Test 2 Flashcards
hemostasis definition
the process of coagulation and lysis of clots in the body
four processes of hemostasis
- narrowing of blood vessels
- platelet activity
- activation of coagulation factors via intrinsic and extrinsic pathways
- fibrinolysis
excessive hemorrhage caused by
- delays in clot formation
- premature clot lysis
excessive thrombosis caused by
- inappropriate clot activation
- localization of the blood coagulation process
hyperreactivity of platelets leads to
arterial thrombosis
accelerated activity of the clotting system leads to
venous thrombosis
impaired coagulation caused by
- thrombocytopenia
- acquired coagulation disorders
- inherited factor deficiencies
activation of platelets steps
- adhesion
- aggregation
- fibrin formation
- clot retraction
platelet count panic values
<20
>1000
causes of thrombocytopenia
- decreased platelet production
- increased platelet destruction or consumption
- increased splenic sequestration
heparin induced thrombocytopenia (HIT)
- life threatening complication of exposure to heparin
- causes platelet activation that causes platelet consumption
- thrombosis risk is higher than bleeding risk
EDTA sensitivity (pseudothrombocytopenia)
- erroneous low platelet counts due to micro clumping of platelets in spite of anticoagulant in tube
- low platelet count without history of thrombocytopenia or bleeding episode*
- redraw specimen in tube with different anticoagulant
causes of thrombocytosis (high platelets)
- essential thrombocythemia (bone marrow over produces)
- reactive thrombocytosis
bleeding time
- measures the primary stage of hemostasis
- interaction of the platelet with the blood vessel wall and formation of hemostatic plug
platelet function analysis
-measures the time to form a platelet/RBC thrombus
platelet aggregation study
- gold standard for testing platelet response*
- measures if platelets aggregate, adhere, or release their granules
von Willebrands Type 1
- most common
- missing some VWF
- mild symptoms
von Willebrands Type 2
- defective VWF
- mild symptoms
von willebrands type 3
- limited or no VWF
- severe symptoms
von willebrand factor role
- VWF helps adhere platelets to exposed collagen in vessel walls
- VWF protects factor 8 from degradation by proteins C and S
von willebrands labs
- platelets = normal
- PTT = normal or increased
- VWF antigen = decreased
- factor 8 antigen = decreased
idiopathic thrombocytopenia purpura (ITP)
- unknown cause but usually follows viral illness in children
- platelets become bound to antibodies
ITP labs
- platelets = decreased
- bleeding time = increased
- PT/PTT = normal
ITP treatment
- splenectomy
- platelet transfusion for super low counts
thrombolytic thrombocytopenia purpura (TTP)
-small blood clots form throughout the body consuming large numbers of platelets
TTP pentad
- consumptive thrombocytopenia
- microangiopathic hemolytic anemia
- neurological
- fever
- renal dysfunction
TTP Labs
- platelets = decreased
- Hb = <10
- PT/PTT = normal
hemolytic uremic syndrome (HUS)
- rare disorder
- can occur with E. coli infection
HUS triad
- microangiopathic hemolytic anemia
- thrombocytopenia
- acute renal failure
HUS labs
- platelets = decreased
- PT, PTT = normal
- BUN/creatinine = elevated
HELLP
- Hemolysis
- Elevated Liver enzymes
- Low Platelet
- seen during pregnancy or within 48 hours post partum
HELLP labs
- platelets = lows
- microangiopathic blood smear
- PT, PTT = normal
- bilirubin/AST = elevated
extrinsic pathway factor
3, 7
intrinsic pathway factor
12, 11, 9, 8
thrombin time (TT)
- measures time needed for plasma to clot when thrombin is added
- can detect DIC
TT clinical implications
- increased = clots faster
- decreased = clots slower
activated partial thromboplastin time (PTT)
- screens for clotting disorders with deficiencies in the intrinsic pathway
- used to monitor unfractionated heparin therapy
heparin
