Kidneys

Front 1

what are the major function of the kidneys

Back 1

regulate 1homeostasis,2filters/regulates content of blood,water content,blood volume
3 concentration of electrolytes
4excretes metabolic waste like urea,uric acid,creatinine,drugs
5 endocrine functions,erythropoieten,renin,calcitrol

Front 2

what is the functional unit of kidney

Back 2

nephron-1.2mil and glomerulus filters blood

Front 3

there r 2 types of nephrons

Back 3

corticol- short loops reduce sodium reabsorption into the blood and filtrate is diluted
Juxtamedullary-long loops of henle, provide increased sodium reabsorption and filtrate is CONCENTRATED

Front 4

normal ph in urine

Back 4

5.0-6.5

Front 5

normal specific gravity

Back 5

1.010-1.020

Front 6

what is normal in urine

Back 6

sediment ,clear light yellow,few or no RBCs,normal urine contains metabolic wastes and few or no plasma proteins blood cells or glucose. produce 1.5 L of urine a day. urine LEFT STANDING MAY CONTAIN LYSED RED BLOOD CELLLS DISINTERGTING CASTS,AND RAPIDLY MULTIPLING BACTERIA.what are casts?molds of distal nephron lumen

Front 7

RBC cast in urine are due to-----, WBC cast due to -------, epitheial cells due to ---------,

Back 7

bleeding, inflammation,necrosis

Front 8

crystals in urine are what

Back 8

r uric acid,calcium oxalate,or phosphate=inflammation,infection,or metabolic disorder

Front 9

protein in urine is due to

Back 9

exercise,stress,fever,cold

Front 10

sugar in urine is due to

Back 10

emotional stress,pregnant,high CO meal

Front 11

GFR

Back 11

is the rate at which plasma is filtered as it flows thru the glomerular capillary filtration membrane---rate at which the glomuerli filters blood. NORMAL IS 125ML/MIN. or 180L/day ITS REGULATED BY THE ARTERIAL BLOOD PRESSURE AND RENAL BLOOD FLOW IN NORMALLY FUNCTIONING KIDNEYS

Front 12

Aldosterone

Back 12

PRODUCED BY-ADRNAL CORTEX, major action is regulates the reapsorption of sodium and excretion of potassium by kidneys,changes urine concentration by sodium reabsorption.
Action in the renal tube to retain sodium,conserve reabsorbtion , and increase potassium excretion

Front 13

ADH

Back 13

antidiuretic hormone that decreases the production of urine BY INCREASING REABSORPTION OF WATER. secreted by hypothalamus and stored in pituitary gland

Front 14

when is ADH is released

Back 14

if there is a decrease in blood volume or increased concentration of sodium or other substances in plasma

Front 15

What is BUN

Back 15

urea is formed in the liver, as a byproduct of protein(nitrogen waste)
normal excretion = 10-20mg

Front 16

when the bun is off this is what ocurs

Back 16

urine flows slower thru nephron,deceased renal blood flow,metabolic rate(fever/infection/trauma)
drugs=damge to kidneys
diet-high protein diet, TPN

Front 17

Creatinine

Back 17

waste product=metabolism is in the muscle which is freely filtered by the glomeruls. Is neither reabsorbed nor secreted by the renal tuble. When it is high it is directly related to nephron damage

Front 18

normal creatinine

Back 18

0.6- 1.2
2x normal=50% nephron damge
3x normal= 75% damage

Front 19

what are renal stones

Back 19

crystaalline structures made by materials the kidney normally excreted in urine

Front 20

how to prevent stones

Back 20

urine test,blood chemestries,stone analysis. FLuids-diet changes-medication-measures to change the PH

Front 21

What are the 2 types of stone pain

Back 21

colic-stretching of the ureters. move into ureters and obstruct flow.acute and intermittent. cool,clammy skin, nausea, vomiting

Front 22

Noncolicky pain

Back 22

distention of the renal pelvis or calices. Dull deep pain from to severe. pain often exaggerated by drinking lots of fluids.

Front 23

types of stones

Back 23

calcium(in blood and urine)
stuvite(form only in alkaline urine in the presecnce of bacteria that possess urease, which splits urine into ammonia and C02
uric acid stones- gout/not seen on xray and high concentraions of uric acids in the urine
cystine stones- rare, genetic, resemble stivute except that infection is unlikely to be present

Front 24

Nephrotic Syndrome

Back 24

protein wasting secondary to diffuse glomerulus damage. Marked by protein in urine,hypoalbunemia,edema, from in creased glomular permeability in the plasma protiens. causes= diseases that produce proliferative inflammatory response that decrease permeabilty of glomular cap membrane EDEMA IS KEY
complications-- open to infections,clots,renal vein clots,hyperlipidemia,liiduria

