MIDTERM ish

Question 1

Is CO2 (carbon dioxide) and acid or a base

Answer 1

Acid; H2O is its counterpart (base)

Question 2

is NH4 (ammonium) an acid or a base

Answer 2

Acid

Question 3

is HCO3 (bicarbonate) an acid or a base

Answer 3

Base

Question 4

is H+ (hydrogen) an acid or a base

Answer 4

Acid

Question 5

Kidneys regulate secretion and resorption of

Answer 5

H+ (acid) and HCO3 (base)

Question 6

How does hyperventilating affect CO2 levels

Answer 6

Increases the amount of CO2 exhaled, raising the pH

Question 7

difference between hyperventilating, hypoventilating, and Kussmaul breaths; and how does each affect CO2 levels?

Answer 7

hypoventilating (slow, shallow breaths): the body produces more CO2 than it can eliminate causing an increase in CO2 in the body, lowering the pH
Kussmaul breaths (fast, deep breaths; a form of hyperventilating): the body is purposely trying to rid the body of excess CO2

Question 8

normal range of PaCO2

Answer 8

35 to 45 mm Hg
Rise in CO2 = blood O2 decrease

Question 9

normal range of HCO3

Answer 9

22 to 26 mEq/L

Question 10

Metabolic Acidosis

Answer 10

(ketoacidosis)
pH: below 7.35
PaCO2: normal (38 to 42 mm Hg)
HCO3: <22 mEq/L $

Increased H+ (hydrogen) / decreased HCO3
Kidneys compensation: retain HCO3, resorption to attempt to raise pH; secretion of H+
Lungs compensation: hyperventilate

Causes: prod./ingestion of acids, renal failure, loss of alkali

Signs: Rapid, deep breaths (Kussmaul); Increased HR; fatigue

Tx: bicarbonate to raise pH;

Question 11

Respiratory Acidosis

Answer 11

pH: below 7.35
PaCO2: > 45 mmHg $
HCO3: increase 1-3.5 mEq/L for every 10 mmHg CO2 (acute - chronic)

Kidneys compensation: increase production of HCO3; acid in urine
Lungs compensation: Hypoventilate

Signs: Hypoventilation; Abdominal distention, evidence of hypoxia

Tx: treating the underlying illness; use suction to remove mucus from the airway

Question 12

Metabolic alkalosis

Answer 12

pH: above 7.45
PaCO2: Normal
HCO3: > 26 mEq/L $
Kidneys compensation: excrete HCO3 or conserve H+
Lungs compensation: hyperventilation or hypoventilation

Causes: excess loss of acids, HCO3 retention, ingestion of alkali

Signs: numbness, prolonged muscle spasms, nausea

Tx: treat the underlying condition

Question 13

Respiratory alkalosis

Answer 13

pH: above 7.45
PaCO2: <35 mmHg $
HCO3: Normal

Kidneys compensation: decreasing production of HCO3 and decreasing acid in urine; acid retention
Lungs compensation:

Signs: hyperventilation; excessive exhalation of CO2

Tx: supplemental O2

Question 14

Name the chemicals in constant acid-base equilibrium

Answer 14

CO2, H2O, HCO3, H+

Question 15

edema

Answer 15

clinical manifestation: accumulation of interstitial fluid. Presentation in the extremities is more notable and palpable; however, presentation in the lungs may cause shortness of breath

Tx: typically diuretics are used to aid in elimination of fluid

Question 16

hyponatremia

Answer 16

Low sodium

Labs: <135 mEq/L

Causes: fluid loss from vomiting and diarrhea or other GI depletion, or an effect from (diuretics); renal dysfunction, adrenal insufficiency (i.e., Addison disease), syndrome of improper ADH secretion, or diabetic ketoacidosis

Signs/symptoms: decreased serum osmolality, headache, anxiety, nausea, hypotension, tachycardia, anorexia, muscle cramps

Tx: focus on underlying etiology, intake/ouput monitoring,

Question 17

hypernatremia

Answer 17

High sodium

Labs: >145 mEq/L

Causes: increased output or decreased intake of water; excessive intake of sodium, diarrhea, burns, and heat stroke

Signs/symptoms: increased serum osmolality, hypotension, tachycardia, dry skin/mucus membranes, headache, decreased skin turgor

Tx: intake/ouput monitoring, nurse lookout for fever or thirst; increase fluid intake if PT excess water output (diabetes insipidus) - synthetic ADH is warranted … seizure watch

Question 18

isotonic

Answer 18

solutions have the same osmolality as body fluids.
Normal saline (0.9% sodium chloride) is an example.

Question 19

hypotonic

Answer 19

the extracellular fluid (ECF) has a lower osmolarity than the fluid inside the cell; water enters the cell
example of a hypertonic solution is 3% sodium chloride.

Question 20

hypertonic

Answer 20

the extracellular fluid has a higher osmolarity than the fluid inside the cell; water leaves the cell
example of a hypotonic solution is 0.45% sodium chloride.

Question 21

hypervolemia

Answer 21

Isotonic fluid volume excess typically results from ECF volume excess; increase in ECF sodium

Cause: a decreased excretion of water and sodium, as in acute kidney injury or chronic kidney disease

Clinical manifest: weight gain, decreased hematocrit, dilution of plasma

Signs: distended neck veins, increased BP, and increased capillary hydrostatic pressure contribute to presence of edema.

Tx: restricting fluid intake and correcting the underlying etiology

Question 22

hypovolemia

Answer 22

Isotonic fluid volume deficit; Normal sodium levels

Causes: hemorrhage, vomiting, diarrhea, fever, excess sweating, burns, diabetes insipidus, and uncontrolled diabetes mellitus

Clinical manifest: decrease in urine output, weight loss, and an increased hematocrit.

Signs: tachycardia, decreased skin turgor and blood pressure, and, potentially, hypovolemic shock

Tx: addressing the cause of the fluid deficit and replacing lost volume

Question 23

RAAS

Answer 23

renin-angiotensin-aldosterone-system

responds to low blood pressure and low serum sodium

Ex:
decrease in BP will stimulate the secretion of renin and subsequent activation of RAAS, resulting in sodium retention, increased fluid volume and BP increase

Question 24

renin

Answer 24

controls production of aldosterone

Question 25

aldosterone

Answer 25

mineralcorticoid hormone synthesized and secreted by adrenal cortex, in response to hemodynamic changes helps control the balance of water and salts in the kidney by retaining sodium in and releasing potassium from the body

Question 26

decreased/increased serum osmolality

Answer 26

low serum osmolality will suppress the release of ADH, resulting in decreased water reabsorption and more concentrated plasma increase of only 2% to 3% in plasma osmolality will produce a strong desire for thirst

Question 27

hyperchloremia

Answer 27

High chloride ions Labs: Causes: Signs/symptoms: Tx:

Question 28

obstructive shock

Answer 28

caused by an obstruction of blood flow least common for nurse to encounter in ICU

Question 29

cariogenic shock

Answer 29

failure of hear to pump

Question 30

distributive shock

Answer 30

abnormal redistribution of blood types: anaphylactic, septic, neurogenic

Question 31

hypovolemic shock

Answer 31

low blood volume

Question 32

septic shock

Answer 32

(or anaphylatic shock) due to inflammatory vascular response a type of distributive shock = most common in ICU

Question 33

sepsis (general)

Answer 33

the bodys extreme response to infection; can lead to tissue damage, organ failure, and death

Question 34

all shock types (etiology)

Answer 34

development of acute circulatory failure resulting in hypotension and inadequate tissue perfusion; heart failure, low blood volume, redistribution of ECF to extravascular sites, and obstruction of blood flow OUTCOME: poor tissue perfusion

Question 35

perfusion

Answer 35

flow rate of blood through capillaries and extracellular spaces, responsible for transport of O2, nutrients, and waste

Question 36

hypoperfusion (clinical manifestation)

Answer 36

cold, clammy skin (a result of vasoconstriction and cyanosis), renal output decrease (oliguria), confusion (obtundation), hyperlactatemia, and hypercoagulability

Question 37

oliguria

Answer 37

production of abnormally small amount of urine

Question 38

hypovolemic shock (cause)

Answer 38

loss of >15% of body fluid severe dehydration, inadequate ECF, sig. blood loss, excess vomit/diarrhea, MODS, burn injury

Question 39

cardiogenic shock (s/s)

Answer 39

decreased CO (cardiac output), MI, HF, cardiac tamponade, restrictive cardiomyopathy, constrictive pericarditis, MODS

Question 40

obstructive shock (s/s)

Answer 40

clinical : disturbance of consciousness, oliguria, hypotension, and tachycardia obstruction of major blood vessels, obstruction of cardiac pumping, cardiac tamponade, pulmonary embolism, MODS

Question 41

distributive shock (s/s)

Answer 41

clinical : imparied distribution of blood flow, extensive vasodilation, loss of vascular tone, septic shock, anaphylactic shock, neurogenic shock, MODS

Question 42

sepsis (s/s)

Question 43

hemodynamics (factors that influence circulation)

Answer 43

blood volume, systemic vascular tone, heart rate, force of contraction

Question 44

MODS

Answer 44

multi-organ dysfunction syndrome

Question 45

stage 1 shock

Answer 45

early, reversible, compensated sympathetic activation cause tachycardia and vasoconstriction kidneys respond with active RAAS to reabsorb sodium and water to maintain fluid strong chance of recovery