- produces immediate anticoagulant effect by enhancing antithrombin
- neutralized by protamine in case of overdose
prothrombin time (PT)
- measure potential defect in extrinsic pathway
- dependent on vitamin K intake and absorption
- PV INR>3.6
- used to manage coumadin therapy
vitamin K dependent factors
- 2 (prothrombin)
- 7
- 4
- 10
- protein C & S
vitamin K deficiency causes
- drug therapy (coumadin, antibiotics)
- disease (malabsorption, biliary obstruction, malnutrition)
coumadin
- delays vitamin K formation interfering with dependent factors
- takes 48-72 hours to cause measurable change in PT/INR
protein C
- prevents thrombosis and enhances fibrinolysis
- inactivates factor 5 and 8
- protein C should be checked in conjunction with protein S
protein S
-enhances activities of protein C
antithrombin
-inhibits factor 10
factor V Leiden
- most common cause of hereditary hypercoagulopathy
- resistant to inactivation by protein C
DIC
-continuous generation of thrombin causes depletion of coagulation factors and platelets resulting in uncontrolled bleeding
DIC treatment
heparin
-blocks thrombin which blocks coagulation factor consumption
DIC labs
- increased PT, PTT, PFA, D-dimer
- decreased platelets, factors 2,5,8, 10
hemophilia A
-factor 8 deficiency
hemophilia B
- factor 9 deficiency
- treated with fresh frozen plasma
hemophilia C
- factor 11 deficiency
- Ashkenazi jews
low molecular weight heparin
- does not require PTT testing
- neutralized by protamine in case of OD
- decreased risk of HIT
urine color
caused by the pigment urochrome
specific gravity
- normal: 1.005-1.030
- dilute: 1.000-1.010
- concentrated: >1.025
measures the ability of the kidneys to concentrate urine and is confirmed with refractometer
pH
useful for the ID of crystals
hemoglobinuria
- no microscopic RBC but color change to “strong”
- pinkish red color
hematuria
- speckled dipstick and microscopic RBC
- ascorbic acid = false negative
myoglobinuria
- cherry red urine
- no microscopic RBC
- increased muscle enzymes
protein
indicator of renal disease
glucose
- critical value = 4+ in pediatrics
- SGLT2 inhibitors can interfere
ketones/acetones
- critical value = ketones in child under 2
- result of fat metabolism
- significant in DKA
nitrite
-produced by gram negative bacteria such as E. coli
WBC
-detect UTI and inflammation
bilirubin
- appears in urine before signs of jaundice
- positive in biliary obstruction
urobilinogen
-most sensitive test for early detection of liver disease
microscopic RBC
can be confused with yeast, oil, or air bubbles
microscopic WBC
-clumps suggest renal origin
microscopic squamous epithelial cells
- normal finding
- large amounts in females can indicate poor collection
transitional epithelial cells
- normal in small numbers
- large numbers due to catherization or trauma
renal tubular cells
-high numbers can indicate necrosis of renal tubules
fatty & waxy/broad casts
-indicative of nephrotic syndrome
cholesterol crystals
- associated with nephrotic syndrome
- broken windowpane
leucine, tyrosine, and bilirubin crystals
associated with liver disease
urine osmolality
-more exact measurement of urine concentration than specific gravity
urine microalbumin
- occurs before clinical proteinuria is evident
- detect early DM and HTN damage
- preeclampsia
sodium
- critical values: <120 >160
- primary determinant of extracellular osmolality
hypernatremia
- all cases will have increased serum osmolality
- low urine osmolality = diabetes insipidis
- high urine osmolality = non renal cause
- thirst, restlessness, seizures
hyponatremia
- lethargy, confusion, seizures
- tachycardia
corrected sodium
- correct sodium to estimate dehydration severity in severe hyperglycemia and DKA
- normal/high Na and high glucose = severe dehydration
- low sodium after correction could be over hydration
osmolality
- measure of number of dissolved particles in solution
- in general increasing sodium increases osmolality
