Renal/fluid/electrolytes/acid/base Test

Front 1

3 types of edema and causes

Back 1

localized edema (venous or lymph obstruction). Bilateral edema isolated to legs and arms of ambulatory individual (congestive heart failure- increased capillary hydrostatic pressure). Face edema alone (hypoproteinemia- can result from liver or kidney failure)

Front 2

treatments of edema

Back 2

support socks, diuretics, elevation of affected area, aldosterone blockers, ACE blockers, blockers of angiotensin II receptors

Front 3

normal hematocrit

Back 3

42-45 for males
38-42 for females

Front 4

hypovolemia causes

Back 4

hemorrhage, draining wounds, abscesses, diarrhea, comiting, sweating, renal disease, decreased aldosterone, burns, intestinal obstruction, fever, ascites, uncontrolled diabetes mellitus

Front 5

Hypervolemia causes

Back 5

excess administration of isotonic fluids, chronic renal failure, liver disease, malnutrition, increase aldosterone when normal feedback inhibited (aldosterone or renin secreting tumor)

Front 6

hyponatremia causes

Back 6

decreased sodium intake (rarely), diuretics, adrenal failure (decreased aldosterone), water replacement after excess diaphoresis, vomiting, diarrhea, or gastrointestinal tract, aspiration; decreased fluid excretion due to renal disease, fluid therapy in patients with high ADH levels

Front 7

clinical hyponatremia

Back 7

cell swelling, muscle weakness due to decreased height of action potentials, lethary, confusion, apprehension, seizure, coma due to action potentials and brain swelling, low BP (due to poor depolarization of heart

Front 8

chronic hypernatremia and hyponatremia

Back 8

osmolites- have to correct slowly to avoid balance to CNS because so good with osmolite action

Front 9

hypernatremia causes

Back 9

impaired thirst, dysphagia, profuse sweating, watery diarrhea, polyuria of diabetes, diet (rare), kidney failure

Front 10

clinical of hypernatremia

Back 10

cells shrink, convulsions, pulmonary edema, thirst, fever, dry mucous membrane, restlessness

Front 11

normal osmolality, hematocrit, Na+ and K+ levels, Ca++ levels, Phosphate levels

Back 11

290-310 mOsm/L. 42-45 for males, 38-42 for females. 135-150 mEq/L. 3.5-5.0 mEq/L. 4.5-5.5 mEq/L. 2.5-4.5 mEq/L

Front 12

things that effect plasma [K+]

Back 12

cell death and growth, diuretic increase K+ loss, Na+ and RAAS (aldosterone increases loss), low activity of sodium/potassium ATPase (low ECF K+)(due to low Oxygen, Insulin, glucose)

Front 13

causes of hypokalemia

Back 13

decreased k+ intake, diuretic, antibiotics, GI surgery, increased aldosterone, malnutrition, trauma, burns, insulin therapy, corrected long term acidosis, acute alkalosis, hypoxia

Front 14

clinical manifestations

Back 14

nausea, vomiting, muscle weakness, cardiac arrhythmias.

Front 15

hyperkalemia causes

Back 15

large increase in uptake (hard to do), kidney failure, low sodium diet, too little aldosterone

Front 16

clinical hyperkalemianess

Back 16

muscle weakness (long refractory period), flaccid, dilated heart (""), ventricular fibrillation, nausea, vomiting, diarrhea, digital numbness and tingling

Front 17

treatment of hyperkalemia

Back 17

correct condition, oral/rectal cation exchange resins (bind K+), dialysis, Insulin and glucose injections

Front 18

three hormones w/ calcium and Phosphate

Back 18

PTH, vitamin D, Calcitonin (aldosterone, angiotensin, ADH with sodium and potassium and water)

Front 19

calcium functions

Back 19

bones and teeth, blood clotting, hormone secretion, exocytosis, cell receptor function

Front 20

hypocalcemia clinicalness

Back 20

increases Na+ into cell- increased excitability (partial depolarization), muscle cramps

Front 21

normal osmolality, hematocrit, Na+ and K+ levels, Ca++ levels, Phosphate levels

Back 21

290-310 mOsm/L. 42-45 for males, 38-42 for females. 135-150 mEq/L. 3.5-5.0 mEq/L. 4.5-5.5 mEq/L. 2.5-4.5 mEq/L