Question 46

stage 2 shock

Answer 46

intermaediate, progressive compensation begins to fail, decrease in persuion = hypoxia PT experience confusion, disorientation, angina (d/t decreased O2 delivery to myocardium), muscle pain reversible if right treatment is implemented promptly

Question 47

stage 3 shock

Answer 47

refractory, irreversible permanent toll on body and organs heart func. decline, kidneys shutdown, cells = hypoxia and cell death PT death due to MODS

Question 48

qSOFA

Answer 48

(Quick Sequential Organ Failure Assessment) bedside diagnosis criteria for septic shock (altered mentation) Glasgow coma scale <10, systolic BP of 100mmHg or less, and respiratory rate of 22/min +

Question 49

Neurogenic shock

Answer 49

blockage of sympathetic nervous system outflow to the intrathoracic sympathetic chain caused by any factor that increases parasympathetic stim common in spinal cord injury above T6, 2nd to parasym. outflow from T1-L2 more severe = higher on spinal cord

Question 50

neurogenic shock (s/s)

Answer 50

decrease in vascular resistance, loss of vascular capacitance with assoc. vascular dilation and bradycardia in the absence of hypovolemia hypovolemia = tachycardia Clinical : systolic hypotension, bradycardia, hypothermia

Question 51

SOFA

Answer 51

evaluates multiple different systems (cardiovascular, respiratory, coagulation, renal, hepatic, neurologic) predicting potential mortality and can guide clinical intervention

Question 52

anaphylactic shock (s/s)

Answer 52

stridor, tachycardia, dyspnea, wheezing, coughing, edema, laryngospasm, bronchoconstriction, angioedema, urticaria, pruritus, hives, gastrointestinal cramps, and hypotension

Question 53

MODS

Answer 53

multi-organ dysfunction syndrome 2+ system dysfunction; homeostasis in PT cannot be maintained without intervention most commonly caused by septic shock

Question 54

MODS (s/s)

Answer 54

6 primaries (respiratory, renal, hepatic, cardio, gastro, neuro) Renal & hepatic = serum creatinine or bilirubin levels. Hematologic = thrombocytopenia Cardio = changes in blood pressure and the heart Neuro = level of consciousness Gastro = tenderness of abdomin, palpable masses Assessment will focus on Glasgow Coma scale scores

Question 55

ischemia

Answer 55

drop in bloodflow to the brain; a lack of O2 and glucose that lead to tissue dmg

Question 56

hematoma

Answer 56

increasing pressure in the skull (bleeding in tissue or excess prod. of CSF)

Question 57

CSF

Answer 57

(cerebral spinal fluid) choroid plexi produces CSF within ventricles flows in the subarachnoid space surrounding the brain and spinal cord, providing buoyancy and nourishment

Question 58

hydrocephalus

Answer 58

excessive accumulation of CSF in brain can cause increased pressure within skull

Question 59

BBB

Answer 59

(blood brain barrier) specialized endothelium in brain capillaries that permits selective entry of substances Highly lipophilic subs are able to cross, H2O by diffusion and most others by facilitated diffusion

Question 60

cerebral autoregulation

Answer 60

critical to providing a steady flow of O2 and nutrients to brain and removing metabolic waste; maintains blood flow to brain and spinal cord despite fluctuation in mean arterial pressure

Question 61

cerebral blood flow

Answer 61

blood supply to the brain in a given time

Question 62

intracranial pressure

Answer 62

pressure exerted by contents of cranium: brain tissue, blood, and CSF

Question 63

TIA

Answer 63

(transient ischemic attack) temporary episode of neurologic dysfunction cause by focal brain, spinal cord, or retinal ischemia without acute infarction cause : clot that blocks bld supply to brain; does not cause permanent damage buildup of fatty deposits on arterial walls (atherosclerosis)

Question 64

TIA (s/s)

Answer 64

facial drooping, extremity weakness (esp. one sided), speech difficulty, sudden trouble seeing, difficulty walking with dizzy, lack of balance, severe headache unkown cause

Question 65

TIA (Tx)

Answer 65

(w/in 24-48hrs) urgent evaluation, risk stratification, and PT education of stroke prevention therapy

Question 66

TIA mimics

Answer 66

hypoglycemia, seizure, intracranial hemorrhage

Question 67

stroke

Answer 67

interruption in bld supply to brain or bleeding vessel that results in brain tissue dmg or infarction

Question 68

ischemic stroke

Answer 68

partial or complete occlusion od cerebral bld flow to an area of the brain d/t a thrombus or embolus athersclerosis = most common lead (conditions = increased risks pg. 672)

Question 69

thrombotic stroke

Answer 69

occlusion of bld vessel as a result of plaque buildup along vessel wall, usually involve internal carotid, mid-cerebral, or basilar artery

Question 70

hemorrhagic stroke

Answer 70

bleeding in brain d/t bursted bld vessel (intraparenchymal) intracerebral = bld in brain tissue (parenchyma) intraventricular = bld in ventricles extracerebral = bld in membrane surrounding brain

Question 71

aneurysm

Answer 71

abnormal bulge along vessel wall that fills with bld and is caused by a weak or thin area of wall symptoms occur when it puts pressure on brain or it leaks/ruptures causing a hemorrhage

Question 72

AVM

Answer 72

(arteriovenous malformation) tangle of abnormal/poorly formed bld vessels can occur anywhere and are at the greatest risk of bleeding Dural AVM = acquired disorder (usually trauma)

Question 73

AVM (s/s)

Answer 73

(would be considered a stroke) sudden onset of neurologic deficit that lasts 24hr and is due to a reduction or occlusion of cerebral circulation or rupture of blood vessels s/s : fig. 27.3

Question 74

ischemic stroke (Tx)

Answer 74

restore bld flow and reduce area of infarction (brain tissue death); area surrounding the infarction (penumbra) can be salvaged if perfusion is restored quickly Acute stroke : O2 is used to improve oxygenation, glycemic control to norm rng, and BP managed for adequate perfusion

Question 75

DCI

Answer 75

(delayed cerebral ischemia) neurologic deficit, cognitive deficit, or both that occur in 3-14 days after hemorrhage

Question 76

hemorrhagic stroke Tx

Answer 76

priority of care = ventilation and BP management osmotic dieuretics = decreased intrcranial pressure

Question 77

subdural hemorrhage

Answer 77

bleed from the bridging veins below inner layer of dura (between dura mater and arachnoid membrane) does not directly occlude bld vessels, so is not considered a stroke; can become large enough to cause a stroke though

Question 78

subdural hemorrhage (s/s)

Answer 78

headache, confusion, behavior change, dizziness, nausea, vomiting, lethargy, weakness, apathy, seizures size of hemorrhage and age of PT affect response

Question 79

subdural hemorrhage (Tx)

Answer 79

surgery must be considered before surgery, ventilation and BP are priority

Question 80

spinal cord hemorrhage

Answer 80

rare but may occur with trauma, vascular malformation, or bleeding disorders (epidural, subdural, subarachnoid, or intramedullary) intramedullary = bleed in white + gray matter epidural/subdural = compression on spinal cord

Question 81

spinal cord hemorrhage (s/s)

Answer 81

sudden, severe, localized back pain with or without radiculopathy intramedullary = hemiparesis, paraparesis, or quadriparesis; sensory loss below the lesion; and loss of sphincter control

Question 82

hemiparesis

Answer 82

weakness or inability to move one side of body

Question 83

paraparesis

Answer 83

partially unable to move legs

Question 84

quadriparesis

Answer 84

(tetraparesis) muscle weakness in all four limbs

Question 85

tetraplegia

Answer 85

inability to move upper and lower body

Question 86

spinal cord hemorrhage (Tx)

Answer 86

surgical resection for decompression or catheter-based intervention, raditation therapy (photon or gamma knife)

Question 87

HF

Answer 87

(heart failure) inability of heart to pump adequate bld to meet bodys metabolic needs

Question 88

HF (causes)

Answer 88

muscular contraction = decreased ejection muscular relaxation = heart not filling adequately combo

Question 89

HF (s/s)

Answer 89

fatigue, SOB, inability to exercise, extremity edema, death

Question 90

CO

Answer 90

(cardiac output) amount of bld pumped out of heart in L/min

Question 91

RAAS (response to CO)

Answer 91

if CO decreases = RAAS & SNS are activated fluid retention and vasoconstriction

Question 92

left side HF

Answer 92

left = responsible systemic circulation; failure results in vol. overload & venous congestion in lungs s/s : fatigue and SOB; decreased CO = RAAS & SNS active = bld volume increase = pulmonary congestion = dyspnea pulmonary congestion = right side works harder against the pressure and may fail as a result

Question 93

right side HF

Answer 93

right = responsible lungs circulation; failure results in systemic venous congestion = elevated jugular ven. pressure, hepatic congestion, peripheral edema *everything behind the failure gets backed up*

Question 94

systolic failure

Answer 94

HF with reduced EF amount of bld present at end of diastole (preload) is important

Question 95

diastolic failure

Answer 95

EF is preserved, contractility is preserved or slightly impaired, but muscle relaxtion impaired = inadequte filling, decreased preload = reduced CO impaired fill (bigger issue) = tachycardia + diastolic fill time decreased = even more reduced SV

Question 96

SV

Answer 96

(stroke volume) amount of blood pumped out of heart with each beat in mL

Question 97

EF

Answer 97

(ejection fraction) measurement of percentage of blood ejected from left ventricle with each contraction