serum osmolality symptom severity
- stupor in hyperglycemia
- grand mal seizure
- increased fatality
urine osmolality
- Increased = kidneys working properly and loss in non renal
- Decreased = kidneys producing dilute urine and not responding to ADH
stool osmolality
- evaluate electrolyte dysfunction in patients with diarrhea
- must be tested in conjunction with serum and urine
potassium
- critical value <2.5 >6.5
- kidneys do not preserve potassium so inadequate intake can cause deficiency
- difficult to fix hypokalemia is usually due to uncorrected hypomagnesemia
hyperkalemia
- acute or chronic renal failure
- peaked T waves and wide QRS
- malaise, muscle weakness, nausea
hypokalemia
- GI loss
- muscle cramps, weakness, ileus, rhabdo
- look for diuretic
- flattened T waves and U waves
hypokalemia and hypomagnesemia
- caused by diarrhea and diuretic therapy
- hypokalemia is refractory to potassium supplementation
hypokalemia treatment
- potassium supplement and rich diet
- potassium sparing diuretic (spironolactone)
hyperkalemia treatment
- bicarb, glucose, insulin
- kayexalate
chloride
- important for acid base balance, water balance, and osmotic pressure
- follows sodium to maintain neutrality
carbon dioxide
-majority is from bicarb, rest is dissolved CO2 and carbonic acid
BUN, urea nitrogen
- formed in the liver
- elevated correlates with impaired kidney function and rapid protein catabolism
- in CKD correlates better with symptoms of uremia and creatinine
creatinine
- critical value >10 (nondialysis)
- freely filtered across glomerulus = better renal function test
- helps estimate GFR
cystatin C
- indicator of GRF
- may be more reliable than creatinine in not affected by muscle mass and nutrition
creatinine clearance
-measurement of kidney function by measuring the rate by which it is cleared from the blood
calcium
- 50% ionized and 50% protein bound
- hypercalcemia = hyperparathyroidism
- hypocalcemia = hypoalbuminemia
phosphorus
- has an inverse relationship with calcium
- levels controlled by PTH
respiratory acidosis labs
- decreased pH
- increased PCO2
- compensation = increased bicarb
respiratory acidosis conditions
asthma, chronic bronchitis, emphysema
respiratory alkalosis labs
increased pH
decreased PCO2
compensated = decreased bicarb
respiratory alkalosis conditions
hyperventilation
metabolic acidosis labs
decreased pH
decreased bicarb
compensated = decreased PCO2
metabolic acidosis conditions
DKA
renal failure
diarrhea
metabolic alkalosis labs
increased pH
increased bicarb
compensated = increased PCO2
metabolic alkalosis conditions
vomiting
hypokalemia
anion gap
Na - (Cl + HCO3)
increased anion gap conditions
methanol uremia dka propylene glycol ioniazid lactic acidosis ethylene glycol salicylates
decreased anion gap conditions
drugs/toxins
cirrhosis
nephrotic syndrome
platelet function analysis with normal epinephrine
normal PFA
platelet function analysis with abnormal epinephrine and normal ADP
aspirin therapy
platelet function analysis with both abnormal epinephrine and ADP
platelet dysfunction disorder
D-dimers
- produced with plasmin breaks apart cross linked fibrin
- diagnose DIC or venous thrombosis
regulation of sodium
- aldosterone = increase Na
- natriuretic hormone = decrease Na
- ADH = increase H2O reabsorption
potassium and acid/base balance
- alkalosis = decreased potassium to get H+ from cell
- acidosis = increased potassium to put H+ into cell
normal calcium with abnormal phosphorus
impaired calcium absorption due to PTH problem
normal calcium and elevated BUN
primary or secondary hyperparathyroidism due to renal disease
normal calcium with decreased albumin
hypercalcemia
magnesium
- involved with calcium absorption from intestines
- hypokalemia and hypocalcemia is always hypomagnesemia
- hypermagnesemia = renal insufficiency
prealbumin
better than albumin at assessing nutritional status
albumin
elevated levels associated with nephrotic syndrome
