Quiz 2 Flashcards

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1
Q

iron-deficiency anemia

A

can be caused by blood loss, pregnancy, poor diet, gastric bypass

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2
Q

vitamin-deficiency anemia

A

low B12 or folate from poor diet

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3
Q

aplastic anemia

A

results when body stops erythropoiesis; from chemicals, drugs, autoimmune causes

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4
Q

hemolytic anemia

A

destruction of RBCs; multiple causes, inherited, infection

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5
Q

anemia of chronic disease

A

results from decreased RBC production by bone marrow, chronic inflammatory and neoplastic states that impair RBC production

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6
Q

sideroblastic anemia

A

multiple causes, bone marrow produces abnormal RBCs which prevent iron from being incorporating in hemoglobin

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7
Q

anemia r/t thalassemia

A

body produces abnormal alpha or beta chain of hemoglobin; genetic

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8
Q

types of WBCs

A

monocyte, eosinophil, basophil, lymphocyte, neutrophil

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9
Q

granulocytes

A

neutrophils, basophils, and eosinophils

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10
Q

fluctuations in WBC count can be due to:

A

time of day, exercise, pain, pregnancy, strong emotional reactions

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11
Q

leukocytosis

A

infections (MOSTLY BACTERIAL), certain medications (corticosteroids), inflammatory processes, bone marrow disorder or malignancy, physical exertion, stress, anesthesia, smoking, increased in newborns

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12
Q

leukopenia

A

infections (VIRAL, parasitic, some bacterial), decreased production (bone marrow malignancy or defect, chemo, nutritional deficiency (B12, folate)), radiation tx for CA, benign ethnic leukopenia, alcohol abuse, poor nutrition, gastric bypass (leading to impaired folic acid absorption leading to decreased WBC production)

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13
Q

neutrophils come in 2 forms:

A

bands (“stabs” or “sticks”) (less mature nucleus) and segmented (segs, polys, PMNs) neutrophils (mature nucleus)

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14
Q

left shift

A

higher predominance of immature neutrophils present; generally occurs in infection or inflammatory response

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15
Q

3 types of lymphocytes

A

T cells, B cells, natural killer cells

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16
Q

lymphocytosis

A

infection (predominately VIRAL: mononucleosis, cytomegalovirus (CMV), primary HIV infection, viral PNA, MMR, varicella, influenza, hepatitis, pertussis, bartonella); higher in infants/young children; drug reactions (esp. anticonvulsants), emergencies/stress/trauma, sz, splenectomy, acute or chronic lymphocytic leukemia, smoking, alcohol use/abuse

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17
Q

lymphocytopenia

A

bacterial or fungal sepsis, post-op state, chemo/radiation, malignancy, glucocorticosteroids, immunosuppressants

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18
Q

causes of increased monocytes

A

infection (bacterial, viral, or parasitic), hematologic or myeloproliferate disorder, hemolytic anemia, autoimmune disorders

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19
Q

eosinophilia

A

PARASITES, ALLERGIC DISORDERS, some drug reactions, occasionally autoimmune disorders

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20
Q

eosinopenia

A

most acute or bacterial infections

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21
Q

basophilia

A

parasitic infections, allergy related illnesses

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22
Q

reactive thrombocytosis (cytokine-driven)

A

infection, post-op, malignancy, post-splenectomy, acute blood loss or iron deficiency

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23
Q

autonomous thrombocytosis (overproduction)

A

malignancy

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24
Q

thrombocytopenia

A

lab error (platelet clumping by EDTA or error in automated cell counter), drug induced, infection (HIV, hep C, epstein-barr virus, sepsis, parasites), alcohol, pregnancy, nutritional deficiencies, malignancies

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25
Q

anemia results from:

A

blood loss, drop in production of RBCs, increase in destruction of RBCs, or lack of iron, B12, or folic acid (co-factors in RBC production)

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26
Q

increased RBC count

A

cigarette smoking (d/t increased presence of carboxyhemoglobin), dehydration, increase in production of erythropoietin (EPO), bone marrow malignancy or disease (myeloproliferative disease), polycythemia (abnormally high RBC count and corresponding high Hgb count)

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27
Q

decreased RBC count

A

anemia, bleeding (GI/GYN primarily), drug-induced (Abx, NSAIDs), hematopoetic failure *(radiation, toxins, or tumors), poor nutrition (B6, B12, folate, iron), pregnancy, overhydration