Question 98

High output HF

Answer 98

heart still pumping high amount of blood (8L/min); vasodilation + BP decrease

Question 99

Low output HF

Answer 99

(simply HF) CO reduced = decreased perfusion

Question 100

acute HF

Answer 100

isolated event without prior hx rapid prog. to critical illness; MI, myocarditis, drug toxicity PT may suffer chronic HF after Tx : underlyting cause

Question 101

chronic HF

Answer 101

management : low-salt diet, medications, monitor symptoms/vitals, lifestyle decisions (ADHF; acute decompensted HF) chronic HF PT can still develop acute HF = worsening symptoms any stress to the heart can result in decomp. (inf./diet/lifestyle/meds) Tx : hospital and underlying cause to be idetnified and treated

Question 102

NYHA Class 1

Answer 102

does not affect daily activity

Question 103

NYHA Class 2

Answer 103

comfortable resting, but slight limit in activity

Question 104

NYHA Class 3

Answer 104

markedly limited in physical activity, still comfort at rest

Question 105

NYHA Class 4

Answer 105

experience symptoms at any level of activity and sometimes at rest

Question 106

ACC/AHA Stages of HF

Answer 106

Stage A: high risk for HF w/o structural dis or symptoms Stage B: structural dis but w/o s/s of HF Stage C: structural dis w/ prior or current symptoms Stage D: refractory HF requiring specialized interventions

Question 107

Killip Classification

Answer 107

Class I: No heart failure. No clinical signs of cardiac decompensation Class II: Heart failure. Diagnostic criteria include rales, S3 gallop and venous hypertension Class III: Severe heart failure. Frank pulmonary edema Class IV: Cardiogenic shock. Signs include hypotension (systolic blood pressure of ≤90 mmHg) and evidence of peripheral vasoconstriction such as oliguria, cyanosis, and diaphoresis. Heart failure, often with pulmonary edema, has been present in a majority of these patients.

Question 108

systolic HF (cause)

Answer 108

dilated cardiomyopathy (weakening of heart muscle) idiopathic, ischemic (related to Coronary Artery Disease), or genetic CAD w/ MI, diabetes, thyroid, hormonal alcohol or cocaine nutritional deficiencies, chemo

Question 109

Preload

Answer 109

amount of blood in the ventricle before contraction, at the end of diastole affected by: body fluid volume, venous return to heart, and EF (ejection fraction)

Question 110

Afterload

Answer 110

amount of pressure the heart needs to generate to pump blood out of the ventricle the ventricle must contract strongly enough to overcome the blood pressure in that system Reducing afterload typically allows the heart to work more efficiently

Question 111

contractility

Answer 111

strength of muscular contraction in the heart muscle. Greater contractility typically leads to increasing stroke volume

Question 112

SVR

Answer 112

(systemic vascular resistance) resistance to forward flow of blood generated by the blood vessels in the systemic circulation Normal SVR is 800-1200 dynes-sec/cm^5. Low SVR = lower pressure needed to provide fwd flow

Question 113

blood flow through the heart

Answer 113

right atrium > tricuspid > right ventricle > pulmonary valve > lungs > left atrium > mitral > left ventricle > aortic

Question 114

cardiac remodeling

Answer 114

physical hypertrophy of heart muscle, becomes less coordinated with opposing ventricles, less elongated fibers, shorter and more rounded Angiotensin II contributes to promoted hypertrophy

Question 115

systolic HF (s/s)

Answer 115

fatigue, sleep disturbances, weight loss, anorexia, and dyspnea depression and cognitive dysfunction is also common peripheral edema, diminished distal pulses, hypotension, tachycardia, and narrow pulse pres-sure pulmonary edema and hepatic congestion may also develop, manifesting in cough, frothy sputum, and right upper quadrant tenderness or pain.

Question 116

systolic HF (Tx)

Answer 116

reducing symptoms by decreasing fluid retention and counteracting the neurohormonal effects of HF. ACE inhibitors are considered first-line therapy in the treatment of systolic HF.

Question 117

diastolic HF (cause)

Answer 117

stiffnes of hear muscles, abnormal electrolyte movement into and out of the myocardial cells causing failure of the heart muscle to completely relax

Question 118

diastolic HF (s/s)

Answer 118

dyspnea with exercise, more fluid retention in abdomin (PT describe as bloating or fullness)

Question 119

diastolic HF (Tx)

Answer 119

No therapy has been shown to improve survival in patients treat PT according to underlying disease

Question 120

left-side HF (cause)

Answer 120

cardiomyopathy, coronary artery disease, alcohol or cocaine abuse, or hypertension

Question 121

left side HF (s/s)

Answer 121

hypertrpophic heart, increase in pulmonary venous pressure = paroxysmal nocturnal dyspnea, activation of RAAS = increase in preload and afterload reduced CO = hypotension, fatigue, decreased urine output, exercise intolerance, dizziness, syncope, distal pulse decrease, cool skin, tachycardia, BP low, weight loss

Question 122

paroxysmal nocturnal dyspnea

Answer 122

sudden shortness of breath while sleeping

Question 123

orthopnea

Answer 123

difficulty breathing while laying flat

Question 124

left-side HF (Tx)

Answer 124

similar to systolic HF: reversing the effects of the body’s natural responses to the HF, Fluid retention is alleviated by the use of diuretics, RAAS is blocked by the use of ACE inhibitors PT educated to weigh themselves, monitor vitals, and low-sodium diet

Question 125

right-side HF (cause)

Answer 125

typically caused by left-side HF pulmonary HTN (pressure too great for afterlod of right ventricle to pump), ischemia, contractility reduction

Question 126

right-side (s/s)

Answer 126

In right ventricular failure, the left ventricle is inadequately filled, leading to reduced CO. Patients may exhibit s/s of reduced CO, including cool extremities, poor distal pulses, fatigue, exercise intoler-ance, and syncope Patients may complain of nausea, vomiting, and early satiety as the liver enlarges and causes pressure on the stomach, liver function may be impaired elevated jugular venous pressure, distended neck veins, peripheral edema

Question 127

pulmonary vascular resistance

Answer 127

the resistance to flow of blood generated by the blood vessels in the pulmonary circulation

Question 128

right-side HF (Tx)

Answer 128

dependent on underlying cause; help reduce RV afterload and improve RV failure; low sodium diet

Question 129

high output HF (cause)

Answer 129

marked by unusually low SVR and elevated CO; caused by dilation of vascular bed or arteriovenous fistula decrease SVR = anemia (nitric oxide > vasodilation), sepsis

Question 130

arteriovenous fistula

Answer 130

abnormal connection between 1+ arteries and 1+ veins = systemic shunting (caused by): Paget disease, multiple myeloma, liver disease, or an artificially created fistula such as one created for dialysis

Question 131

high output HF (s/s)

Answer 131

similar to systolic, (and right side HF) signs of volume overload such as hepatic congestion, elevated jugular venous pressure, and peripheral edema. Patients may also experience fatigue and dyspnea

Question 132

high output HF (Tx)

Answer 132

treating cause of vasodilation, control symptoms, and support vital functions

Question 133

cardiac index

Answer 133

value obtained when the CO is divided by body surface area

Question 134

CAD

Answer 134

(coronary artery disease) bloodflow to myocardium is reduced sometimes interchangeable w/ (coronary heart disease) buildup of plaque (made of cholesterol) [fatty] deposits in the coronary arteries (atherosclerosis) Dx included with CHD: silent myocardial ischemia, myocardial infarction, angine pectoris, acute coronary syndrome (ACS)

Question 135

angina

Answer 135

(angine pectoris) chest pain, discomfort, pressure, squeezing symptoms of CAD when the heart is not receiving enouhg perfusion blood

Question 136

CVD

Answer 136

(cardiovascular disease) commonly atherosclerosis, causes disease of the heart and coronary and systemic circulation Dx include: stroke, TIA, claudication, and limb ischemia

Question 137

claudication

Answer 137

leg pain that is induced by exercise, typically caused by decreased arterial blood flow

Question 138

myocardial ischemia

Answer 138

restriction or decrease in bld supply to the heart muscle tissues = shortage of O2

Question 139

myocardial infarction

Answer 139

complete occlusion of bld flow leading to cell death, or necrosis athersclerosis > thromboembolism thrombus (blood clot) is carried through the vessel and becomes lodged (embolism)

Question 140

ideal cardiovascular health

Answer 140

w/o cardiovascular disease Life Simple 7: BP, physical activity, cholesterol, diet, weight, smoking habits, blood glucose

Question 141

thrombosis

Answer 141

process of formation of a thrombus that obstructs blood flow to organs depending on where it comes from; when formed in coronary artery, the block can cause an MI

Question 142

vasospasm

Answer 142

a sudden contstriction of a blood vessel that decreases the vessels diameter and thus decreases blood flow

Question 143

aneurysm

Answer 143

a localized, blood-filled, balloon-like bulge in the wall of a blood vessel

Question 144

a name for atherosclerosis that can affect all arteries in the body?

