Monday Reassement Review

Front 1

platelets increase when ?

Back 1

inflammation
or if the pt had a splenectomy (reason being that platelts are removed form the blood via the spleen, so not having a spleen means and increase in platelets)
thrombocytosis or thrombocythemia

Front 2

platelets decrease when?

Back 2

there is a decreased production due to vitamin B12/folic acid deficiency or if there is a leukemia (cancer of the blood) or if there is sepsis (blood infection)

or can be due to increased destruction

or medication induced (heparin, chemo)

Front 3

monocytes increase?

Back 3

cancer, infection, autoimmune disorder

Front 4

monocytes decrease?

Back 4

chemotherapy, corticosteroids, bacterial toxins

Front 5

eaosinophils increase?

Back 5

medication/drug induced allergic reaction, parasite infection

Front 6

eosinophils decrease when?

Back 6

cushings syndrome, acute stress, corticosteroids

Front 7

basophils increase?

Back 7

allergic reaction, histamine reaction, hypothyroid

Front 8

basophils decrease/

Back 8

infection, acute hypersensitivity reaction, hyperthroidism

Front 9

neutrophils increase when?

Back 9

infection, stress, trauma, inflammation, steroids will also increase the % of neutrophils

Front 10

neutrophils decrease when?

Back 10

chemotherapy, bone marrow failure

Front 11

neutrophils do what?

Back 11

phagocytosis

Front 12

lymphocytes do what?

Back 12

immune response against invading pathogens

B cells: humoral immunity (antibodies)
T cells: cell-mediated immnuity

Front 13

lymphocytes increase?

Back 13

viruses (such as epstein-Barr), cancer, TB, Crohn's disease

Front 14

lymphocytes decrease?

Back 14

HIV, malnutrition, steroids, chemotherapy, chronic disease (lupus, TB)

Front 15

what do monocytes do?

Back 15

regulate immnunity, destroy cancer cells, clean up dead/damaged tissues

Front 16

eosinophils

Back 16

drug induced allergic reaction

Front 17

basophils

Back 17

allergic reactions/parasitic reactions these are your mast cells

Front 18

platelets

Back 18

clot formation

Front 19

% amts of each type of white blood cells?

Back 19

neutrophils (70%)
lymphocytes (15-40%)
monocytes (1-10%)
eosinophils (<7%)
basophils (<3%)

Front 20

stimulus for PTH release?

Back 20

low ionized calcium

Front 21

corrected calcium equation

Back 21

Corrected calcium (mg/dL) =

measured Ca2+ + [0.8 x (4-albumin)]

the problem with this equation is that it tends to overestimate the degree of hypercalcemia and can fail to identify hypocalcemia...therefore if given ionized calcium use that to see if pt is hyo or hyper calcemic

Front 22

in terms of calcium metabolic acidosis causes?

Back 22

decreased binding

Front 23

when it comes to calcium metabolic alkalosis?

Back 23

increases binding

Front 24

primary hyperthyroidism is?

Back 24

an excessive amount of PTH secretion just all on its own, has nothing to do with calcium levels (calcium would be in normal range of 8-10)

Front 25

secondary hyperparathyroidism?

Back 25

increase level of PTH because there is a decreased level of calcium (hypocalcemia)

Front 26

tertiary hyperthyroidism is?

Back 26

happens due to a consequence of secondary hyperparathyroidism going on for way too long, so then it will cause hypertrophy of the parathyroid glands

Front 27

lisinopril does what to potassium levels?

Back 27

it increases

Front 28

hemolytic anemia is?

Back 28

premature destruction of RBCs
can be caused due to infection, medication (such as Bactrim!) or can be an autoimmune disorder (sickle cell, or G6PD)

Front 29

aplastic anemia is?

Back 29

the bone marrow is unable to produce RBC

this can be due to an autoimmune disorder (the body is attacking itself) can be due to medications, or can be due to radiation or chemotherapy
usually results in pancytopenia (the lack/loss of all blood cells including wbc, platelts, and rbc)

Front 30

if you vasocinstrict the efferent arterioles what happens to filtrations rates

Back 30

they would increase becuase you would be keeping the blood in the bowman's capsule longer

Front 31

high specific gravity in a urine sample means?

Back 31

dehydration, high quantity of glucose or IV contrast dye

Front 32

low specific gravity in a urine sample means?