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28
Q

increased Hgb

A

tobacco use, advanced COPD, alcohol abuse, living at high altitude, dehydration (false elevation), EPO abuse, myeloproliferative disease, polycythemia

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29
Q

decreased Hgb

A

acute blood loss anemia, malnutrition (B12, iron, folate), myeloproliferative disorders or CA, chemo, renal failure (EPO produced in kidneys), disorders of Hgb structure (thalassemia, sickle cell)

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30
Q

hematocrit

A

percentage of whole blood that is made up of RBCs; AKA packed cell volume (PCV)

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31
Q

RDW

A

RBC distribution width; refers to variation of RBC volume (as a percentage); higher = larger variation in RBC volume

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32
Q

calculate RDW

A

(Standard deviation of MCV ÷ mean MCV) × 100

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33
Q

RDW significance

A

earliest manifestation of iron deficiency anemia; frequently increased in nutritional-linked anemias

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34
Q

anisocytosis

A

cells of varying size

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35
Q

MCV

A

mean corpuscular volume; measures the average volume of the RBC by dividing the Hct/Hgb; categorizes the size of RBCs and divides them into 3 categories

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36
Q

microcytic

A

decreased MCV

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37
Q

normocytic

A

normal MCV

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38
Q

macrocytic

A

increased MCV

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39
Q

MCH

A

mean corpuscular hemoglobin; measures the avg WEIGHT of Hgb within the RBC by dividing Hgb/RBC; rises or falls w/ rise and fall of MCV

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40
Q

MCHC

A

mean corpuscular hemoglobin concentration; measures the proportion of each RBC that is taken up by hemoglobin (increased Hgb = increased iron = increased red color of RBC)

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41
Q

hypochomic RBCs

A

decreased concentration of Hgb (decreased MCH or MCHC)

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42
Q

normochromic RBCs

A

normal concentration of Hgb (normal MCH/MCHC)

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43
Q

hyperchromic RBCs

A

increased concentration of Hgb (increased MCH or MCHC)

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44
Q

most frequently encountered anemias

A

normocytic anemias; decreased RBC production or increased RBC destruction (Hgb/Hct decreased but MCV nl)

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45
Q

causes of normocytic anemias

A

acute blood loss, hypersplenism (increased sequestering and RBC destruction), anemia of chronic disease, hemolytic anemia

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46
Q

causes of microcytic anemias

A

iron deficiency anemia (most common), alpha-thalassemia, beta-thalassemia, anemia of chronic disease (25% is microcytic), lead poisoning

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47
Q

causes of macrocytic anemia

A

alcoholism, B12/folate deficiency, hypothyroidism, multiple myeloma, acute leukemia, aplastic anemia, liver disease, myeloproliferative disease, drugs

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48
Q

reticulocytes

A

immature red blood cells that are visible d/t presence of ribosomal RNA that turns blue when stained; used to investigate bone marrow disorders

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49
Q

increased reticulocyte count

A

hemolysis or hemolytic anemia, acute blood loss, infiltrative marrow disorders

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50
Q

decreased reticulocyte count

A

represents decrease in RBC production; vitamin deficiency anemia, iron deficiency anemia, bone marrow failure, decreased EPO production (renal disease/failure)

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51
Q

Hgb A

A

2 alpha and 2 beta chains

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52
Q

Hgb A2

A

2 alpha and 2 delta chains

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53
Q

Hgb F (fetal)

A

2 alpha and 2 gamma chains (higher O2 affinity in utero)

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54
Q

alpha thalassemia

A

impaired production of alpha chains

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55
Q

beta thalassemia

A

impaired or very reduced beta Hgb chains, common in Mediterranean, Asian, African descent

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56
Q

Hgb S

A

sickle cell trait or disease

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57
Q

Hgb C

A

mild anemia

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58
Q

Hgb E

A

mild anemia, common in Asian descent

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59
Q

medications that can alter iron level

A

antibiotics, birth control pills, estrogen, hypertension medication, cholesterol medications, Deferoxamine (removes excess iron from the body), gout medication, testosterone

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60
Q

causes of increased iron level

A

beta-thalassemia, alcoholic cirrhosis, high iron intake, hereditary hemochromatosis