Front 22

things that effect plasma [K+]

Back 22

cell death and growth, diuretic increase K+ loss, Na+ and RAAS (aldosterone increases loss), low activity of sodium/potassium ATPase (low ECF K+)(due to low Oxygen, Insulin, glucose)

Front 23

causes of hypokalemia

Back 23

decreased k+ intake, diuretic, antibiotics, GI surgery, increased aldosterone, malnutrition, trauma, burns, insulin therapy, corrected long term acidosis, acute alkalosis, hypoxia

Front 24

clinical manifestations of Hypokalemia

Back 24

nausea, vomiting, muscle weakness, cardiac arrhythmias.

Front 25

hyperkalemia causes

Back 25

large increase in uptake (hard to do), kidney failure, low sodium diet, too little aldosterone

Front 26

clinical hyperkalemianess

Back 26

muscle weakness (long refractory period), flaccid, dilated heart (""), ventricular fibrillation, nausea, vomiting, diarrhea, digital numbness and tingling

Front 27

treatment of hyperkalemia

Back 27

correct condition, oral/rectal cation exchange resins (bind K+), dialysis, Insulin and glucose injections

Front 28

three hormones w/ calcium and Phosphate

Back 28

PTH, vitamin D, Calcitonin (aldosterone, angiotensin, ADH with sodium and potassium and water)

Front 29

calcium functions

Back 29

bones and teeth, blood clotting, hormone secretion, exocytosis, cell receptor function

Front 30

hypocalcemia clinicalness

Back 30

increases Na+ into cell- increased excitability (partial depolarization), muscle cramps

Front 31

hypercalcemia clinicalness

Back 31

decreases Na+ movement into the cell- decreased excitability, muscle weakness, increased bone fractures, kidney stones, constipation (most immediate). Either come from diet of calcium or failure of D3 (liver failure) so break down bone

Front 32

hypophosphatemia clinicalness

Back 32

osteomalacia, muscle weakness, bleeding disorders (platelet impairment), anemia, Leukocyte alterations, antacids bind phosphate

Front 33

hyperphosphatemia clinicalness

Back 33

hypocalcemia- high levels associated with low calcium levels

Front 34

compensation vs. correction

Back 34

comp- getting normal pH through renal and resp. Correction- reestablishment of normal blood pH, [bicarbonate], and [carbonic acid]

Front 35

extracellular pH and how it affects plasma potassium

Back 35

remember acute and chronic alkalosis and acidosis and how H+ push K+ out of the cell etc and how the body adjusts to chronic conditions to give overall lower or higher [K]

Front 36

renal bicarbonate buffer mechanisms

Back 36

secretion of H+ into urine and recovery of bicarbonate from urine and creation of new bicarbonate from the kidneys (primary active secretion of H+, buffering of secreted H+ by phosphate, direct production of ammonium (through glumaine breakdown), and buffering of H+ by ammonia (combine in tubule to form ammonium)

Front 37

sources of intracellular H+

Back 37

anaerobic (non-mitochondrial) metabolism of glucose (ATP hydrolysis and production through Pyruvate to Lactate production) and diabetic ketoacidosis (prominent source of H+)

Front 38

normal blood pH

Back 38

7.4

Front 39

pCO2 and HCO3- arterial blood pressures to determine acid/base status

Back 39

basic< pCO2 of 40 mm Hg<acidic
acidic<HCO3- of 24 mM<Basic

Front 40

Respiratory acidosis causes

Back 40

depression of respiratory center (drugs or head trauma), paralysis or trauma of respiratory or chest muscles, chronic pulmonary disease

Front 41

respiratory acidosis symptoms

Back 41

change in awareness and muscle control (restlessness and apprehension to lethargy and muscle twitches to coma). shallow breathing

Front 42

Respiratory Alkalosis (most common)

Back 42

caused by: O2 deficiency at high altitudes, fever, acute anxiety

Front 43

respiratory alkalosis symptoms

Back 43

dizziness, confusion, tingling in extremities, coma (late)