Answer 144

ASCVD (atherosclerotic cardiovascular disease)

Question 145

dysrhythmia

Answer 145

abnormal heart rhythm that can be irregularly slow or fast (aka arrhythmia)

Question 146

coronary angiography

Answer 146

(aka coronary arteriography) invasive procedure that is usually used to confirm the diagnosis of CAD after noninvasive test have been inconclusive

Question 147

coronary perfusion pressure

Answer 147

the pressure of blood through coronary circulation as a result of the pressure gradient between the aortic pressure and the right atrial pressure

Question 148

autoregulation

Answer 148

the phenomenon that maintains the constant regulation of coronary blood flow through the myocardium despite changes in coronary perfusion pressure

Question 149

tachycardia

Answer 149

(abnormal rapid heart rate, generally more than 100 beats per minute)

Question 150

stable angina

Answer 150

occurs with increased myocardial oxygen demand and reduced blood flow during exertion or emotional stress, commonly caused by atherosclerosis

Question 151

stable angina (cause)

Answer 151

gradual narrowing of the arteries: endothelial dysfunction, coronary microvascular disease (MVD), vasospasms

Question 152

stable angina (s/s)

Answer 152

chest discomfort {usual complaint}, may also result as postpandrial (after eating), dyspnea, fatigue, belching same as angina pectoris, sqeezing, tightness, crushing, suffocating, and pressure

Question 153

stable angina (Tx)

Answer 153

stress test (cardio-vascular magnetic resonance (CMR) myocardial perfusion imaging) Beta blockers, ACE inhibitors, or ARBs when ACE are not tolerated short-acting nitroglycerin

Question 154

silent ischemia

Answer 154

higher prevalence being likely for patients with diabetes

Question 155

silent ischemia (cause)

Answer 155

thought to be due to defective anginal warning as a result of an issue with peripheral and neural processing of pain

Question 156

silent ischemia (s/s)

Answer 156

chest pain may not always be present; ST-segment depression may or may not be present

Question 157

IHD

Answer 157

ischemic heart disease

Question 158

silent ischemia (Tx)

Answer 158

tx of symptomatic and asymptomatic ischemia would be similar = nitrates, beta blockers, CCBs (reduce or eliminate episodes) lipid-lowering therapy as secindary

Question 159

MVD (cause)

Answer 159

not currently known, could be d/t ischemic process or other causes such as endothelial and microvascular dysfunction, coronary vaso-spasms, or myocardial metabolism problems

Question 160

MVD

Answer 160

(microvascular dysfunction or coronary microvascular dysfunction) damage to the walls and inner linings of small coronary arteries that can lead to narrowing, spasms, and decreased blood flow

Question 161

MVD (s/s)

Answer 161

angina in the absence of ischemia caused by CAD is a common characteristic, difficult to differentiate from angina with ischemia

Question 162

MVD (Tx)

Answer 162

standard test used to detect CAD do not work for MVD; noninvasive methods: Doppler echocardiography, SPECT scan, and CMR myocardial perfusion imaging, have proved helpful in detecting MVD

Question 163

ACS

Answer 163

(acute coronary syndrome) acute form of CAD; any cluster of clinical signs and symptoms that are related to acute myocardial ischemia and infarction Types: - non–ST-segment elevation acute coronary syndrome (NSTE-ACS), which formerly was known as unstable angina - non–ST-segment elevation myocardial infarction (NSTEMI) - ST-segment elevation myocardial infarction (STEMI)

Question 164

NSTE-ACS

Answer 164

(non–ST-segment elevation acute coronary syndrome) formerly known as unstable angina presents as myocardial ischemia without ST elev. accelerates in frequency and severity but does not result in myocardial necrosis {ischemic}

Question 165

NSTEMI

Answer 165

(non-ST-segment elevation mycardial infarction) myocardial ischemia in the absence of ST elevation on ECG but the presence of elevated biomarkers of myocardial necrosis = acute MI major difference between NSTEMI and unstable angina is the biomarker of necrosis {infarction}

Question 166

STEMI

Answer 166

(ST-segment elevation mycardial infarction) myocardial necrosis more precise term for heart attack {infarction}

Question 167

unstable angina

Answer 167

chest discomfort or pain related to lack of blood flow through coronary arteries and subsequent myocardial ischemia that is less predictable than stable angina and may occur at rest

Question 168

STEMI (cause)

Answer 168

state of heightened inflammation and prothrombotic components adv. atherosclerosis, nonobstructive plaque rupture, embolus exposure to fine particle pollution could increase risk of ACS,

Question 169

atrial fibrillation

Answer 169

dys-rhythmia that may cause pooling and clotting of blood and the risk of embolization if the clot breaks free and obstructs an artery

Question 170

STEMI (s/s)

Answer 170

ischemic nerve endings cause pain, but necrotic myocardium will not angina, dyspnea, malaise (radiate to shoulder, arms neck), fatigue, diaphoresis, palpitations

Question 171

bradycardia

Answer 171

less than 60BPM

Question 172

STEMI (s/s)

Answer 172

ischemic nerve endings cause pain, but necrotic myocardium will not angina, dyspnea, malaise (radiate to shoulder, arms neck), fatigue, diaphoresis, palpitations

Question 173

STEMI (Tx)

Answer 173

ECG alone is not sufficient to Dx a STEMI timely reperfusion and function of caridomyocytes Timely Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a nonsurgical technique for treating obstructive coronary artery disease, including unstable angina, acute myocardial infarction (MI), and multivessel coronary artery disease (CAD) will greatly increase survival chance.

Question 174

automaticity

Answer 174

ability of specialized myocardial cells, or pacemaker cells, to generate an electrical impulse (depo-larize) to regulate the heart rate in accordance to the body’s needs.

Question 175

absolute refractory period

Answer 175

time after the firing of a nerve fiber during which the nerve fiber can-not be stimulated, regardless of the strength of the stimulus applied

Question 176

VF

Answer 176

(ventricular fibrillation) most serious dysrhythmia; has greatest risk of occurence within first hour of MI related to absolute refractory period

Question 177

which electrolyte imbalances have the greatest risk for heart dysrhythmias?

Answer 177

hypokalemia and/or hypomagnesemia

Question 178

ventricular aneurysm

Answer 178

defect in the left or sometimes right ventricle wall in which there is bulging outward dur-ing both systole and diastole, usually as a result of a MI (cause) female, LAD artery occlusion, no Hx of angina (s/s) 3-4 heart sound present, systolic murmur TTE (transthoracic echocardiography) used to identify

Question 179

ventricular septal rupture

Answer 179

type of ventricular septal defect in which there is an abnormal opening between the left and right ventricles causing oxygenated blood (from the left ventricle) to mix with deoxygenated blood (from the right ventricle) as a result of left-to-right shunting.

Question 180

pericarditis

Answer 180

swelling and inflammation of the pericar-dium, the thin double-layered sac surrounding the heart, as a result of injury such as an acute MI, infection, inflam-matory disorder, trauma, cancer, or congenital causes 10% chance to accour 23-96hrs post-MI

Question 181

Dressler syndrome

Answer 181

also known as post-MI syndrome, is the late pericarditis and possibly has an autoimmune pathogenesis

Question 182

pericarditis (s/s)

Answer 182

pleuritic chest pain, pain worsens with deep inspiration, cough, swallow, lying down pericardial friction may rub and be auscultated

Question 183

pericarditis (Tx)

Answer 183

hospitalization for management and OBS of possible cardiac tamponade, aspirin every 4-6hr to reduce inflammation and treat pain

Question 184

cardiac tamponade

Answer 184

life-threatening condition of increased pericardial pressure as a result of blood or fluid buildup between the myocardium and the pericardium

Question 185

cardiac tamponade (cause)

Answer 185

pericardial effusion (fluid accumulation), trauma, inf, cancer, med side effect, HF, MI, raditation, Dressler, PCI, surgery, inflammatory disease

Question 186

cardiac tamponade (s/s)

Answer 186

dyspnea, edema, oliguria (low urine output), jugular venous distention, tachypnea {pant}, and tachycardia

Question 187

cardiac tamponade (Tx)

Answer 187

prompt surgical Tx is needed, MRI can confirm presence, fluid removed and examined to identify cause

Question 188

valvular disorders

Answer 188

problems that disrupt blood flow through the atria and ventricles as a result of abnormal func-tioning of one or more of the four heart valves such as stenosis, regurgitation, or prolapse

Question 189

the four heart valves?

Answer 189

atriventricular: tricuspid and mitral semilunar: pulmonic and aortic

Question 190

valvular disorders (cause)

Answer 190

Increased risk of valvular disorders is associated with age, gender, tobacco use, high cholesterol levels, hypertension, and diabetes

Question 191

regurgitation

Answer 191

leaking valve; not closing completely

Question 192

prolapse

Answer 192

valves don't close smoothly, or overextend into next chamber (balloon)

Question 193

stenosis

Answer 193

hardening or fusion; in the case of mitral valve, may be fused together and restrict blood flow; or could be hardened in an open state and function improperly

Question 194

valve disorder (Tx)

Answer 194

surgical replacement

Question 195

coronary collateral circulation

Answer 195

can develop in the heart as an adaptation to ischemia; as an alternative path for blood supply

Question 196

PVD

Answer 196

(peripheral vascular disease) general term referring to conditions affecting circulation in the tissues other than the brain or heart affects veins; chronic venous insuffi-ciency, deep vein thrombosis, leg ulcers, and varicose veins

Question 197

PAD

Answer 197

(peripheral artery disease) affects arteries, caused by arteriosclerosis

Question 198

arteriosclerosis

Answer 198

thickening, loss of elasticity, clacification of walls of arteries

Question 199

atherosclerosis

Answer 199

build up of plaque within artery that harden and narrow

Question 200

plaque is made of

Answer 200

cholesterol, calcium

Question 201

hyperlipidemia

Answer 201

(form of dyslipidemia) elevated level of blood lipids

Question 202

LDL

Answer 202

(Low-density lipoproteins) primary carriers of cholesterol "Less-Desireable Lipoproteins"

Question 203

HDL

Answer 203

(high-density lipoproteins) help to clear cholesterol from the arteries "highly-desireable lipoproteins"