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61
Q

causes of decreased iron level

A

iron deficiency anemia, anemia of chronic disease, chronic renal failure, inadequate absorption (antacid use, competition w/ other metals such as copper or lead, bowel resection, celiac disease, inflammatory bowel disease), increased loss (from GI tract, epistaxis, menstruation, CA, trauma, phlebotomy), increased demand (pregnancy)

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62
Q

function of ferritin in the body

A

storage unit for iron (15-20% of the body’s iron), releases iron when needed by body; is an acute phase reactant

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63
Q

“gold standard” in diagnosis of iron deficient anemia

A

serum ferritin

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64
Q

serum ferritin value in anemia of chronic disease

A

ferritin >10 ng/mL

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65
Q

acute phase reactant

A

concentration increases in response to inflammation

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66
Q

causes of increased ferritin

A

hereditary hemochromatosis, excess iron intake/poisoning, chronic hepatitis, other chronic disease states (CA, alcoholism)

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67
Q

causes of decreased ferritin

A

iron deficiency anemia

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68
Q

transferrins

A

glycoproteins that are responsible for the transport of iron to almost all tissues of the body; can bind 2 iron molecules

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69
Q

total iron binding capacity

A

maximum amount of iron that serum proteins (mainly transferrin) can bind to; reflects the potential for iron binding if ALL of the binding sites on transferrin were filled

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70
Q

TIBC in iron deficient states

A

increased. less iron in body = more sites available for iron to bind to

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71
Q

TIBC in iron overload states

A

decreased. too much iron in body = fewer sites for iron to bind to

72
Q

increased TIBC

A

iron deficiency anemia, pregnancy, oral contraceptives, viral hepatitis

73
Q

decreased TIBC

A

anemia of chronic disease, hemochromatosis, sideroblastic anemia

74
Q

transferrin saturation

A

measurement of percentage of transferrin binding sites that are actually bound by iron; increase represents increase in iron absorption (serum iron/TIBC)

75
Q

increased transferrin saturation

A

megaloblastic anemia, sideroblastic anemia, iron overload states, hemochromatosis

76
Q

decreased transferrin saturation

A

iron deficiency anemia, chronic infection, malignancy, pregnancy, anemia of chronic disease

77
Q

plasma components

A

55% of blood. contains: blood proteins (7%), nutrients (2%), hormones, electrolytes (1%); water (91%)

78
Q

major plasma proteins

A

albumin (50-60%), fibrinogen (?%), globulins (36%)

79
Q

albumin

A

most abundant blood plasma protein. synthesized in liver. involved in maintenance of oncotic pressure, transportation of fatty acids, hormones, drugs, and other substances

80
Q

increase in serum albumin

A

dehydration (false)

81
Q

decrease in serum albumin

A

liver disease, malabsorption/malnutrition, abnormal loss (renal disease, GI loss, skin loss, severe burns), dilution by IVF, genetic variants

82
Q

prealbumin

A

synthesized mainly in liver, functions as a transport protein for thyroxine and vitamin A

83
Q

prealbumin test

A

much better assessment of pt’s nutritional status than albumin b/c has a shorter half-life and is more sensitive to rapid changes in nutrition (may not be accurate in pts with inflammation, infection, or trauma)

84
Q

increased prealbumin

A

pregnancy, hodgkin’s lymphoma

85
Q

decreased prealbumin

A

renal/liver disease, malabsorption/malnutrition, Crohn’s disease, low protein diet, severe illness/inflammation/infection

86
Q

alpha-1-antitrypsin

A

an alpha-1 globulin; inhibits the action of many key enzymes that are released during inflammatory rxns in the lungs; deficiency can lead to early-onset COPD. abscence causes damage to lung parenchyma. can also caused liver disease

87
Q

decreased/deficient alpha-1-antitrypsin manifestations

A

early-onset COPD, prolonged jaundice or hepatitis in infants, liver dysfxn in children, portal HTN, chronic hepatitis, cirrhosis, hepatocellular carcinoma

88
Q

ceruloplasmin

A

alpha-2 globulin that is made in liver; transports 6-7 copper atoms; is an acute phase reactant

89
Q

Wilson’s disease results from:

A

low ceruloplasmin; impaired transport of copper can lead to liver disease (excess copper in the liver)