Front 44

metabolic Acidosis causes

Back 44

diabetic ketoacidosis, extreme prolonged exercise, renal failure, severe diarrhea

Front 45

metabolic acidosis symptoms

Back 45

headache, lethargy, coma, deep and rapid respiration (Kussmaul breathing), nausea, vomiting, diarrhea

Front 46

Metabolic Alkalosis causes

Back 46

loss of gastric juices due to vomiting or suction of stomach, excess bicarbonate ingestion or infusion

Front 47

Metabolic Alkalosis symptoms

Back 47

weakness, muscle cramps, hyperactive reflexes, respiration slow and shallow, confusion, convulsions

Front 48

pH and calcium

Back 48

acidosis increase plasma [Ca++] and leads to depression of CNS. Alkalosis decreases plasma [Ca++] and leads to hyper-excitability of CNS

Front 49

what are the hormones the Kidneys secrete?

Back 49

renin-angiotensin-aldosterone system, erythropoetin, conversion of Vitamin D to usable form

Front 50

remember weight loss reduced obesity-associated RAAS activity

Back 50

RAAS activity overactive cause adipose tissue making more of those things

Front 51

remember renin KO mice are resistant to both weight gain and insulin resistance

Back 51

doesn't produce renin, maintain insulin sensitivity and not get fat. Also have higher metabolic rate and poorly absorb and create fat

Front 52

remember reduced Ang II explains effects of Renin KO

Back 52

also, adipose expresses MR, obese adipose has more MR, blocking MR improves IS and reduces inflammation

Front 53

hydroureter

Back 53

blockage leading to dilation of ureter

Front 54

hydronephrosis

Back 54

blockage leading to dilation of the renal pelvis and calyces

Front 55

tubulointerstitial fibrosis

Back 55

deposition of excessive amount of extracellular matrix in kidneys, result of prolonged blockage

Front 56

apoptosis

Back 56

blockage can result in loss of some functioning nephrons

Front 57

compensatory hypertrophy

Back 57

counteracts negative consequences of unilateral damage- causes an increase in size of functioning nephrons in unaffected kidney (not any new nephrons)- obligatory growth- caused by somatomedins (growth factor) and compensatory growth (unknown)

Front 58

postobstructive diuresis

Back 58

transient increase in urine production after removal of obstruction

Front 59

kidney stone formation

Back 59

supersaturation of one or more salts, precipitation of salt due to pH lowering or temperature increases, growth into a stone via crystallization or aggregation. Also affected by crystal growth-inhibiting substances, particle retention, and matrix (organic material from urea metabolism of pathogens during infection)

Front 60

Kidney stone manifestation

Back 60

renal colic- pain in the flank and radiation to the groin, very mild hematuria and constipation

Front 61

acontractile detrusor with or without urethral sphincter incompetence

Back 61

damage below S1 vertebrae- bladder will not contract until super full so have problem excreting

Front 62

detrusor hyperreflexia

Back 62

damage above C2 vertebrae- bladder constantly trying to rid self of uring

Front 63

detrusor hyperrreflexia with vesicosphincter dyssynergia

Back 63

damage between C2 and S1 vertebrae- bladder trying to purge but sphincter not relaxing

Front 64

persistent UTI

Back 64

stays infected after antimicrobial therapy for >3 days

Front 65

complicated vs. uncomplicated UTI

Back 65

patient has other health problems vs. has no other health problems

Front 66

cystitis

Back 66

inflammation of the bladder. (form of UTI)
Manifestations: frequency, painful, urgent urine and lower abdominal and/or suprapubic pain

Front 67

pyelonephritis

Back 67

inflammation of ureter, renal pelvis, or renal parenchyma (form of UTI)- Chronic or acute- "drug or bug"

Front 68

pyelonephritis clinicalness

Back 68

fever, chills, frequent and painful urination, tenderness in back, bacteria in urine, white blood cell casts, bipsy reveals scarring and tissue destruction in chronic disease, repeated episodes can cause kidney failure and high urine flow

Front 69

pyelonephritis treatment

Back 69

antibiotics or anti-fungal agents, remove urinary obstruction if present, stop taking drug if drug toxicity