Question 204

atheroma

Answer 204

region of plaque consists of calcium, macrophages, lipids, and fibrous connective tissue, where atherosclerotic narrowing begins to build up

Question 205

vulnerable plaque

Answer 205

more inflammation and thinner fibrous cap, more susceptible to rupture with subsequent thrombi formation

Question 206

arterial dissection

Answer 206

caused by a tear in the tunica intima in which the blood vessel splits and blood goes between the inner and outer layers, separating the walls trauma, heredity, cocaine use, pregnancy, and hyperten-sion are associated risk factors

Question 207

angioplasty

Answer 207

stent placement is the minimally invasive procedure A balloon-tipped catheter is placed into an artery and advanced to the area of blockage. The balloon is inflated, pressing the plaque against the arterial wall. Once opened, the balloon is deflated, and a small wire mesh tube called a stent is placed in the vessel to keep it from narrow-ing or closing again

Question 208

NAPAD

Answer 208

(Nonatherosclerotic peripheral arterial disease) group of disorders in which blood flow is decreased for reasons other than plaque buildup coarctation of the aorta, thoracic outlet syndrome, and Raynaud disease

Question 209

TOS

Answer 209

(thoracic outlet syndrome) thoracic outlet starts at the base of the neck and goes behind the clavicle, over the first rib, and down the arm If the path is narrowed, it can restrict the flow of blood and nerve function (s/s) poor bld flow or decreased nerve function

Question 210

coarctation

Answer 210

birth defect resulting in narrowing of aorta

Question 211

Raynaud disease

Answer 211

condition characterized by attacks of vasospasm in the small arteries and arterioles in the fingers often triggered by cold weather and emotional stress Primary (idiopathic), secondary (caused by another condition) (s/s) skin devoid of color, cyanotic, numbness, tingling, ischemia may result in ulceration or necrosis

Question 212

Raynaud (Tx)

Answer 212

events may not be severe enough for medical attn. tx for 2nd addresses underlying condition prime med is calcium channel blockers

Question 213

CVI

Answer 213

(chronic venous insufficiency) disorder in which the veins are unable to return adequate blood to the heart long-term disorder that most com-monly occurs as a result of blood clots in the deep veins of the legs, a condition called deep vein thrombosis (DVT)

Question 214

CVI (causes)

Answer 214

genetic predisposition, gender (the disorder is more com-mon in women), pregnancy, age over 50 years, smoking, lack of physical activity, obesity, and occupations requiring long periods of standing or sitting. Use of oral contracep-tives

Question 215

CVI (s/s)

Answer 215

leg cramps and pain that worsens when standing, edema of leg, thickening or discoloration of skin on calves

Question 216

leg ulcers

Answer 216

(CVI is most common cause) sores on the skin that persist for more than 6 weeks and take several months or longer to heal

Question 217

varicose veins

Answer 217

veins that have become enlarged and twisted because of the rupture of valves superficial thrombophlebitis = inflam of varicose veins

Question 218

DVT

Answer 218

(deep vein thrombosis) a thrombus (blood clot) occurs in a vein deep in the body; the thrombus may become an embolism that can travel to the heart, lungs, brain, or other vital organs of the body. (s/s) pressure builds, fluid starts to leak out of the swollen veins, causing edema and additional pain. The area may become reddened, hard, and warm as a result of blood backing up in the area.

Question 219

DVT (Tx)

Answer 219

a positive D-Dimer indicates high amount of fibrin degradation and suggests clot formation Obesity is the main culprit for DVT

Question 220

Elevated BP

Answer 220

120-129 AND < 80

Question 221

Stage 1 HTN

Answer 221

130-139 OR 80-89

Question 222

Stage 2 HTN

Answer 222

>140 OR >90

Question 223

Stage 3 HTN

Answer 223

>190 AND/OR >120

Question 224

essential HTN

Answer 224

(primary HTN) HTN that does not have a known cause 90% of the cases

Question 225

secondary HTN

Answer 225

identifiable and categorized cause

Question 226

hypertensive urgency

Answer 226

patient presents with severe HTN without evidence of organ damage

Question 227

hypertensive crisis (s/s)

Answer 227

myocardial ischemia or infarction. Renal function is diminished, and blood or protein may be found in the urine. Acute renal failure may occur. In the brain, thrombotic or hemorrhagic stroke may occur. The capillaries in the brain become leaky, producing hypertensive encephalopathy (edema of the brain), with symptoms of headache, paralysis, seizures, or coma. Reti-nal hemorrhages and edema of the retina (papilledema) are signs of severe HTN.

Question 228

hypertensive crisis

Answer 228

rare condition that occurs when systolic pressure exceeds 180 and/or diastolic pressure exceeds 120 mmHg. formerly called malignant hypertension or hypertensive emergency Organ damage occurs primarily in the cardiovascular system, kidneys, or brain

Question 229

HTN lifestyle changes

Answer 229

□■Restrict sodium consumption □■Limit alcohol consumption □■Stop smoking □■Maintain an optimal weight □■Reduce intake of saturated fat and cholesterol, and increase consumption of fruits and vegetables □■Increase physical activity □■Reduce stress levels

Question 230

hemostasis

Answer 230

cessation of blood flow, particularly through the action of coagulation related to conditions of excess coagulation or bleeding

Question 231

hemorrhage

Answer 231

copious bleed-ing, which can be outside of the skin (as from a laceration) or in the skin (ecchymoses) bruise

Question 232

ecchymoses

Answer 232

(bruise) bleeding within skin

Question 233

thrombocytes

Answer 233

(platelets)

Question 234

phases of hemostasis

Answer 234

vascular (initiation): constriction of vessels + platelet activation aggregation (amplification): platelet begin to clump and form plug coagulation (propagation): platelet rel. factors = form fibrin = layer over plug to stop blood loss

Question 235

thrombocytopenia

Answer 235

(reduction in number of platelets)

Question 236

primary hemostasis

Answer 236

associated with abnormalities in the number or function of platelets Ex: von Willebrand, a lack of a certain factor prevents platelets from adhering to the site of injury, prevent clot

Question 237

secondary hemostasis

Answer 237

lack of, or reduction in, factors tied to coagulation Ex: lack of factor VIII = hemophilia

Question 238

hereditary hemostasis

Answer 238

vWD and hemophilia

Question 239

aquired hemostasis

Answer 239

liver disease and vitamin K utilization

Question 240

thrombocythemia

Answer 240

an excess of platelets can lead to spontaneous blood clot formation

Question 241

bleeding precautions

Answer 241

Patients who are at risk of excessive bleed-ing need to be educated about their condition and provided with instructions about preventing bleeding. soft toothbrush, wearing shoes at all times, avoiding contact sports, and using stool softeners to prevent straining

Question 242

intrinsic factor pathway

Answer 242

XII > PF3 > VIII & IX > X

Question 243

extrinsic factor pathway

Answer 243

III > VII > X

Question 244

common pathway

Answer 244

X > Prothrombin activator > Prothrombin > Thrombin > Fibrinogen > Fibrin

Question 245

hematopoiesis

Answer 245

the process behind the formation of blood cells

Question 246

megeakaryocytopoiesis

Answer 246

(aka thrombocytopoiesis) formation of thrombocytes, reflecting their emergence from megakaryocytes

Question 247

vWD

Answer 247

(von Willebrand Disease) most common bleeding disorder; a lack of a certain factor prevents platelets from adhering to the site of injury, prevent clot 1% population, M&F

Question 248

type 1 vWD

Answer 248

70–80% of all cases of the disease and is characterized by either a failure to manufacture the factor or an increase in clearance

Question 249

type 2 vWD

Answer 249

binding ability of the factor is either significantly enhanced or delayed, resulting in functional deficits

Question 250

type 3 vWD

Answer 250

more severe form in which there is a complete absence of production of the factor

Question 251

D-dimer

Answer 251

measures a fragment of fibrin degradation

Question 252

aPTT

Answer 252

(Activated partial thromboplastin time) Measures the same parameters as PTT but with the addition of a clotting activator to enhance the speed of clotting. This results in a test that is seen as more sensitive

Question 253

PTT

Answer 253

(Partial thromboplastin time) Measures the effectiveness of factors I (fibrinogen), II (prothrombin), V, VIII, IX, X, XI, and XII

Question 254

PT

Answer 254

(Prothrombin time) Measures the functional ability of the extrinsic clotting pathway. Examines factors II (prothrombin), V, VII, and X and fibrinogen

Question 255

vWD (s/s)

Answer 255

varies per type and blood type type 1: asymp.; becomes apparent during surgery = excess bleeding type 3: similar to hemophilia, life-threat + internal bleed

Question 256

Tx for spontaneous bleeding episode

Answer 256

DDAVP (desmopressin) and transfusion with plasma-derived vWD products

Question 257

thrombocytopenia

Answer 257

norm platelet range : 150,000-450,000 /muL increased bleed occurs : 80,000-100,000

Question 258

thrombocytopenia (causes)

Answer 258

artifact, deficient prod.; increased destruction, consumption, or both pseudothrombocytopenia = use of anticoagulant

Question 259

HIT

Answer 259

(heparin-induced thrombocytopenia) type 1 : modest transient decrease in platelet count within the first 2–3 days after initiation of heparin therapy type 2 : (heparin-induced thrombocytopenic thrombosis or white clot syndrome) antibodies to platelet factor IV on the heparin complex. It is seen about 4–14 days after initiation of heparin therapy

