Pathophysiology EX3 - Renal

6 functions of the kidney

1. f/e balance
2. acid/base maintenance
3. removes water-soluble nitrogenous wastes (BUN, creatinine, etc)
4. helps control BP (RAA system)
5. maintains RBC levels (releases erythropoietin in response to hypoxia)
6. activates vitamin D

what is the functional/parenchymal unit of the kidney?

nephron!!!

3 components of urine formation

1. filtration
2. reabsorption
3. secretion

where does filtration start?

glomerulus

where does blood enter the glomerulus? exit?

enters through the afferent arteriole and exits through the efferent arteriole

afferent vs efferent arteriole - WHICH IS BIGGER AND WHY?

afferent, because it creates the pressure needed to filter the blood

difference between filtrate and plasma?

filtrate does NOT contain any IMPORTANT things our body needs, such as proteins, RBCS, and WBCs, as we do not want to excrete these

what types of things are in filtrate?

water, electrolytes, wastes (anything our body does not need)

glomerular filtration (2 types of cells that sit along basement membrane?)

1. glomerular capillary cells
2. Bowman's capsule epithelial cells

glomerular filtration - bowman's capsule cells stand up away from the membrane on what? which does what?

stand away from membrane via PSEUDOPODS, which provide space between the epithelium and blood vessel

glomerular filtration - fluid filters across the membrane between what?

pseudopods of the bowman's capsule epithelial

what is considered a good GFR?

125cc/min

after blood goes through glomerulus, what structure does it encounter next?

proximal convoluted tubule

which structure is responsible for reabsorption and secretion? why is this structure important?

vasa recta; makes it possible for kidney to reabsorb/secrete ions/water/other components in most perfect amounts possible to ensure our blood is as perfect as possible

reabsorption - definition

when water, electrolytes, amino acids, glucose, acid/base elements are returned to the BLOOD

secretion - definition

the FINAL adjustment; when components that were brought back into the blood LEAVE the blood and are excreted in urine

where does secretion occur?

distal convoluted tubule

juxtaglomerular apparatus - composed of what 2 cells?

1. juxtaglomerular cells
2. macula densa cells

juxtaglomerular apparatus - juxtaglomerular cell (function)

senses the stretch being put on by AFFERENT arteriole, initiating kidney to secrete renin, starting the RAA system (low blood volume/BP in afferent arteriole will start this system)

juxtaglomerular apparatus - macula densa cells (function)

adjust GFR when the concentration of sodium in blood entering the kidney is at an abnormal level (too high, GFR increases to let it out faster)

renin release - stimulated by what 2 things?

1. decreased BP
2. increased urine Na+

RAA system (steps)

1. renin converts angiotensinogen to angiotensin I
2. angiotensin I meets with ACE in lungs to created angiotensin II, which is a strong vasoconstrictor that also helps conserve fluid in the body
3. angiotensin II also stimulates the release of aldosterone

aldosterone (functions)

1. reabsorbs Na+ and water into the blood, INCREASING BLOOD VOLUME
2. excretes K+, DECREASING SERUM POTASSIUM

ADH - what stimulates its release?

hypothalamus senses increase in osmolality (blood is becoming hypertonic)

ADH - what it does?

makes the collecting duct MORE permeable to water, meaning water is reabsorbed from initial urine filtrate back into the body

atrial natriuretic peptide vs. B-type natriuretic peptide

ANP - made by overstretched atria
BNP - made by overworked ventricles

ANP and BNP (BOTH cause what?)

cause the kidneys to STOP reabsorbing Na+ and water (working against ADH), making them get lost in the urine

ANP and BNP (effects on blood volume, stretch/workload of heart)

ALL DECREASE!!!

why would someone with severe renal disease have anemia?

kidney can't properly filter out blood, therefore releasing unhealthy RBCs back into vascular space

why would a patient with severe renal disease have weak bones?