Front 70

nephritic sediment

Back 70

hematuria, blood cell casts

Front 71

nephrotic sediment

Back 71

proteinuria (3.5 g or more/day), lipiduria. Due to glomerular injury- find hypoalbumenia, edema, hyperlipidemia, and lipiduria)

Front 72

sediment of chronic glomerular disease

Back 72

waxy casts, granular casts

Front 73

nephrotic syndrome types

Back 73

glomerulonephritis, IgA nephropathy (Berger disease), membranous glomerulonephritis, focal and segmental glomerulosclerosis, minimal change disease (lipid nephrosis)

Front 74

glomerulonephritis

Back 74

immunoligic abnormalities, drugs or toxins, vascular disorders, systemic disease, viral causes- due to deposition of circulating soluble antigen-antibody complexes, formation of antibodies against glomerular basement membrane, and strep release of neuraminidase

Front 75

IgA nephropathy

Back 75

Berger's disease- form of acute glomerulonephritis- seen 2-3 days after URT or GI viral infection - IgA binds glomerular mesangial cells, inducing proliferation- not able to filter

Front 76

membranous glomerulonephritis

Back 76

deposition of antibodies in basement membrane- activation of immune complex- increased membrane permeability and thickening (thickening but more holes)

Front 77

focal and segmental glomerulosclerosis

Back 77

scarring of glomerulus

Front 78

minimal change disease

Back 78

lipid nephrosis- most common form in children- no glomerular changes discernible with microscope- slight structural change in epithelial cells

Front 79

nephritic syndrome

Back 79

slight proteinuria (<3.5 g/day). Hematuria (RBC casts). small pored in podocytes

Front 80

types of nephritic syndrome

Back 80

acute postinfection glomerulonephritis (2-3 weeks after strep infection- immune complexes deposits in the glomerulus- macrophage recruitment- capillary endothelial cell proliferation) and Crescentic glomerulonephritis (antiglomerular basement membrane disease or Goodpasture syndrome. Ab form against basement membrane)

Front 81

renal insufficiency

Back 81

decline to about 25% of normal GFR (our kidneys adapt so well that we don't notice inefficiency till less than 25% of function

Front 82

renal failure

Back 82

less than 10% of renal function remaining- Azotemia/Uremia

Front 83

Acute Renal Failure (ARF)

Back 83

happens w/in hours, Oliguria (low urine output), most cases reversible if treated

Front 84

types of ARF

Back 84

preprenal (most common- cause by impaired renal blood flow- renal vasocontriction, hypotension, hypovolemia, hemorrhage. GFR rate declines due to decrease in filtration pressure). Intrarenal (acute tubular necrosis is most common cause- ischemia post surgery, nephrotoxic toxin induced kidney damage- sue to some antibiotics, anesthetics, chemotherapeutics, and imaging dyes- damage to tubular epithelium). Postrenal (rare)(occurs when urinary tract obstructions affect the kidneys bilaterally- back leak)

Front 85

three stages of ARF

Back 85

initiation phase: phase where filtration is decreasing, toxicity is occurring (prevention of injury possible)
Maintenance phase: when filtration has stabilized in its still compromised state (oliguria, Azotemia- weeks to months)
Recovery phase: when renal function is re-established (diuresis)

Front 86

oliguria

Back 86

low urine output

Front 87

azotemia

Back 87

increased creatinine and urea

Front 88

chronic renal failure

Back 88

is the irreversible loss of renal function that affects nearly all organ systems (Diabetes mellitus and hypertension)

Front 89

Chronic Renal Failure Progression

Back 89

Reduced renal reserve- GFR goes to ~50%
Renal insufficiency- when symptoms first start showing
Renal failure- azotemia, acidosis (not excreting H+ and conserving HCO3-), hypernatremia, hyperkalemia, etc
End-stage renal disease (ESRD): almost no GFR

Front 90

Chronic renal failure can lead to osteoporosis because?

Back 90

kidneys are last step of Vitamin D activation, so not absorbing Ca++ w/out vitamin D

Front 91

kidney dialysis

Back 91

works by simple diffusion- takes 3-5 hours, 3 days/week