatory growth
- compensatory growth
postobstructive diuresis
- it is caused by relief of the obstruction
- may cause fluid and electrolyte imbalance
kidney stones
- are also called renal calculi or urolithiasis
- masses of crystals, protein, or mineral salts form in the urinary tract and may obstruct the urinary tract
risk factors for kidney stones
- male
- most develop before 50 years of age
- inadequate fluid intake: most prevelant
- geographic location: temp, humidity, rain fall, and dietary patterns