Question 260

ITP

Answer 260

(immune thrombocytopenic purpura) autoimmune disease that causes increased destruction of platelets

Question 261

TTP

Answer 261

(Thrombotic thrombocytopenia purpura)

Question 262

purpura

Answer 262

bleeding associated with thrombocytopenia is usu-ally mucocutaneous in nature—on the skin in the form of tiny pinprick hemorrhages or bruises

Question 263

TTP (s/s)

Answer 263

(1) microangiopathic hemolytic anemia (2) thrombocytopenia (3) renal insufficiency (4) fever (5) mental status changes that can wax and wane

Question 264

TTP (Tx)

Answer 264

plasmapheresis = cornerstone of therapy, slowing the destruction of platelets

Question 265

hemophilia

Answer 265

hereditary bleeding disorder resulting from the loss of select clotting factors 2 forms: A&B Male; carrier females have a 50% chance to pass on

Question 266

hemophilia A

Answer 266

a lack of factor VIII

Question 267

hemophilia B

Answer 267

a deficiency in factor IX

Question 268

hemophilia (Tx)

Answer 268

episodic home administration of factor deficient concentrates

Question 269

DIC

Answer 269

(Disseminated intravascular coagulation) life-threatening condition in which the proteins that control clot-ting become overactive; individual faces an increased risk of hemorrhage. (s/s) increased tissue ischemia and bleeding

Question 270

DIC (cause)

Answer 270

sepsis, shock, trauma Dmg to blood vessels and tissue and inflammation can lead to an increase in the concentration of a protein known as tissue factor

Question 271

DIC (s/s)

Answer 271

formation of numerous clots, organ dysfunction DVT or pulmonary embolism testing is critical dyspnea, hemoptysis, SOB, tachycardia, hypotension

Question 272

DIC (Tx)

Answer 272

evaluation of vital signs, assessment of intake and output, and monitoring circulatory status for either the obstruction of blood flow or the presence of hemorrhage determine underlying cause

Question 273

what presents similarly as DIC

Answer 273

thrombocythemia (excess platelets = numerous clots)

Question 274

anemia

Answer 274

characterized by a reduction in the number RBCs or a decline in the ability of erythrocytes to carry oxygen

Question 275

erythrocytes

Answer 275

RBC

Question 276

Hb

Answer 276

(hemoglobin)

Question 277

polcythemia vera

Answer 277

excess of RBCs blood is more viscous = decrease in flow of blood = depriving organs of O2

Question 278

anemia (cause)

Answer 278

1) decrease in prod of erythrocytes 2) reduction in survival time of erythrocytes 3) loss of erythrocytes d/t acute/chronic blood loss 4) func. change in structure of erythrocytes

Question 279

MVC

Answer 279

(mean corpuscular volume) Changes in erythrocyte size; this reflects average RBC size HCT/number of cells in blood

Question 280

fL

Answer 280

(femoliters) unit of measurement equal to 1mm^3; reported value of MVC norm: 80-100

Question 281

HCT

Answer 281

(hematocrit) the proportion of red blood cells in a volume of blood

Question 282

microcytic/macrocytic anemia

Answer 282

presence of small or large erythrocytes micro: cells are smaller than normal, generally as a result of lack of mat-uration time or lower levels of iron macro (megablastic): cells that are larger than normal, generally because of a lack of certain nutrients necessary for successful (DNA) replication

Question 283

MCH

Answer 283

(mean corpuscular hemoglobin) Cell color is determined and reported in picograms norm: 27-34 pg

Question 284

hypochromic

Answer 284

Cells with a lower amount of hemoglobin appear washed out and pale

Question 285

normochromic

Answer 285

Cells that resemble the normal cell color normochrom. anemia = decreased in cell number through blood loss or premature destruction

Question 286

folic acid

Answer 286

B vitamin that is necessary for cell maturation and DNA repair

Question 287

thalassemia

Answer 287

a group of genetic disorders that affect hemoglobin

Question 288

aplastic anemia

Answer 288

reduction in number of stem cells present

Question 289

erythropoietin

Answer 289

hormone commonly provided in the clinical setting as a pharmacologic therapy to aid in the treatment of anemia (hemolytic anemia = destruction of RBC)

Question 290

anemia risk factors

Answer 290

(1) patients with nutritional deficits (iron and B vitamins) (2) patients with intestinal disorders preventing the ability to absorb nutrients (3) patients with chronic health problems (4) patients who are pregnant (5) patients who are experiencing gastrointestinal bleeding (6) patients who have genetic risks such as those with sickle cell disease

Question 291

anemia (s/s)

Answer 291

decreased O2 can lead to muscle weakness, headaache, dizziness (not enough O2 to brain), pallor, tachycardia, hypotension, increased respirations,

Question 292

anemia (Tx)

Answer 292

blood transfusions, replacement of iron or B12, stim factors to promote maturation of RBCs

Question 293

iron deficiency anemia

Answer 293

occur through either a reduc-tion in dietary iron or a loss of iron loss of iron most commonly occurs through hemorrhage, menstrual blood loss in females, and gastrointestinal bleeding in males and females

Question 294

cobalamin deficiency

Answer 294

(vitamin b12) Intrinsic factor is a necessary step in the utilization of cobalamin; changes in the release or absorption of this factor can have adverse effects on red blood cell function. most common cause: pernicious anemia

Question 295

Folic Acid Deficiency

Answer 295

Folic acid works in conjunction with cobalamin, and in its absence, a macrocytic anemia can result

Question 296

folate

Answer 296

B vitamin that is essential for maintenance of DNA

Question 297

SCD

Answer 297

(sickle cell disease) cluster of autosomal recessive disorders that results in misshapen forms of hemoglobin that resemble a sickle or crescent in shape individual has inherited a mutated form of hemoglobin referred to as hemoglobin S (HbS) from both parents chrom 11

Question 298

SCD (s/s)

Answer 298

ischemia anywhere in body, resulting in pain, swelling, tenderness, rapid respiratory rate, HTN chronic tissue hypoxia and tissure dmg

Question 299

SCD (Tx)

Answer 299

prevention, screening, sup-portive care, disease-modifying strategies, and curative procedures O2 supp, blood transfusion, chronic pain management (vaso-occlusive crisis) opiod analgesics

Question 300

thalassemia (cause)

Answer 300

a defect in production of one or more of the globin chains. Hemoglobin comprises four protein chains: a set of two alpha chains and two beta chains alpha: mutation occurs on chromosome 16 beta: mutation of a gene on chromosome 11 is the causative agent

Question 301

thalassemia (s/s)

Answer 301

Growth retardation and cognitive deficits, often identified in early infancy jaundice

Question 302

aplastic anemia (cause)

Answer 302

immune-mediated attack: Activated T cells lead to a process of apoptosis (programmed cell death) within the bone mar-row. These apoptotic processes result in a relative deple-tion of both immature and stem cell populations within the bone marrow.

Question 303

ACD

Answer 303

(anemia of chronic disease) aka anemia of chronic inflammation patients with chronic disease, being associated with inflammatory infectious processes such as infection, chronic immune activation, or malignancy

Question 304

normocytic

Answer 304

the cell size is within the normative range

Question 305

hypoproliferative

Answer 305

number of RBCs are reduced

Question 306

ACD (cause)

Answer 306

iron is a necessary nutrient for bacterial growth, in ACD the body is attempting to deplete iron so not to feed the bacteria

Question 307

ACD (s/s)

Answer 307

generally mild, tired, SOB; no differnt from other anemic forms

Question 308

ACD (Tx)

Answer 308

focused on chronic condition underlying disease as ACD is an adaptive response

Question 309

Polycythemia vera

Answer 309

disorder of the bone marrow in which too many red blood cells are produced; white blood cells and platelets may increase as well primary (absolute): increase in the production of erythrocytes on the part of bone marrow (myeloproliferative) secondary: genetic modifications related to the production of erythropoietin

Question 310

polycythemia vera (s/s)

Answer 310

headache, dizziness, and blurred vision associated with the increased blood volume, increased preload = HTN, blood viscosity = blood clots

Question 311

polycythemia vera (Tx)

Answer 311

anitcoagulation to prevent thrombi, blood-letting to reduce RBC amount and dilute concentration

Question 312

benign

Answer 312

grwoths that contain nonmalignant cells

Question 313

malignant lung tumors (cause)

Answer 313

smoking (responsible for 80-90%) - cigarettes - cigar/pipe - weed/cocaine - 2ndhand smoke - occupational exposure - genetics - benign chronic lung conditions - viral inf - diet - gender : women more susceptible to carcinogen

Question 314

Adenocarcinoma

Answer 314

most common form of lung cancer more common in F than M

Question 315

large cell carcinmoa aka...