Back 32

potential inability to concentrate renal failure, glomerularnephritis (a type of kidney disease in which the part of your kidneys that helps filter waste and fluids from the blood is damaged.) or diabetes insipidus

Front 33

if there is protein in the urine this means that....

Back 33

fever, kidney disease/damage, excercise

Front 34

if there are glucose/ketones in the blood this means?

Back 34

diabetes

Front 35

if pH of a urine sample is high (alkaline) this means?

Back 35

urea-splitting bacteria (proteus)

normally pH of urine is low/acidic becuase this helps prevent any bacterial growth

Front 36

if urine is cloudy this mean?

Back 36

may indicate crystals, bilirubin, blood, porphyrins or protein

Front 37

if there is bilirubin in the urine sample that means?

Back 37

jaundice, or internal bleeding

Front 38

if there is blood/rbc in the urine that means?

Back 38

damage to urinary tract, or pt is on theri period

Front 39

if there are leukocyte esterases in a pt's urine sample that means?

Back 39

UTI (urinary tract infection)

Front 40

if there are squamous epi in the urine sample this means?

Back 40

it was a dirty catch

should be < or equal to 5

Front 41

what causes urine to be red/orange in color?

Back 41

rifampin or phenazopyridine (pyridium)

Front 42

if crystals show up in the urine this means?

Back 42

crystals are due to uric acid therofore pt can have gout.....

or can be due to calcium/phosphate crystals (parathyroid disorders)

Front 43

what are the 3 main functions of the nephron?

Back 43

1) filtration: done passively in the glomerulus into the Bowman's capsule..only water and small molecules

2) secretion: active process, majority done in the proximal tubule but can be done throughout the nephron

3) reabsorption: water and solutes throughout the nephron, medication in the distal tubule and the collecting duct

Front 44

what does endocrine do in terms of the nephron functions?

Back 44

produces erythropoetin

Front 45

what are metabolic function os the nephron?

Back 45

activation of Vitamin D3

Front 46

are proteins ably to be filtered into the glomerulus?

Back 46

no, becuase they are large molecules therefore they do not get into bowman's capsule, but if you see protein in your urine means then kidney damage going on that its allowing proteins to come in

glomerular filtration is passive filtration

Front 47

what is absorbed in the proximal tubule?

Back 47

majority of NaCl and water
and 100% of filtered glucose and amino acids
however can only reabsorb up to 180-200 mg/dL
so say you get more than 200 mg/dL of glucose/amino acid in the filtrate at proximal tubule then only 200 will get reabsorbed out and the rest of it will show up in the urine

this differes from blood glucose

also reabsorb 90% of filtered HCO3 (bicarb) this is saturable up to 26 meq/L so if more than this will spill out into urine therefore will alkalinize the urine

Front 48

what do carbonic anhydrase inhibitors do?

Back 48

blocks the reabsorbtion of sodium bicarb thereofore it will stay in the urine and cause an alkalinization of the urine......since there is sodium as well then water will follow so get more water in urine ie diuresis

Front 49

what is a medication that is a carbonic anhydrase inhibitor?

Back 49

acetazolamide

Front 50

where do carbonic anhydrase inhibitors work?

Back 50

at the proximal tubule

Front 51

what would be a good reason to use a carbonic anhydrase inhibitor?

Back 51

if there is too much bicarb in the blood/body, helps the body to excrete it by blocking its reabsorbtion and forcing it out via the urine

Front 52

what are the names of the loop diuretics?

Back 52

torsemide, bumetanide, and furosemide

Front 53

what co-transporter do the loop diuretics work on?
what does it do to Na, K, Cl, Mg and Ca also water?

Back 53

blocks the Na+/K+/2Cl- cotransporter found in the asceninding loop of Henle

so Na is not reabsorbed goes int ourine, water follows therofre diuretic

K also follows therefore loop diuretics cause hypokalemia

they also rebabsorb Mg and Ca

Front 54

the descending loop of Henle is permeable and impermeable to?

Back 54

permeable to water...water goes out and solutes stay in...osmolality increases because water decreases and a lot of solutes left

Front 55

ascending loop of Henle is permeable to and impermeable to?

