Pathophys Exam 3

main functions of the kidneys

filters blood, removes waste/toxins, regulate water/electrolytes, maintain acid base balance

what are the two main regions of the kidney

cortex and medulla

functional unit of the kidney

nephron

two major nephron types

cortical and juxtamedullary nephrons

which neuron type is most important for concentrating urine

juxtamedullary neuron

what forms the renal corpuscle

glomerulus and bowmans capsule

what is the function of the glomerulus

filters blood to create filtrate

what is the order of filtrate flow through the nephron

proximal convolated tubule (PCT) to the loop of Henle to the distal convolated tubule (DCT) to the collecting duct

what three cell types make up the juxtaglomerular apparatus (JGA)

macula densa cells, juxtaglomerular cells, extraglomerular mesangial cells

what is the function of the juxtaglomerular apparatus

regulates blood pressure, renal blood flow, and GFR

what do juxtaglomerular cells produce

renin

what does the macula densa detect

sodium chloride conentration in the distal tubule

what triggers renin release from the macula densa pathway

decreased NaCl delivery

what is the role of mesangial cells

strucutural support and blood flow regulation

what is the function of peritubular capillaries

reabsorption of water, ions, and nutrients into blood

what is the function of the vasa recta

maintains the meduallary osmotic gradient through countercurrent exchange

why is the loop of Henle called a countercurrent multiplier

fluid flows in opposite directions while salt transport multiples the medually osmotic gradient

why does water leave the descending limb

presence of aquaporin channels are present

what transprter is found in the thick ascending limb

Na+/K+/2Cl- co-transporter

what are the three major steps of urine formation

filtration, reabsorption, secretion

what is glomerular filtration

movement of water and solutes form blood into nephron filtrate

what is tubular reabsorption

movement of substances from filtrate back into blood

what is tubular secretion

movement of substances from blood into filtrate

what happens in the ascending loop of Henle

Na+ and Cl- leave the filtrate, diluting tubular fluid

what ions are secreted in the distal convoluted tubule

K+ and H+

what ions are reabsorbed in the distal convoluted tubule

Na+, Cl-, and HCO3-

what substances must be heavily reabsorbed to maintain homeostasis

Na+, Ca2+, glucose, and amino acids

what common waste products are secreted into filtrate

creatinine, urea, ammonia, frugs, and K+

how do kidneys regulate pH

by secreting/reabsorbing H+ and HCO3-

which system responds fastest to acid-base disturbances

buffer systems (seconds-minutes)

which system responds slowest to acid-base disturbances

kidneys (hours-days)

what does RAAS regulate

blood pressure, blood volume, electrolyte balance, vascular resistance

what are the three major components of RAAS

renin, Angiotensin II, Aldosterone

what stimulates renin release

decreased renal perfusion, decreased NaCl delivery, increased sympathetic activity

what is produces from prorenin

renin

what are the major causes of chronic kidney disease

diabetes mellitus and hypertension

difference between acute kidney injury and chronic kidney disease

acute kidney injury is sudden and often reversible; chronic kidney disease is chronic and progressive

what is diabetic nephropathy

kidney damage caused by diabetes that may lead to ESRD

what are hallmark findings of diabetic nephropathy

persistent albuminuria and declining GFR

what causes diabetic kidney damage

hyperglycemia causing oxidative stress, inflammtion, fibrosis, podocyte injury, and GBM thickening

what are the three major lesions of diabetic nephropathy

mesangial expansion, GMB thickening, arteriolar hyalinization

what is one of the earliest pathological changes in diabetic nephropathy

hyperfiltration

what injury causes proteinuria in diabetic nephropathy

hyperfiltration

what injury causes proteinuria in diabetic nephropathy

podocyte injury

main treatments for diabetic nephropathy

glycemic control, ACE inhibitors, ARBs, GLP-1 receptor agonists

where is ADH produced and released

produced in the hypothalamus and released from the posterior pituitary

what is the primary function of ADH

increase water reabsorption by the kidneys

where does ADH act in the nephron

late distal tubule and collecting duct

how does ADH increase water reabsorption

inserts aquaporin channels into principal cells

when is ADH secretion increased

during hydration and hypovolemia

what stimulates renin release

decreased renal arterial pressure, decreased NaCl delivery to the macula densa, and reduced afferent arteriole strech