calcium is taken from bones as a result of kidneys not functioning to maintain proper calcium levels

gold standard for detecting kidney failure? what is also a good indicator?

gold standard = serum creatinine (should be about 1mg/dL)
-BUN is the other indicator

pyelonephritis

infection of the kidney pelvis and parenchyma (where filtration, reabsorption, and secretion are taking place)

ACUTE pyelonephritis - what type of bacteria is usually associated? (+/-)

gram negativ

acute pyelonephritis - what can it lead to? (WORST ENDGAME)

sepsis, as the bacteria can get into the blood

acute pyelonephritis - treatment?

antibiotics

acute pyelonephritis - 4 symptoms

chills, fever, headache, back pain

CHRONIC pyelonephritis - what happens during it?

progressive process where the kidney is trying to heal itself in a place of chronic inflammation, leading to scar tissue; chronic inflammatory process creates obstruction, which prevents healing and promotes the inflammatory process even more

cystic disease of the kidney

deals with the development of fluid/urine filled sacs in weakened areas of the tubules of the kidney

cystic disease of the kidney - characterized by what 2 things?

urinary stasis and infections

simple cystic disorder (does it affect renal function?)

NOPE

acquired cystic disorders (result of what?)

hemodialysis

medullary cystic disease (another name)

sponge kidney

medullary cystic disease (specifically affects what part of the kidney?)

collecting ducts

hydronephrosis (results from what?)

the dilation of renal tubules/tract due to cysts

hydronephrosis

the expansion of the kidney with urine, due to the cysts that have formed in the tubules of the kidney

hydronephrosis - what it leads to ? what does this cause?

compartment syndrome, which compresses the blood vessels inside the kidney, causing renal ischemia

stasis of urine (increases risk for what 2 things?)

1. infection
2. development of kidney stones (renal calculi, urolithiasis)

3 theories for renal calculi development

1. saturation theory
2. matrix theory
3. inhibitor theory

renal calculi - saturation theory

urine is supersaturated with stone components, encouraging the formation of stones

renal calculi - matrix theory

organic materials in kidney act as a nidus (a starting place) for stone formation

renal calculi - inhibitor theory

patient has a deficiency of substances that inhibit stone formation

overall, renal calculi cause what?

OBSTRUCTION of urine flow

4 types of kidney stones

1. calcium stones
2. struvite stones
3. uric acid stones
4. cystine stones

what is the most common type of kidney stone?

calcium (oxalate) stones

struvite stones and uric acid stones (what do they have in common)?

BOTH happen as a result of specific metabolic disorders, such as gout

cystine stones (how does one get these?)

GENETICALLY

5 general (noninvasive) treatments for renal calculi

1. increase fluids to flush stone out
2. decrease Calcium intake (avoid eating chocolate, nuts, spinach)
3. drugs to bind Ca+ oxalate in the gut
4. diet changes to inc/dec pH of urine
5. thiazide diuretics to decrease Ca+ excretion (decrease urine calcium)

3 invasive methods of kidney stone removal

1. lithotripsy
2. ureteroscopic removal
3. open removal

lithotripsy

breaking up the stone via the use of sound waves

ureteroscopic removal

going up into the ureter and into the kidney in an attempt to snag the stone to remove it

open removal

opening up the kidney to pull the stone out (surgical)

UTI (how do they usually come into the kidney?)

from the bladder

4 defenses hosts have against UTIs

1. washout phenomenon
2. protective mucus in bladder, ureters, and urethra
3. local immune responses and IgA (macrophages)
4. normal bacterial flora (keep bad bacteria down)

washout phenomenon

the flushing out of bacteria every time we urinate

ureteral reflux

backflow of urine from the bladder into the kidneys

glomerulonephritis (description)

occurs when there is IMMUNE damage to the glomerulus

2 types of glomerulonephritis

1. type 2
2. type 3

type 2 glomerulonephritis

antibodies are created AGAINST the glomerular proteins themselves

type 3 glomerulonephritis

antigen-antibody complexes get lodged into tissue of the glomerulus and cause damage

why is it important to treat strep infections right away? (hint: think glomerulonephritis)

group A b hemolytic strep infections MAY lead to subsequent immune damage to the kidneys (glomerulonephritis)

during glomerulonephritis, the glomerulus is exposed to what?