Back 55

loose NaCl and water stays
thereofe by the time you reach the distal tubule and have a more normal osmolality

Front 56

function of vasa recta?

Back 56

goes in opposite direction of the loop of henle and picks up what the loop has reabsorbed back into blood, so passive diffusion of NaCl in ascending and water in descending thats comine out

Front 57

thiazides work where?

Back 57

distal convoluted tubule

Front 58

what drugs work on the distal convoluted tubule?

Back 58

hydrothiazide, amiloride and triamterene

spironolactone blocks aldosterone action here

Front 59

thiazdies work on what cotransporter?

Back 59

Na/Cl cotransported in the distal convoluted tubule of the nephron

reabsorbs NaCl

also calcium is reabsorbed here

Front 60

which is stronger loop or thiazide?

Back 60

loops

Front 61

where does aldosterone work?

Back 61

distal convoluted tubue and the collecting duct

reabsorbs sodium and secretes potassium

spironolactone blocks this therefore sodium goes into urine, potassium is saved and not secreted (potassium-sparing diuretic)

becuase sodium is not reabsorbed it gets excreted into urine, water follows so spironolactone causes diuresis and is potassium sparing

Front 62

where does ADH work?
what does it do?

Back 62

collecting duct

reabsorbs water by putting in aquaporins

ADH another word for vasopressin

Front 63

mannitol works where in the nephron?

Back 63

in the glomerulus, osmotic diuretic pulls water with it as it goes into the bowman's capsule
it is filtered in the glomerulus

Front 64

what drugs work in the distal tubule?

Back 64

thiazide, amiloride, spironolactone, triamterene

Front 65

what drugs work in the collecting duct?

Back 65

spironolactone, vasopressin, amiloride, triamterene

Front 66

what drugs work in the proximal tubule?

Back 66

carbonic anhydrase inhibitors such as acetazolamide

Front 67

what drugs work in the glomerulus?

Back 67

mannitol

Front 68

what drugs work on the loop of henle?

Back 68

loop diuretics (furosemide, butanemide, torsemide)

Front 69

what part of the nephron does calcium get reabsorbed?

Back 69

proximal tubule, ascending loop of henle, and the distal convoluted tubule

Front 70

what part of the nephron does phosphate get reabsorbed?

Back 70

proximal tubule only

Front 71

how to calculate plasma osmolality?

Back 71

(2x Na) + (glucose/18) + (BUN/2.8)

Front 72

primary ECF anion

Back 72

chloride and bicarbonate

Front 73

priamry ECF cation

Back 73

sodium

Front 74

primary ICF cation

Back 74

potassium

Front 75

primary ECF anion

Back 75

phosphate

Front 76

what is intracellular fluid?

Back 76

fluid within the cells, also known as cytosol

2/3 of total body water

Front 77

what is extracellular fluid?

Back 77

the fluid found outside of the cells

1/3 of total body water

Front 78

what is interstital fluid

Back 78

is it the fluid that surrounds the cells (also called extravascular)

3/4 of ECF

Front 79

what is plasma?

Back 79

the fluid component of blood (also called intravascular)

1/4 of ECF

Front 80

name some isotonic solutions

Back 80

have the same osmolality as body fluids

0.9% NaCl (normal saline)
D5W
LR (lactate ringers)

Front 81

name some hypotonic solutions

Back 81

they have a lower solute concentration than cells=>cells expand

use in patients with hypernatremia
0.45% NaCl
2.5% dextrose

Front 82

name some hypertonic solutions

Back 82

have higher solute concentrations than cells=>cells shrink


D5/0.45NS
D5/0.9NS
D5/RL

Front 83

what are crystalloids?

Back 83

0.9NS, D5W
small molecules
ECF
can be used for rapid/large volume replacement
IV diluenet
maintenence fluid
inexpensive

Front 84

what are colloids?

Back 84

blood, albumin, hetastatrch
large molecules
have colloid osmotic pressure therefore will pull water into the intravascular space
useful for hemorrhagic shock
no difference found between outcomes using crystalloids vs colloids
very expensive

Front 85

where is calcium passively reabsorbed and where is calcium actively reabsorbed in the kidney nephron?

Back 85

passively in the proximal tubule and ascending limb of Henle

actively reabsorbed in the distal tubule by PTH

Front 86

what stimulates the release of PTH?