90
Q

increased ceruloplasmin

A

oral contraceptives, 1st trimester pregnancy, infections

91
Q

decreased ceruloplasmin

A

wilson’s disease, hereditary low ceruloplasmin, liver failure or hepatitis

92
Q

haptoglobin

A

plasma protein; produced in liver, function is to bind to free Hgb when RBCs are destroyed, then trasport Hgb to liver where heme is converted to bilirubin. acute phase reactant. useful when looking for signs of hemolytic anemia

93
Q

increased haptoglobin

A

infection, inflammation, neoplastic disease, pregnancy, trauma, acute MI

94
Q

decreased haptoglobin

A

hemolytic anemia, transfusion rxn, artificial heart valves

95
Q

complement proteins

A

supplement the action of antibodies to destroy and eliminate pathogens from the body via opsonization; 9 different proteins (C1-C9) in plasma. typically synthesized in liver. C3 and C4 are acute phase reactants.

96
Q

complement pathway

A

C1 recognizes antibody-antigen complex or bacteria/virus. C3 is cleaved causing inflammation and opsonization. pathway goal is to produce membrane attack complex (MAC) and insert into membrane of pathogen causing lysis

97
Q

CH50 total complement activity

A

test used to measure immune processes or detect complement deficiency. measures ability of human serum to lyse RBCs that have been coated w/ antibody (measures amount of hemolysis); all 9 C proteins must be present

98
Q

decreased CH50

A

decreased complement activity

99
Q

CH50 = 0

A

one of the complement pathyway components is absent

100
Q

C3 and C4 test

A

often used to investigate the undetectable CH50 level or monitor some diseases (ex. lupus)

101
Q

decreased C3, C4

A

systemic lupus erythematosus, bacterial infections, cirrhosis, hepatitis, malnutrition

102
Q

increased C3, C4

A

cancer, ulcerative colitis

103
Q

immunoglobulins

A

AKA antibodies. developed to target specific foreign invaders (bacteria, viruses, toxins); produced by B lymphocytes and develop to become very specific

104
Q

IgA

A

usually found in and defends secretions and along mucosal epithelium; allows for clearance of pathogens by cilia or of toxins in GI tract; present in saliva, tears, colostrum, and mucus (think: SECRETIONS)

105
Q

IgA deficiency

A

can by asymptomatic, or can cause frequent resp infections, inflammation of GI tract, unexplained asthma sx

106
Q

IgD

A

fxn/clinical significance unknown. only 0.25% of immunoglobulins. ound to activate basophils and mast cells. increases w/ chronic infections; highest in leprosy, TB, malaria, AIDS, hepatitis, staph infections

107
Q

IgE

A

involved in allergic rxns and parasitic infections; binds to mast cells to initiate a chain of immune responses; increase most likely r/t allergies

108
Q

IgG

A

major antibody when antigen is encountered. most prevalent and longest half life. responsible for immunity to bacteria and other microorganisms. crosses the placenta so that the fetus can be protected

109
Q

IgM

A

INITIAL antibody secreted. usually indicate recent infection. deficiency is rare

110
Q

IgG and IgM testing

A

useful when trying to determine if someone has an active infection currently or has already had the infection in the past. commonly used in: epstein-barr virus, cytomegalovirus, herpes I/II, varicella, MMR

111
Q

protein electrophoresis indications

A

detecting some forms of CA or pre-CA, immune abnormalities, kidney or liver dysfxn, multiple myeloma

112
Q

multiple myeloma

A

incurable. neoplastic disorder when causes proliferation of a monoclonal immunoglobulin (usually IgG and IgA); clones of a single structurally-identical antibody multiplies rapidly and becomes “M protein” (monoclonal protein)

113
Q

protein electrophoresis in multiple myeloma

A

spike in gamma portion (M protein); can also occur in alpha-2 or beta range. M protein a/w plasma cell disorder. poss. signifies neoplastic process

114
Q

conditions a/w M protein on protein electrophoresis

A

multiple myeloma, smouldering muyeloma, monoglonal gammopathy of undetermined significance, solitary plasmacytoma, AL amyloidosis, heavy chain deposition disease, light chain deposition disease, chronic lymphocytic leukemia, any B- or T-cell lymphomsa, breast CA, colon CA, cirrhosis, sarcoidosis, autoimmune disorders