Answer 315

undifferentiated tumors, least common form of NSCLC (Non–small cell lung cancer)

Question 316

lung cancer (s/s)

Answer 316

persistent cough w/ or w/o sputum, (cough is usually attributed to smoking, COPD, respiratory inf) blood in sputum, recurrent pneumonia or bronchitis, dyspnea, chest pain, hoarseness, and paraneoplastic syndromes (adv lung cancer)

Question 317

NSCLC (Tx)

Answer 317

Clinical staging is based on the tumor size (T), location of cancer in lymph nodes (N), and metastases (M) stage 0-1 : surgery stage 2-4: surgery is performed, radiation and/or chemotherapy

Question 318

SCLC (Tx)

Answer 318

surgery typically is not indicated multiple chemotherapeu-tic agents and radiation untreated survival = 2-4 months

Question 319

TB

Answer 319

(tuberculosis) primary TB infection: M. tuberculosis organisms have seeded areas in the lung but have not caused significant tissue damage (s/s) : fever and pleural effusion are infrequent disease tuberculosis: clinically significant tissue damage has occurred and the infection is contagious

Question 320

risk factors of TB

Answer 320

□■HIV/AIDS □■Foreign immigration □■Low income, homelessness, and/or malnourishment □■Residing in crowded urban conditions □■Incarceration □■Ethnic minorities (e.g., Hispanics, African Americans, Asians) □■Old age □■Chronic disease (e.g., diabetes mellitus, chronic lung disease, Hodgkin disease, chronic renal failure, alcohol-ism, immunosuppression) □■Currently smoking cigarettes

Question 321

TB (causes)

Answer 321

in US, primary transmitted between infected person and susceptible person via inhalation of aerosolized droplet

Question 322

secondary TB

Answer 322

reactivation of latent TB

Question 323

TB (s/s)

Answer 323

cough, weight loss and anorexia, fever, night sweats, dull aching chest pain, and hemoptysis,

Question 324

TB (Tx)

Answer 324

10 meds; 2-7 months

Question 325

BCG

Answer 325

(bacillus Calmette-Guérin) vaccine that provides immunity to TB

Question 326

dimorphic fungal infection

Answer 326

endemic to particular geo-graphic areas and cause primary infections in both healthy and immunocompromised individuals.

Question 327

histoplasmosis

Answer 327

caused by inhaling spores of Histoplasma capsulatum, is endemic to the Ohio, Missouri, and Mississippi; Caribbean and Central and South America

Question 328

Coccidioidomycosis

Answer 328

(San Joaquin Valley fever) caused by Coccidioides immitis, which is endemic in the soil in the southwestern United States but can be found throughout the world grows best in bird feces

Question 329

Blastomycosis

Answer 329

caused by Blastomyces dermatitidis, an uncommon fungus that is found in Ohio, the Great Lakes region, and the Mississippi; common in dogs, horse, bats, and cows pulmonary granulomas

Question 330

fungal inf (s/s)

Answer 330

competent immune systems: asymp and discovered incidentally immunocompromised: cough and fever plus hemoptysis, dyspnea, and chest pain, weight loss, and hepatosplenomegaly

Question 331

URI

Answer 331

(upper respiratory tract infections) acute infection of one or more structures of the upper respi-ratory tract, including the nose, paranasal sinuses, pharynx, larynx, trachea, and bronchi

Question 332

URI increased risk

Answer 332

very old or very young malnourished = alcoholics cigarette smoke COPD, CF Impaired immune status (HIV, immunosuppressive therapy)

Question 333

URI (cause)

Answer 333

most are passde between human contact

Question 334

URI (s/s)

Answer 334

rhinorrhea (profuse, watery discharge from nose), cough that may or may not be productive, localized mucosal edema with erythema (redness)

Question 335

URI (Tx)

Answer 335

increase the individual’s comfort as well as treating the specific cause of the infection rest, increased fluids to dilute respiratory secretions and replace fluid loss, and antipyretics for systemic symptoms, lozenges, antihistamines

Question 336

croup

Answer 336

(laryngotracheobronchitis) acute viral infection of the upper respiratory tract commonly caused by parain-fluenza viruses that spread among children younger than 5 years of age acute inflammation of the larynx and trachea, narrowing obstructs breathing upon inhalation, wheezy, hoarse cough, fever, dyspnea, and restlessness s/s improve within 3-4 days Tx: moisture and nebulized bronchodilators

Question 337

Epiglottitis

Answer 337

rapidly progressive inflammation of the epiglottis and adjacent structures that is usually caused by bacterial infection, most commonly Haemophilus influen-zae type b (Hib) peaks in children at 3 y/o; but incidence has decreased with infant vaccination

Question 338

acute bronchitis

Answer 338

very common, self-limited lower respiratory tract inflammation, that is often referred to as a “chest cold.” can occur at the same time as a URI or follow one. Acute bronchitis is most often diagnosed in children younger than 5 years of age

Question 339

acute bronchitis (s/s)

Answer 339

broncial inflammation w/ mucousal congestion cough lasting 10-20 days, can persist longer with pertussis hyperreactivity can last 5-6 weeks

Question 340

pertussis aka

Answer 340

(whooping cough) highly contagious respira-tory infection that is usually caused by Bordetella pertussis common among young adults, outgrew child vaccination immunity (s/s) spasmatic cough that ends in loud inspiratory whoop; inf 6 weeks, cough 3-4months

Question 341

bronchiolitis

Answer 341

inflammation of the bronchioles; similar causation as acute bronchitis increased risk for bronchiolitis in premature infants and children with underlying pulmonary problems recurrent = d/t CF

Question 342

bronchiolitis

Answer 342

Symptoms of fine crackles and expiratory wheezing with deep breaths are similar to asthma symptoms, but asthma is uncommon in children under 2 years of age

Question 343

influenza

Answer 343

highly contagious viral infection that sweeps through a geographic region as an epidemic that lasts 6–8 weeks during the winter months flu + pneumonia = 8th leading cause of death in US

Question 344

those at risk for influenza

Answer 344

children < 5, esp. < 2 pregnant >50 y/o chronic medical cond. care home worker, healthcare worker

Question 345

flu types

Answer 345

Type A: most severe vs B or C

Question 346

antigenicity

Answer 346

ability to stimulate the formation of antibodies Major shifts in antigenicity are associated with epidemics and pandem-ics of influenza

Question 347

flu (s/s)

Answer 347

fever, headache, myalgias, and severe malaise after 1–2 days (photophobia and pain with eye movements can occur early) postinfluenza asthenia (postflu syndrome) can occur

Question 348

flu (Tx)

Answer 348

yearly flu shot is recommended alleviate symptoms if intiated within 48hrs

Question 349

pneumonia

Answer 349

inflammation of the lung parenchyma that is typically characterized by lung consolidation with alveoli filled with exudate

Question 350

HAP

Answer 350

(hospital-aquired pneumonia) not incubating at the time of hospital admission and develops 48 hours or more after hospital admission

Question 351

VAP

Answer 351

(ventilator-aquired pneumonia) develops more than 48–72 hours after tracheal intu-bation

Question 352

HCAP

Answer 352

(healthcare-associated pneumonia) patients who were hospitalized in an acute care hospital for 2 or more days within 90 days of developing the infection, or who resided in a long-term care facility or nursing home at the time of infection.

Question 353

CAP

Answer 353

(community-aquired pneumonia) bacteria or viruses, and bacterial pneumonias frequently follow URIs

Question 354

bacterial pneumo vs viral pneumo

Answer 354

bacterial: consolidation of lung tissue primarily by bacterial exudates within alveoli, but there is very little interstitial involvement viral: interstitial pneumonitis with patchy inflammatory changes in the lung interstitium and septa

Question 355

egophony

Answer 355

increased resonance of voice sounds heard on auscultation Lung consolidation is indicated by these bronchial breath sounds

Question 356

pneuomnia (Tx)

Answer 356

supp O2 in serious cases, may be treated with antibiotics for bacterial inf, antiviral meds for viral

Question 357

PH

Answer 357

(pulmonary HTN) increased blood pressure in the pulmonary arteries may represent disease (pulmonary arterial hypertension) can occur secondary to adv. COPD

Question 358

PH (cause)

Answer 358

increased blood flow d/t septal defects of heart, increased vascualr resistance in response to hypoxemia, inflam that cause vasoconstriction, left side HF, drugs like coke and meth

Question 359

PH (s/s)

Answer 359

dyspnea on exertion, lethargy, and fatigue because the heart is not able to increase cardiac output with exercise left side HF progresses to right ventricular failure, individuals may experience angina or syncope with exercise and develop edema hepatic congestion, jugular vein distention, abdominal pain

Question 360

PH (Tx)

Answer 360

vasodilators, specifically prostacyclin

Question 361

PAH

Answer 361

(Pulmonary arterial hypertension) increased pulmonary arterial resistance in the absence of left ventricular failure or chronic thromboembolism (cause): idiopathic

Question 362

embolus

Answer 362

substance or object that travels via the bloodstream to a blood vessel and subsequently lodges in the blood vessel, creating a partial or complete obstruction

Question 363

embolism

Answer 363

a condition in which an embolus travels via the bloodstream and subsequently lodges in a blood vessel

Question 364

PE

Answer 364

(Pulmonary embolism) an embolus is pumped from the right heart into progressively smaller pulmonary arteries until it wedges in a vessel that is too small for it to pass through

Question 365

those at risk of PE

Answer 365

prior Hx of DVT prolonged immobilization recent surgery pregnancy and 6-12 wks post delivery oral contraceptive older adults CVD active cancer hypercoagulability, burns, HIV, drug abuse

Question 366

PE (s/s)

Answer 366

shortness of breath or dyspnea that is not related to activity; hemoptysis; and chest pain that is worse with a deep breath, cough, eating, or bending. The chest pain is worse with exertion but does not go away with rest.