name three conditions that increase renin release

hemorrhage, aortic constriction above renal arteries, and renal artery stenosis

which nephron strucutre detects reduced sodium chloride delivery

macula densa

what is the major vascular effect of Angiotensin II

vasoconstriction

how does angiotensin II affect blood pressure

increases total peripheral resistance and blood pressure

how does angiotensin II affect sodium and water balance

increases sodium and water reabsorption

what hormone release is stimulated by angiotensin II

aldosterone

what is aldosterone produced

adrenal cortex (zona glomerulosa)

what is aldosterone’s major effect on the kidney

increased sodium reabsorption and water retention

what receptor does aldosterone bind to

mineralocorticoid receptor

what is hypovolemia

decreased circulating blood volume

how does the kidney respond to hypovolemia

increases ADH secretion and activates RAAS

why is ADH beneficial during hypovolemia

conserves water and helps restore blood volume

what defines POTS

heart rate increase >30 bpm within 10 minutes of standing without major BP drop

what defines orthostatic hypotension

significant decrease in blood pressure within 3 minutes of standing

who typically develops POTS

younger women and adolescents

who typically develops orthostatic hypotension

older adults

common symptoms of POTS

tachycardia, dizziness, fatigue, brain fog, palpitations

common symptoms of orthostatic hypotension

lightheadedness, weakness, visual dimming, syncope

what is polycystic kidney disease

genetic disorder causing multiple fluid-filled cysts in the kidneys

why is polycystic kidney disease considered a form of CKD

gradually reduces kidney function and may lead to kidney failure

major complications of polycystic kidney disease

hypertension, kidney failure, and vascular abnormalities

what causes polycystic kidney disease

gene mutations, usually inherited

two major forms of polycystic kidney disease

autosomal dominant polycystic kidney disease and autosomal recessive polycystic kidney disease

what gene is most commonly affected in autosomal dominant polycystic kidney disease

PKD1

common symptoms of polycystic kidney disease

hypertension, flank pain, hematuria, enlarged kidneys, headache, kidney stones, UTIs

is there a cure for autosomal dominant polycystic kidney disease

no

what medication can slow cyst growth

tolvaptan

how does tolvaptan work

blocks vasopressin receptors, reducing aquaporin insertion and water reabsorption

why is vasopressin important in polycystic kidney disease

vasopressin promotes cyst growth

what is the most common cause of renovascular hypertension

renal artery stenosis due to atherosclerosis

other causes of renovascular hypertension

fibromuscular dysplasia, artery compression, artery infarction, artery dissection

is renovascular hypertension primary or secondary hypertension

secondary hypertension

what initiates renovascular hypertension

decreased renal perfusion

what system becomes activated

RAAS

what happens to renin-producing cells with prolonged ischemia

their numbers increase

classic clues of renovascular hypertension

early-onset severe hypertension, worsening hypertension, declining kidney function, pulmonary edema

first line medications for renovascular hypertension

ACE inhibitors and ARBs

what do ACE inhibitors and ARBs do

block Angiotensin II effects, causing vasodilation and sodium/water excretion

what procedure is often used for fibromuscular dysplasia

percutaneous angioplasty

major complications of uncontrolled renovascular hypertension

renal failure, MI, stroke, CHF, LV hypertrophy, pulmonary edema, retinopathy

why are diuretics used in kidney disease

recuced fluid overload, edema, hypertension, and electrolyte accumulation

in what syndrome are diuretics used to treat massive edema from protein loss

nephrotic syndrome

where do loop diuretics work

thick ascending limb of the loop of henle

what transporter do loop diuretics block

Na+/K+/2Cl- co-transporter

why are loop diuretics considered powerful

cause significant diuresis and natriuresis

where do thiazide diuretics work

distal convoluted tubule

what transporter do they inhibit

sodium-chloride transporter

why can loop and thiazide diuretics cause hypokalemia

increased sodium delivery to distal nephron increases potassium secretion

how does aldosterone contribute to hypokalemia

increases potassium and hydrogen ion excretion