115
Q

polyclonal gammopathy

A

infectious, inflammatory and reactive processes may be a/w a broader based peak in the gamma region. ex. liver disease (cirrhosis, hepatitis), autoimmune disease (SLE/lupus, RA), infection (HIV, hepatitis, osteomyelitis, endocarditis), hematologic disorders/malignancies (non-hodgkins, sickle cell, thalassemia), non-hematologic malignancies

116
Q

complete metabolic panel

A

proteins, electrolytes, renal and liver function, monitoring DM and HTN

117
Q

monitoring electrolyte fxn and abnormalities on CMP

A

Na, K, Cl, CO2, anion gap, Ca

118
Q

monitoring renal fxn on CMP

A

BUN/Cr

119
Q

monitoring liver fxn on CMP

A

bilirubin, alk phos, AST, ALT

120
Q

monitoring proteins on CMP

A

albumin, total protein

121
Q

monitoring diabetes on CMP

A

glucose

122
Q

sodium

A

predominant cation in the extracellular space; major determinant of ECF osmolality (tonicity)

123
Q

sodium regulation via:

A

hormones such as aldosterone, naturietic hormone, primarily antidiuretic hormone (ADH) AKA vasopressin; functions to increase renal free water reabsorption

124
Q

hypernatremia

A

typically occurs in unreplaced water loss; elderly pts who have impaired mental faculties w/ diminished thirst stimulation, or pts w/o free access to water (hypertonic saline solutions)

125
Q

hyponatremia

A

dietary/nutritional intake, thiazide diuretics, renal insuffiency

126
Q

potassium

A

major intracellular cation; affects potential across cell membrane (involved in muscle/nerve excitability). secreted via kidneys. changes can affect muscle contractility (esp. cardiac muscle)

127
Q

causes of hyperkalemia

A

increased dietary or IV intake, crush injuries or infection (cellular injury releases K), acidotic states

128
Q

causes of hypokalemia

A

deficient dietary or IV intake, fluid and electrolyte loss, alkalotic states, DIURETICS

129
Q

glucose

A

levels are controlled by glucagon and insulin. increases after eating, insulin is then released to decrease levels. can be affected by several hormones.

130
Q

hyperglycemia

A

diabetes, acute stress response, pancreatitis, certain diuretics, corticosteroid therapy

131
Q

hypoglycemia

A

insulinoma (insulin secreting tumor), insulin OD, starvation, hypothyroidism

132
Q

glomerulus

A

main filtering structure of the kidney

133
Q

glomerular filtration rate (GFR)

A

of mL of body fluid cleared by the kidneys per unit of time (mL/min)

134
Q

blood urea nitrogen (BUN)

A

urea formation in liver as a result of carabolism of protein into amino acids; free amonia is formed in the process. ammonia molecules combine to form urea; BUN reflects the metabolic functioning of the liver and excretory fxn of kidneys

135
Q

increased BUN

A

high protein diets, GI bleed (via deceased kidney perfusion), dehydration, certain meds, sepsis

136
Q

decreased BUN

A

primary liver disease/failure, low protein diets, overhydration

137
Q

creatinine

A

byproduct of catabolism of creatinine phosphate; filtered by glomerulus of kidney; secreted by kidneys at a constant rate; marker for renal fxn, NOT AFFECTED BY LIVER FXN; production dependent on muscle mass

138
Q

increased creatinine

A

disorders of renal fxn, urinary tract obstruction, diabetic neuropathy, rhabdomyolysis, gigantism/acromegaly

139
Q

decreased creatinine

A

debilitation, decreased muscle mass

140
Q

calcium

A

more abundant in ECF than ICF; involved in muscle contraction, cardiac fxn, neural transmission, clotting cascade

141
Q

calcium exists in the body in 3 forms:

A

protein-bound (mostly albumin, but also alpha, beta 1 & 2, gamma globin); complexed (w/ phosphate, citrate, bicarb, sulfate); ionized (“free” calcium in its active form)

142
Q

calcium is regulated by

A

parathyroid hormone (PTH); as Ca decreases, PTH is released and Ca is reabsorbed by kidneys, released from bone and absorption from GI tract is increased

143
Q

calcitonin function

A

released by thyroid gland in response to rising Ca levels in blood; leads to increased excretion of calcium by kidneys and calcium deposition in bone.

