ch 9 renal system text

kidneys 3 primary sections

cortex - glomeruli and capillaries, most of proximal tubules and arteries

medulla - collecting ducts, pyramids, most blood vessels and distal tubules

pelvis

vital functions of kidneys

maintain fluid concentration

regulate electrolyte concentration

detoxify blood

eliminate wastes

regulate blood pressure - renin

regulate acid-base balance - acid and base

regulate release of excess potassium into urine

RBC production - erythropoietin

produce part of vitamin D

hormone control kidneys based on

osmoreceptors responding to changes in osmolality - ionic or solute concentration of a solution

hormones in kidney fluid balance

ADH- made by pituitary gland, works at collecting duct of nephrons

aldosterone- made by adrenal cortex, works at distal tubule of nephrons

ADH

antidiuresis

stops water loss from body

stimulates collecting duct to reabsorb water back into bloodstream

renin-angiotensin-aldosterone system RAAS

key regulator of fluid and blood pressure

RAAS step 1

when kidney senses low perfusion due to hypovolemia it secretes renin

RAAS step 2

renin stimulates liver to secrete large protein angiotensinogen

RAAS step 3

angiotensinogen is broken down in circulation into angiotensin I

RAAS step 4

essential enzyme angiotensin-converting enzyme ACE transforms angiotensin I into angiotensin II

RAAS step 5

angiotensin II stimulates arterial vasoconstriction which raises BP

angiotensin II also stimulates adrenal gland to secrete aldosterone

aldosterone

produced and released by adrenal cortex but works in kidney

causes reabsorption of sodium and water into bloodstream at distal tubule of nephron- raises blood volume and blood pressure

stimulates secretion of potassium from bloodstream into distal tubules

kidney other important hormones

calcitriol

erythropoietin

renin

calcitriol

assists with converting vitamin D to its active form

erythropoietin

stimulates RBC production

renin

helps regulate blood pressure through RAAS

kidneys concentrate urine through

countercurrent exchange system in nephron’s loop of Henle

loop of Henle countercurrent exchange

reabsorbs water from tubule fluid

releases waste products into tubule fluid

to regulate acid-base balance kidneys

secrete hydrogen ions

reabsorb sodium and bicarbonate ions

acidify phosphate salts

produce ammonia

acidosis occurs at

pH below 7.34

alkalosis occurs at

pH above 7.45

kidneys collect and eliminate wastes step 1

glomerular filtration

glomeruli, collection of nephron capillaries, filter blood flowing through them to form filtrate

kidneys collect and eliminate waste step 2

tubular reabsorption

tubules reabsorb filtered fluid into surrounding blood vessels

kidneys collect and eliminate waste step 3

tubular secretion

filtered substance aka glomerular filtrate passes through tubules to collecting tubules and ducts and eventually becomes urine

clearance

complete removal of a substance from blood

creatinine

muscle breakdown product that needs to be almost completely cleared from blood and excreted into urine

serum creatinine is used to measure

how well kidneys are clearing creatinine from bloodstream

glycosuria

in diabetes mellitus excess glucose in blood overwhelms renal tubules and causes glucose to appear in urine

proteinuria

when glomeruli are damaged protein appears in urine because large protein molecules pass into urine by a damaged glomerulus

kidneys help regulate blood pressure by producing and secreting the enzyme

renin

in response to decreased perfusion of kidney usually due to hypovolemia

angiotensin II raises low arterial blood pressure levels by

increasing peripheral vasoconstriction

stimulating aldosterone secretion by adrenal gland

two essential functions of aldosterone

sodium and water reabsorption into blood raises blood volume and blood pressure

aldosterone enhances excretion of potassium at distal tubule of nephron

hypertension can stem from

fluid and electrolyte imbalance

RAAS hyperactivity

hypertension can

damage blood vessels

cause hardening of kidneys - nephrosclerosis a leading cause of chronic renal failure

kidneys secrete erythropoietin when

oxygen in blood drops/hypoxia

active vitamin D helps regulate

calcium and phosphorus balance

bone metabolism

calcium and phosphate have an

inverse relationship in blood

renal osteodystrophy

osteoporosis from kidneys unable to activate vitamin D leading to hypocalcemia and hyperparathyroidism from PTH activating bone to release calcium

renal disorders

acute kidney injury AKI

acute tubular necrosis

glomerulonephritis

hydronephrosis

kidney disease, chronic (chronic renal failure)

renal calculi aka kidney stones aka nephrolithiasis

urinary tract infection UTI, pyelonephritis aka kidney infection, urosepsis

acute kidney injury AKI aka acute renal failure

sudden interruption of renal function

if untreated permanent damage can lead to chronic renal failure

prerenal failure results from

conditions that diminish blood flow to kidneys

prerenal failure can also be termed prerenal azotemia

which means excessive nitrogenous wastes in blood

increased blood urea nitrogen BUN

intrarenal failure aka intrinsic renal failure

results from damage to filtering structures of kidneys usually from acute tubular necrosis, kidney infection, autoimmune disease, or nephrotoxic substances

postrenal failure results from

obstruction of urine outflow as in nephrolithiasis, prostatic hyperplasia, prostate cancer, or bladder outlet obstruction due to tumor

with treatment AKI three distinct phases

oliguric - decreased urine output

diuretic - increased urine output

recovery - glomerular filtration rate normalizes

oliguric phase AKI

2 weeks - several months

oli