inflammatory mediators

why does proteinuria and hematuria result from glomerulonephritis?

glomerulus is not working right, making it more permeable to things that our body is SUPPOSED TO KEEP (RBCs, proteins, etc)

glomerulonephritis - loss of plasma proteins yields what? why?

periorbital edema, as our blood becomes HYPOTONIC due to lack of plasma proteins, causing the fluid to go out to the tissues

oliguria (what is it?)

decreased urine output

oliguria - causes what 2 things?

1. sodium and water retention
2. hypertension (more fluid I hold on to, higher the BP)

glomerulonephritis (3 treatments)

1. drugs (diuretics, antihypertensive, anti-inflammatory)
2. sodium restriction diet
3. MAY need ultra-filtration or hemodialysis

4 elements of nephrotic syndrome

1. edema
2. hyperlipidemia
3. hypercoagulability
4. decreased immune competence

nephrotic syndrome - what is it?

collection of symptoms that are caused by glomerular disease

nephrotic syndrome - edema (why?)

fluid retention and protein loss (fluid moves into interstitial space/tissue from vascular space)

nephrotic syndrome - hyperlipidemia (why?)

cholesterol production is increased (by liver) to balance the plasma protein loss

glomerulonephritis vs. nephrotic syndrome

glomerulonephritis = disease process
nephrotic syndrome = collection of symptoms BECAUSE of glomerulonephritis

nephrotic syndrome - hypercoagulability (why?)

altered levels of clotting factors (usually excess are secreted in urine, but due to decreased urine, factor concentration builds up)

nephrotic syndrome - decreased immune competence (loss of which 2 things)

1. globulin
2. albumin

nephrotic syndrome - decreased immune competence (loss of globulin results in what?)

decrease of antibodies and complement proteins

nephrotic syndrome - decreased immune competence (loss of albumin results in what?)

inability to respond to drugs/hormones

globulin (function)

used to make antibodies and complement proteins

albumin (function)

binds and carries drugs and hormones

Acute Kidney injury (caused by what 3 things?)

1. prerenal
2. intrinsic (intrarenal)
3. postrenal

prerenal AKI

decreased blood supply to kidney, causing ischemia (can result from shock, dehydration, hypertension, etc)

intrinsic (intrarenal) AKI

kidney tubule function is decreased, due to ischemia, toxins, aminoglycosides, organic solvents, myoglobin in blood

postrenal AKI

urine flow is blocked, causing back flow into the kidneys, leading to stones, tumors, enlarged prostate (won't allow urine to pass)

4 phases of AKI

1. initial phase
2. oliguric phase
3. diuretic phase
4. recovery phase

AKI - initial phase

starts from event that caused it to symptoms (hours to days), which include decreased urine output, buildup of creatinine/BUN

2 things that control progression of AKI

1. extend of the damage
2. how long this damage has been there

AKI - oliguric phase

when urine output is decreased, and toxins build up (days to weeks); may even progress to anuric; may need HD, while also hoping kidney is healing itself

AKI - diuretic phase

kidney is repairing itself; phase where we see urine output again; BUT kidney still not functioning correctly, causing us to lose lots of water; normal saline IV may be ordered

AKI - recovery phase

when kidney is repaired and returned back to normal function

hemodialysis

blood is run through semipermeable tubules of machine, of which is surrounded by dialysate; particles from blood will move into dialysate via simple diffusion; dialysate is hypertonic, meaning it will pull water out of the blood

why is it significant that dialysate can be adjusted?

we can provide the person with the perfect amount of electrolytes/water that are good for functioning

a-v fistula (where is blood pulled from?)

vein