Exam #3 - still need to learn

what does the nephron contain

glomerulus

what does the glomerulus do

filter blood

what do you need to consider if GFR decreases

end-organ damage

signs and symptoms of end organ damage

decreased urine, alterations in mental status, glucose abnormalities

where is the primary site of urine concentration

juxtamedullary nephrons

what age does normal physiological aging of kidneys begin

40

why does the glomerulus require hydrostatic pressure

to force fluids and solutes into Bowman’s capsule

what is the movement of fluid through the glomerular capillaries determined by

capillary hydrostatic pressure

capillary colloidal osmotic pressure

capillary permeability

what does the glomerular filtration rate (GFR) tell you

how well the kidneys are working

what is transported in the tubules by passive transport

water and urea

no energy required

what is transported in the tubules by active transport

sodium, potassium, chloride, calcium, phosphate, urate, glucose, amino acids

need energy → if body doesn’t have energy it cannot filter these things causing abnormalities

what does a countercurrent system do?

increase osmolality by promoting exchange of solutes between the adjunct tubules of the loop of Henle and the vasa recta

what does antidiuretic hormone do?

regulates the ability for kidneys to concentrate urine

where is ADH secreted

posterior pituitary gland

what is ADH secretion stimulated by

increase in serum osmolality (increased sodium), changes in BP or blood volume

what happens to water when ADH is present

water is returned to the circulatory system from the tubules

what happens to water when ADH is absent

water is excreted in urine

what is the kidneys function other than getting rid of wastes

regulation of pH

what do high uric acid levels in urine cause

kidney stones

what happens to drugs not bound to plasma proteins

go through glomerulus and eliminated by kidneys

what system do drugs use in the kidneys to be eliminated

same transport as uric acid → if lots of drugs in the system uric acid may build up causing kidney stones

endocrine functions of kidneys

renin-angiotensin-aldosterone system

erythropoietic synthesis

calcium homeostasis

how is the glomerular filtration rate measured

with timed blood and urine tests

what is creatinine

a byproduct of creatine metabolism

what is the estimated GFR (eGFR)

accounts for lifestyle → “what is normal”

what does prostaglandin cause

vasodilation

explain the RAAS system

hypotension causes the body to release renin which converts angiotensinogen in the liver to angiotensin I which goes to the lungs and converting enzyme converts it to angiotensin II. Angiotensin II causes the secretion of aldosterone which causes an increase in sodium reabsorption and thus water reabsorption as well as vasoconstriction to raise BP

other than hypovolemia what may happen with thiazide and loop diuretics

electrolyte abnormalities like hyponatremia and hypokalemia

what are the two most damaging effects of urinary obstruction

stasis of urine

progressive dilation of collecting ducts and tubules

what does the stasis of urine cause in urinary obstruction

infection and stone formation

what does the progressive dilation of collecting ducts and tubules cause in urinary obstruction

destruction and atrophy

what does hydronephritis mean

urine-filled dilation of the renal pelvis and calices

what does hydronephritis cause

progressive atrophy of the kidney d/t urine outflow

usually unilateral

what are the manifestations of hydronephritis

can be asymptomatic for days

pain d/t distention of the collecting ducts and renal capsule

oliguria → anuria → renal failure

• this can cause complete bilateral obstruction

HTN d/t renin release

how is hydronephritis diagnosed

US

CT

UA

treatment of hydronephritis

depends on the cause

urinary stone removal

infection management

pain management

supportive therapies

fluid administration → prevents AKI

what is the most common cause of an upper urinary tract obstruction

renal calculi

what are the types of pain you can have with a renal calculi

colicky or noncolicky pain based off the anatomical position of the calculi

colicky pain

stretching of tube causes sudden severe pain, NV

noncolicky pain

dull, deep ache in the flank or back that is exaggerated with excess fluid intake

how do you diagnose a renal calculi

US

XR

UA
CT

treatment of renal calculi

supportive therapies to manage pain, treat infection and fluids for hydration

if larger than 5 mm → surgery

what causes a renal calculi

increase in blood and urine levels of stone components and interactions among components

anatomic changes

metabolic and endocrine influences

dietary and intestinal factors

UTIs

types of renal calculi

calcium (most common)

uric acid → associated with obesity

what is the second most common infection in the older adult

urinary tract infection

what does the urine look like in someone with a UTI

cloudy and foul-smelling

what kind of pain is present in UTIs

lower-abdominal or back discomfort

flank pain

who is at risk for a UTI

females

people with multiple sexual partners

older adults → hygiene issues

prior UTI

changes in vaginal flora

urinary obstruction and reflex

neurogenic bladder

postmenopausal women

men with prostate disorders

urinary catheterization

what is tubulointerstitial disorders

inflammation of tubules

where do tubulointerstitial disorders affect

renal tubular structures, specifically the proximal and distal tubules

why do fluid and electrolyte imbalances occur in tubulointerstitial disorders

inability to concentrate urine

acidification of urine

diminished tubular reabsorption

what is acute pyelonephritis

upper UTI that has spread to kidneys

risk factors for acute pyelonephritis

Dm, catheterization, pregnancy, neurogenic bladder

manifestations of acute pyelonephritis

abrupt onset of fever and chills

costovertebral angle (CVA) tenderness → flank area

dysuria

abdominal pain with NV

what is the manifestation triad of acute pyelonephritis

fever, NV, dysuria

what is the treatment of acute pyelonephritis

antibiotics for 10-14 days

IV hydration

pain management

antiemetics

what affects the kidneys ability to tolerate renally toxic meds

renal function, hydration status, BP, urine pH

how does kidney damage occur in drug related nephropathies

it is due to a decrease in renal blood flow, obstructing urine flow, damaging the structures, and hypersensitivity reactions