Front 25

diuretic

Back 25

promotes formation and excretion of urine
a diuretic reduces the volume in the extracellulr fluid in hypetension,edema,CHF
loop and thiazide

Front 26

polycystic renal disease

Back 26

cystic formation and hypertrophy of the kidneys which lead to rupture , infection, fibrosis and damged nephrons
autosomal dominant trait that ends in renal disease

Front 27

hydro nephrosis

Back 27

distention of renal pelvis and calyces of kidney by urine that cannot flow past an obstruction in a ureter with progressive atrophy of kidneyURINE IS STAGNANT

Front 28

WHAT CAUSES HYDRO NEPHROSIS

Back 28

tumor,stone in ureter,inflammation of prostate gland,edema from UTI
stasis of urine predisposes to an infection or stones
Surgery and removal of obstruction

Front 29

Nephritic syndrome

Back 29

caused by diseases that provoke a proliferation inflammatory response that decreases the pemeabilty of the glomular capillary mmebrane , RBCS escape into the urine and damge to cap walls from inflammtion

Front 30

What are symptoms of nephritis

Back 30

blood in urine,red cell casts,diminished GFR,azotemia,oliguria,hypertension

types are
1.acute proliferative glomerulnephrits
2.rapid progressive glomerulonenephritis
3. chronic glomerulonephritis

Front 31

Causes of nephrtis

Back 31

occurs in glomerular abnormality is the only disease present or it can be secondary condtion to disease s like diabetes or SLE

Front 32

Erythopoeiten

Back 32

glycoprotein hormone that regulaaets the differentiation in RBCs in bone marow. made in the kidneys and released in the blood in response to anoxia. stimulated by tissue hypoxia. This increases oxygen carrying capapcity in the blood.

Front 33

ABG

Back 33

measures the dissolved o2 and oxygen in the arterial blood and reveals the acid base state and how well the oxygen is being carried to the body

Front 34

respiratory failure

Back 34

cant eliminte co2 from alveoli
02 reaches the alveoli but cant be absorbed, can vntilate but cant oxygenate the pulmonry blood

Front 35

ARDS

Back 35

extravascular lung fluid, alveolar cap membrane damage, reduced complince= bc of edema and compression of terminal airways, respiratory acidosis and hypxemia

Front 36

Pnuemonia

Back 36

inflammation that stiffens the lungs, and decreases lung compiance, causes hypoxemia

Front 37

Pulmonary embolism

Back 37

clot forms in deep vein and detaches and travels to right side of the heart and then lodges in a branch of the pulmonary artery

Front 38

In copd how much 02 is given

Back 38

no more than 2l bc of long standing hypercapnia, the respiratory drive is triggered by low 02 levels rather than increased C02 like in normal lungs

Front 39

pursed breathing

Back 39

helps in maximal expiration breathing with obstructive disease like asthma by increasing airway pressure keeps passages open during exhalation

Front 40

low Pa02 arterial in ARDS

Back 40

increasing hypoxemia

Front 41

Acute tubular necrosis

Back 41

destruction of tublar epithelial cells with acute suppression of renal function. sudden failure of the kidney tubular.COMMONLY CAUSED BY AN INTERRUPTION OF BLOOD SUPPLY TO THE TUBES RESULTING ISCHEMIA

Front 42

DIFFER STAGES OF ATN

Back 42

1. ONSET-HRS TO DAYS UNTIL INJURY OCCURS
2. MAINTANENCE-DECREASE IN GFR,SUDDEN RETENTIONOF METABOLITES THAT ARE NORMALLY CLEARED BY THE KIDNEYS, FLUID RETENTION AND LOW OUTPUT
3. RECOVERY-REPAIR OF OF TISSUE TAKES PLACE AND SLOW INCREASE OF URIN OUTPUT, EDEMA
destruction of tubular epithelial cells with acute suppression of renal fnction

Front 43

causes of ATN

Back 43

ischemia of tubulars, nephotoxic effects of drugs, obstruction, toxins from massive infection, major surgery, hypovolemia,sepsis severe, trauma, and burns

Front 44

kidney failure is what

Back 44

kidneys fail to remove metabolic end products from the blood and regulate fluid,electrolyte, and ph balance of extrcellular fluid

Front 45

CHRONIC VS ACUTE

Back 45

chronic is slow to develop
acute is sudden onset and can be reversed if caught early, rapid decline in renal function

Front 46

manifestations of kidney failure

Back 46

inability to concentrate urine,hypertension,cardio issues, uremia, anemia

Front 47

diagnosis of kidney failure

Back 47

look at urine output,tests for osmoality sodium concentration and inabilty to concentrate urine

Front 48

causes of kindney failure

Back 48

conditions that cause acute shutdown in renal funciton like renal disease systemic disease urinary tract disorders