Back 86

low ionized calcium

can also be stimulated by hyperphosphatemia
or a vitamin D deficiency

Front 87

what inhibits PTH release

Back 87

severe hypomagnesemia (if patient has a low Mg and Ca must first correct the Mg to be able to correct the Ca later)

also too much calcium will inhibit PTH release

Front 88

what does PTH do in the kidney?

Back 88

stimulates the reabsorption of calcium

inhibits phosphate reabsorption in the proximal tubule (becuase this would bind to calcium lowering its levels...defeat the purpose of PTH production)


stimulates the production of active vitmain D

Front 89

What does PTH do in the bone?

Back 89

stimulates calcium release from bone mineral compartment
stimulates the osteroblastic cells
causes bone resorption/breakdown via an indirect effect on osteoclasts
enhances bone matrix degradation

Front 90

what does active vitamin D do to calcium levels?

Back 90

Ca increases because vitamin D helps to increase calcium reabsorbtion via the GI tract

Front 91

what stimulates the release of vitamin D

Back 91

increase in PTH
decrease in calcium
decrease in phosphate
estrogen/prolactin

Front 92

what inhibits the release of vitmain D

Back 92

decrease in PTH
increase in calcium
increase in phosphate

Front 93

what percent of calcium is bound vs ionized vs complexed? which is diffusable?

Back 93

bound 40% to albumin
ionized 50%
complexed 10% (no affected by protein binding)


only ionized and complexed are diffusable

Front 94

what causes an increase in unbound calcium?

Back 94

acidosis (because it will decrease binding)

Front 95

what drugs interact with calcium reabsorption in the kidney?

Back 95

loops in the ascending tubule will block the reabsorption if calcium

thiazides in the distal will increase the reabsorption of calcium

Front 96

causes for hypercalcemia?

Back 96

cancer
priamry hyperparathyroidism
thiazide diuretic
lithium (b/c increases bone reabsorption)
milk-alkali syndrome (pt is taking in too much calcium)

Front 97

signs/symptoms of hypercalcemia

Back 97

fatigue, lethargy, muscular weakness, difficulty conentratin, confusion, acute pancreatitis
polyuria, constipation, N/V, kidney stones, hypertension, short QT interval on the EKG

Front 98

treatment of primary or tertiary hyperparathyroidism?

Back 98

remove the abnormal glands

Front 99

what should u do to treat hypercalcemia?

Back 99

Increase renal Ca2+ excretion
Increase volume (NS infusions) + loop diuretic
Decrease intestinal absorption
Corticosteroids to decrease calcitriol production
Phosphate-containing drugs
Slow bone resorption
Calcitonin, bisphosphonates
Remove Ca2+ from circulation
Dialysis with low-no Ca2+ concentration in dialysate
Control underlying disease

Front 100

what is cacitonin used for and what does it do?

Back 100

hypercalcemia

it is a homone the drug brand is Miacalcin
it inhibits osteoclast resorption (breakdown of bone to release mroe clacium)
it also increase the urinary excretion of calcium by decreasing its reabsorption in the kindneys

Front 101

what are bisphosphonates and what do they treat?

Back 101

treat hypercalcemia

block osteoclast activity, used for longterm decrease of calcium levels

Front 102

name the bisphosphonates and their cautions

Back 102

pamidronate (Aredia)
may cause renal toxicity, preganancy D

etidronate(Didronate)
use in caution in renal impairment

zoledronic acid (Reclast, Zometa)
reclast not recommended if CrCl <35ml/min

Zometa dont if <30ml/min, preg D

ibandronate(Boniva)
do not give if CrCl<30ml/min

Front 103

what is sensipar and how does it work?

Back 103

used to treat hypercalcemia

it enhances the calcium-sensing receptor sensitivity to extracellular Ca therefore inhibiting PTH secretion

Front 104

causes for hypocalcemia?

Back 104

hypoparathyroidism, magnesium deficiency, vitamin D deficiency, can also be due to hyperphosphatemeia (chronic renal failure) or osteoblast metsatsis

Front 105

signs/symptoms of hypocalcemia?

Back 105

increased neuromuscular (tetany, Chvostek's sign, Trousseau's sign, paresthesias, muscle cramps, seizures)
CV: prolonged QT interval, hypotension
chronic: depression, anxiety, memory loss, confusion, dry skin, brittle nails, course brittle hair

Front 106

how should you treat hypocalcemia?