what can cause acute prerenal failure

diuretics, contrast media, immunosuppressants

what is acute renal injury (AKI)

rapid decline in function within hours to days

what is azotemia with AKI

accumulation of nitrogenous wastes in blood which decreases GFR and impairs fluid and electrolyte balance

what is the most common AKI

prerenal

why does a prerenal AKI occur

decrease in renal blood flow d/t

• severe depletion of vascular volume

• impaired perfusion d/t HF and cardiogenic shock

• decreased vascular filling in anaphylaxis or shock

• toxins, drugs, mediators

what are the clinical manifestations of a prerenal AKI

sharp decrease in urine output

increase in BUN and creatinine

what is the compensatory mechanism of prerenal AKI

fractional excretion of sodium (FENa) < 1%

tries to preserve vascular volume by not excreting sodium

what does an intrarenal AKI result from

damage to structures within the kidney

causes of an intrarenal AKI

ischemia d/t prerenal AKI

toxic insult to tubules in nephrons (diuretics)

intratubular obstruction

acute glomerulonephritis

acute pyelonephritis

during intrarenal AKI a decrease of glomerular filtration and epithelial injury occurs d/t

intrarenal vasoconstriction

decreased hydrostatic pressure in glomeruli

changes in arterial tone

decreased capillary permeability

increased tubular hydrostatic

backflow of glomerular filtrate

what is postrenal AKI a result from

obstruction of urine outflow from kidneys causing retrograde pressure which damages nephrons

phases of a postrenal AKI

onset (hours to days)

oliguric (anuric) (8-14+ days)

diuretic

recovery

what occurs during the onset phase of a postrenal AKI

time from onset until tubular injury occurs

oliguric (anuric) phase of postrenal AKI

marked decrease in the GFR causing retention of urea, potassium, sulfate and creatinine → may cause HTN, hyperkalemia, and uremia

diuretic phase of a postrenal AKI

kidneys try to heal and urine output increases, but tubule scarring and damage occurs

levels of retained metabolites may continue to rise

recovery phase of a postrenal AKI

tubular edema resolves and renal function improves

BUN, creatinine, and GFR return to normal

how do you diagnose an AKI

observe urine output and characteristics

blood tests of creatinine, BUN, and GFR

how do you treat an AKI

balanced fluid resuscitation

prevent and treat infection

hemodialysis or continuous renal replacement therapy (CRRT) for more severe AKIs

what is chronic kidney disease (CKD)

loss of function in the nephrons due to damage

what are two main causes of CKD

HTN and DM

what are the indicators used for renal function

GFR → best (decreased in CKD)

albuminurea

azotemia in CKD

accumulation of urea happens first

BUN levels rise as CKD progresses

uremia in CKD

alters fluid, electrolyte ,and acid-base balance

alters regulatory functions like BP, erythropoiesis, and Vit. D synthesis

can cause uremic encephalopathy (mental status altered d/t increased urea), peripheral neuropathy, pruritus

weakness, fatigue, nausea → extreme weakness, frequent vomiting, lethargy, confusion → coma, death

ECF volume regulation in CKD

eliminating or conserving sodium and water

may need potassium supplements

what occurs with potassium in CKD

can retain it causing heart issues

what occurs with pH in CKD

elimination of H+ and regeneration of HCo3- can cause metabolic acidosis

what happens with calcium and phosphorus in CKD

d/t PTH release bone calcium is reabsorbed causing hypocalcemia and hyperphosphatemia

what occurs due to impaired Vit. D synthesis in CKD

can develop hyperparathyroidism d/t direct suppressive effect on PTH

how does CKD affect cardiovascular disease

10-20x greater in people with CKD

how does CKD create HTN

increased vascular volume

increase of peripheral vascular resistance

decreased renal vasodilator prostaglandins

increased activity of the RAAS

when does pericarditis come about in CKD

stage 5 CKD

how does CKD cause heart disease

left ventricular hypertrophy → heart failure

ischemic heart disease → cardiomyopathies

what GI changes occur due to CKD

anorexia, NV, and metallic taste due to uremia

uremic encephalopathy

altered mental status and motor function disturbances

what occurs with peripheral neuropathies

lower limbs > upper limbs

uremic toxins cause atrophy and demyelination of nerve fibers

how does azotemia and uremia in CKD affect immune function

decrease immunity

decreased granulocyte count

impaired humoral and cell-mediate immunity

defective phagocyte function

what skin changes occur with CKD

pale due to anemia

dry skin and mucous membranes

pruritus → itchy

thin and brittle fingernails

what needs to be treated and avoided to prevent CKD progression

risky conditions like HTN and DM

avoid renally toxic meds

what needs to be restricted in the diet with CKD

protein, sodium, potassium, phosphorus, and fluid

what is the dialysis that is hooked up to a machine

hemodialysis

what are the 3 parts of hemodialysis

dialysis fluid, dialyzer, blood delivery system