144
Q

parathyroid hormone (PTH) function in calcium

A

released by parathyroid glands in response to decreased calcium levels in blood. leads to increased reabsorption of calcium by kidneys, calcium release from bone, increased calcitriol production (causing Ca2+ absorption from digestive system)

145
Q

hypercalcemia

A

hyperparathyroidism, vit. D intoxication, MALIGNANCY, acromegaly

146
Q

hypocalcemia

A

hypoparathyroidism, vit. D deficiency, hypoalbuminemia, malabsorption

147
Q

bilirubin

A

formed from breakdown of RBCs; is a component of bile

148
Q

unconjugated (indirect) bilirubin

A

RBC is broken down to form heme + globin molecules. heme is catabolized and formed biliverdin which then becomes unconjugated bilirubin

149
Q

conjugated (direct) bilirubin

A

unconjugated bilirubin becomes conjugated with glycuronide when in the liver

150
Q

total bilirubin =

A

direct + indirect

151
Q

causes of indirect hyperbilirubinemia

A

hepatocellular disfunction (hepatitis, cirrhosis, neonatal hyperbilirubinemia), any disease process that increases RBC destruction (transfusion rxn, sickle cell anemia, hemolytic anemia), many medications

152
Q

causes of direct hyperbilirubinemia

A

OBSTRUCTION of extrahepatic ducts! via gallstones, tumor

153
Q

serum protein

A

reflects synthesis and maintenance of total amount of protein in circulation

154
Q

low serum protein

A

can be d/t renal disease; glomerulus becomes less able to filter proteins –> less reabsorbed, so excreted in urine

155
Q

hyperproteinemia

A

dehydration (less water leads to increased concentration of proteins), malignancy (overproduction of immunoglobulins), infection (overproduction of immunoglobulins)

156
Q

hypoproteinemia

A

hepatic failure/disease, malnutrition, malabsorption, renal failure/disease

157
Q

hyperalbuminemia

A

dehydration d/t concentration of albumin

158
Q

hypoalbuminemia

A

malnutrition, pregnancy, hepatic disease or failure, protein-losing nephropathies

159
Q

liver enzyme tests/LFTs

A

alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT)

160
Q

alk phos

A

functions in growth and development of bones, teeth, and other tissues (essential for bone mineralization)

161
Q

increased alk phos

A

cirrhosis of liver, obstruction of biliary tract, liver tumors, drugs that are toxic to liver; cancers that metastasize to bone, primary CA of bone, post-fx, hyperparathyroidism, growing children

162
Q

decreased alk phos

A

malnutrition

163
Q

aspartate aminotransferase (AST)

A

found in highly metabolic tissue w/in the body (heart, liver, skeletal muscle); damage to tissue or cell inflammation/injury/death releases AST in circulation

164
Q

elevated AST

A

liver disease, liver tumors, infectious mononucleosis, skeletal muscle disease or trauma (burns, myositis, muscular dystrophy)

165
Q

alanine aminotransferase (ALT)

A

found primarily in liver!!!! but can be found in smaller amount in other tissue. released when liver damage occurs. in jaundiced pt, elevated ALT = liver as source (not RBC hemolysis). elevated ALT = liver abnormality!

166
Q

increased ALT

A

hepatitis, cirrhosis, hepatotoxic drugs, MI, myositis

167
Q

AST:ALT ratio >1

A

alcoholic cirrhosis (frequently >2!!!!!!!); metastatic tumor of liver

168
Q

AST:ALT ratio less than 1

A

acute/viral hepatitis, mononucleosis

169
Q

azotemia

A

refers to increase in nitrogen containing compounds in the blood

170
Q

pre-renal azotemia

A

results from abnormalities in systemic circulation that decrease blood flow to kidney

171
Q

intra-renal azotemia

A

results from abnormalities w/in the kidneys themselves

172
Q

post-renal azotemia

A

results from obstruction of collecting system of kidneys

173
Q

BUN/Cr ratio >/= 20:1 pre-perfusion

A

volume depletion, sepsis, hypotension, CHF

174
Q

BUN/Cr ratio less than/= 10:1 intra-renal

A

nephrosclerosis, glomerulonephritis

175
Q

early: BUN/Cr ratio >/= 20:1 or late: BUN/Cr ratio less than/= 10:1 post-renal

A

urinary tract obstruction, nephrolithiasis, prostatic hyperplasia, metastatic disease

176
Q

normal BUN/Cr ratio

A

10:1 to 20:1

177
Q

serum ferritin in iron deficient anemia

A

less than 10 ng/mL