Back 106

can give calcium gluconate or calcium chloride until pt can take oral calcium/vitamin D
trat co-exisiting hypo-Mg
treat hyperphosphatemia

Front 107

what drugs can you use to treat hypocalcemia?

Back 107

calcium carbonate, calcium chloride, calcium citrate, calcium lactate, and calcium gluconate
(gluconate preferred becuase less irritating to veins but carbonatte contains more elemental carbon

can also give teriparatide(Forteo) it is a recombinant PTH, it is indicated for treatment of osteoporosis, stimulates osteoblast activity, increases Ca absorption, increases renal tubular reabsorption of Ca

can also give Vitamin D supplements to help absorb calcium (ex calcitiol, cholecalciferol, doxercalciferol, ergocalciferol, paricalcitol)

Front 108

causes for hyperphosphatemia?

Back 108

impaired glomerular filtration, hemolysis of cells (tumor lysis syndrome)
medications(sodium phosphate, vitamin D)

Front 109

signs/symptoms of hyperphosphatemia?

Back 109

hypocalcemia: tetany, seizures
nephrolithiasis: cardiac/pulmonary calcification

Front 110

what is calciphylaxis?

Back 110

calcium X phosphate>55

precipitates into soft tissue

Front 111

how should you treat hyperphosphatemia?

Back 111

IV calcium if the atient has tetany/seizures
volume expansion
phosphate binders (calcium acetate, calcium carbonate, sevelamer, lanthanum carbonate)
hemodialysis

Front 112

name the phosphate binders?

Back 112

calcium acetate(Phoslo)
binds about 45mg phosphate per 1gm calcium acetate

calcium carbonate(Tums, Oscal, Caltrate)
binds 39 mg of phoshate er 1 gram of calcium carbonate

sevelamer (Renagel, Renvela)
first line in patients with hypercalcemia, also lowers LDL

lanthanum carbonate(Fosrenol)
available as a chewable tablets

Front 113

what are the causes for hypophosphatemia?

Back 113

decreased intestinal absorption (binders, fasting/starvation)
excessive renal excretion (hyperparathyroidism b/c PTH causes phosphate excretion)
redistribution from extracellular to intracellular (parathyroidectomy, dextrose/insulin, refeeding syndrome)

Front 114

signs/symptoms of hypophosphatemia?

Back 114

severe acute in hospitalized patients, respiratory failure, cardiac dysfunction, seizures, coma
chronic: musculoskelatal (pain, osteomalacia)

Front 115

how should you treat hypophosphatemia?

Back 115

correct hypocalcemia first
give oral phosphate if not severe, IV if it is severe

phosphate replacement therapy (neutra-phos, K-phos neutra, fleets phosphosoda, sodium phosphate, potassium phosphate) last 2 are IV only

Front 116

what can causes kidney stones (nephrolithasis)

Back 116

dehydration, high protein diet, high sodium diet, hypercalciuria, hyperuricosuria, hyperparathyroidism

Front 117

signs/symptoms fo kidney stomes (nephrolithiasis)

Back 117

pain, hematuria, anuria, azotemia

Front 118

how to treat kidney stones?

Back 118

drink alot of fluid to pee it out, give analgesics for the pain

give an oral a1-adrenergic blocker (doxazosin, terazosin, or prazosin)

give a thiazide diurteic (this will help reabsorb calcium so less calcium will go into urine to form the stone)

can to extracorporeal shock wave lithotripsy, percutaneous nephrolithotomy, or ureteroscopy

or give an alkalinizing agent such as potassium citrate or sodium citrate

Front 119

how would you know you have renal dysfunction?

Back 119

increase BUN, increased SCr, might be protein or blood in urine sample
pt would have a decreased GFR

Front 120

causes of pre-renal kidney failure?

Back 120

intravascula volume depletion, arterial hypotension, decreased cardiac output, renal hypoperfusion

Front 121

what is intrinsic renal failure?

Back 121

damage inside the kidney, vascular damage, glomerular damage, acute tubular necrosis, acute interstitial nephritis

Front 122

what is postrenal failure?

Back 122

damage after the kidney, bladder outlet obstruction, ureteral, renal pelvis or tubules