Question 367

PE (Tx)

Answer 367

thrombolytic therapy to dis-solve the clot, anticoagulation to prevent further clots, and oxygen supplementation

Question 368

pulmonary contusion

Answer 368

bruising in lung tissue from a shock wave of force common in motor vehicle accidents or explosion in young adults; potentially lethal

Question 369

alveloar hemorrhage sydromes

Answer 369

(Goodpasture syndrome and granulomatous vasculitis) autoimmunie disorders that affect lung and kidneys of young white adults cause : idiopathic

Question 370

goodpasture syndrome

Answer 370

uncommon antiglomerular basement antibody disease that targets the lungs and kidneys antibodies initiate inflammation of the basement membranes of alveoli and renal glomeruli (s/s): cough, dyspnea, fatigue, hemop-tysis, and burning on urination (Tx): Treatment includes immunosup-pressant drugs combined with intensive plasmapheresis

Question 371

Wegener granulomatosis

Answer 371

rare systemic vasculitis that restricts blood flow, causing damage that may be limited to the upper and lower respiratory tracts but can involve the kidneys and other organs; ANCAs (Antineutrophilic cytoplasmic antibodies) dmg tissue and intiate inflam (Tx) longer term immunosuppression with cytotoxic agents

Question 372

COPD

Answer 372

(chronic obstructive pulmonary disease)

Question 373

air trapping

Answer 373

during exercise, increased inspiratory volume combined with exhalation through contricted airway leads to air trapping impairs venitlation and gas exchange = lung hyperinflation

Question 374

TV

Answer 374

(tidal volume) Volume of air inhaled and exhaled during one cycle of normal unconscious breathing

Question 375

IRV

Answer 375

(Inspiratory reserve volume) after TV, IRV is the maximal volume of air that can be inhaled take a max deep breath

Question 376

ERV

Answer 376

(expiratory reserve volume) maximal amount of air you can exhale

Question 377

RV

Answer 377

(residual volume) the amount of air still in the lungs after ERV

Question 378

FRC

Answer 378

(func residual capacity) ERV + RV

Question 379

IC

Answer 379

(insp. capacity) TV + IRV

Question 380

vital capacity (VC)

Answer 380

ERV + TV + IRV

Question 381

hyperreactivity

Answer 381

an exaggerated response to a stimulus

Question 382

asthma

Answer 382

chronic inflammatory disorder of the airways characterized by recurrent episodes of reversible airway obstruction and hyperreactive airways

Question 383

risk factors of asthma

Answer 383

genetic atopy (predisposition to develop allergies) females after puberty obesity exposure to allergens, irritants, smoke (maternal smoking)

Question 384

classes of asthma

Answer 384

allergic (extrinsic or atopic): triggered by allergens that are external to the individual; type 1 hypersensitivity nonallergic (intrinsic or nonatopic): generate an inflammatory response that involves IgE

Question 385

asthma (s/s)

Answer 385

- chest tightness/SOB - wheeze - cough that is worse in am/pm - prod. thick sputum strings

Question 386

asthma (Tx)

Answer 386

environmental control, asthma education for patients and families, and bronchodilator and anti-inflammatory medications The gold standard treatment for persistent asthma is inhaled corticosteroids

Question 387

hypercapnia

Answer 387

Air trapping and impaired ventilation produce an increase in retained carbon dioxide

Question 388

hyperinflation

Answer 388

overexpansion of the lungs due to air trapping

Question 389

chronic bronchitis

Answer 389

increase in the thickness of the basement membrane and loss of structural support for small airways = airway fixation

Question 390

Emphysema

Answer 390

irreversible loss of walls between alveoli with no evidence of fibrosis = loss of alveoli results in fewer walls available for diffusion of gases (cause) cig smoking prime

Question 391

pulmonary acini

Answer 391

functional units of the lung in which gas exchange occurs

Question 392

chronic bronchitis (s/s)

Answer 392

defined by a productive cough in the absence of a pulmonary infection on most days for 3 months in 2 consecutive years

Question 393

hemoptysis

Answer 393

expectorationof blood from the airways as a result of an erosion through a pulmonary or bronchial blood vessel wall

Question 394

emphysema

Answer 394

common case: smoker in his 60s who reports increased DOE but has little or no cough or sputum production unless he has a pulmonary infection

Question 395

DOE

Answer 395

(dyspnea on exertion)

Question 396

bronchiectasis

Answer 396

characterized by excessive mucus accumulation leading to irreversibly dilated bron-chi that readily collapse, airway obstruction, and frequent inf congenital = infants and children acquired = children and adults

Question 397

bronchiectasis (s/s)

Answer 397

severe persistent cough with a daily production of tenacious, mucopurulent (mucus and pus) sputum that can persist over months or years Tx: long term antibiotics, bronchial hygiene w/ chest physiotherapy

Question 398

volatile acid

Answer 398

dissociate, forming a gas that is eliminated by the lungs carbonic acid (H2CO3) = volatile

Question 399

nonvolatile

Answer 399

(fixed acids) not gases and therefore cannot be eliminated by the lungs; eliminated by kidneys in urine lactic acid, ketoacids, sulfuric acid, and phosphoric

Question 400

base

Answer 400

an acceptor of H+

Question 401

sodium normal range

Answer 401

135-145 mEq/L

Question 402

potassium normal range

Answer 402

3.5-5.0 mEq/L

Question 403

pKa

Answer 403

the dissociation constant of the weak acid

Question 404

compensation

Answer 404

when the renal or respiratory function return the pH closer to or actually back within the normal range

Question 405

correction

Answer 405

condition responsible for the acid–base imbalance is controlled or no longer present

Question 406

antiport

Answer 406

transport molecule that moves two different electrolytes in opposite directions across a cell membrane

Question 407

symport

Answer 407

transport molecule that moves two different electrolytes in the same direc-tion across a cell membrane

Question 408

simple acid/base imbalance

Answer 408

presence of one type of acid–base imbalance □■Respiratory acidosis □■Respiratory alkalosis □■Metabolic acidosis □■Metabolic alkalosis

Question 409

chvostek sign

Answer 409

when there is increased neuromuscular excitability, the facial nerve causes contraction of the lips, nose, and face on the side that was tapped

Question 410

trousseau sign

Answer 410

(during inflation of BP cuff) if neuromuscular excitability is present, the pressure will result in a carpal spasm of the hand

Question 411

ABG

Answer 411

(arterial blood gas) measure of the pH, PaCO2, PaO2, and bicarbonate in the arterial blood.

Question 412

TCO2

Answer 412

(total CO2) measure of carbon dioxide in the form of HCO3 - ions, H2CO3, and CO2attached to proteins such as hemoglobin, as well as the CO2dissolved in plasma

Question 413

venous blood gases

Answer 413

measure of the pH, PaCO2, PaO2, and bicarbonate in the venous blood

Question 414

BE

Answer 414

(base excess) measure of all bases in the blood, including bicarbonate, phosphate, and proteins such as albumin and hemoglobin

Question 415

mixed acid/base imbalances

Answer 415

2+ types of acid–base imbalances in an individual at the same time

Question 416

ROME

Answer 416

respiratory opposite: pH up / CO2 dwn; pH dwn / CO2 up metabolic equal: pH up / HCO3 up; pH dwn / HCO3 dwn

Question 417

hypochloremic metabolic alkalosis

Answer 417

Cl- deficit due to the loss of gastric fluid results in the next most abundant anion, which is bicarbonate

Question 418

hyperchloremic metabolic acidosis

Answer 418

administration of intravenous fluids containing chloride, can cause metabolic acidosis if the chloride accumulates because the increase in chloride results in increased renal excretion of HCO3 -

Question 419

electrolyte

Answer 419

any substance that dissociates into ions in water

Question 420

Chloride normal levels

Answer 420

95-105 mEq/L

Question 421

Calcium normal levels

Answer 421

4.5-5.5 mEq/L

Question 422

ICF

Answer 422

(intracellular fluid) largest portion of fluid spacing in the body; 63–70% of the total volume

Question 423

ECF

Answer 423

(extracellular fluid) component includes the remaining 30–37% of the fluid volume; 3 categories: intravascular, interstitial, and transcellular sodium is prime cation for ECF

Question 424

intravascular ECF

Answer 424

fluids within blood and lymphatic vessels and includes blood plasma and lymphatic and transcellular fluids K, Mg, Ph, proteins

Question 425

interstitial ECF

Answer 425

fluid in tissues and surrounding the cells; transport nutrients, waste, and gas exchange

Question 426

transcellular ECF

Answer 426

reflects fluid found in defined spaces, such as the cerebral spinal fluid, synovial fluid Na, Cl, HCO3

Question 427

osmosis

Answer 427

flow from less concentrated to more concentrated; movement between ICF and ECF

Question 428

osmolality

Answer 428

amount of solute per kilogram of solution

Question 429

diffusion

Answer 429

higher concentration to an area of lower concentration

Question 430

hydrostatic pressure

Answer 430

pressure of fluids or their properties when in equilibrium

Question 431

colloid osmotic pressure

Answer 431

(oncotic pressure) concentration of proteins, particularly albumin, that gives rise to water-pulling forces of a particular compartment at the arterial end of the capillary, resulting in the movement of fluid to the interstitial space

Question 432

increased hydrostatic pressure (cause)

Answer 432

sodium and water retention, usually results from an increased systemic venous pressure due to HF

Question 433

decreased colloid osmotic pressure

Answer 433

may cause edema,

Question 434

third spacing

Answer 434

class of edema: accumulation of fluid in areas (typically the intestinal space) that normally have no fluid or a minimal amount of fluid Ex: ascites and edema associated with burns

Question 435

RAAS

Answer 435

(renin–angiotensin–aldosterone system) sodium retention, increased fluid volume and subsequent blood pressure increase

Question 436

ANP

Answer 436

(atrial natriuretic peptide) produced by atrial cells released in response to the elevated atrial pressure result-ing from the increased circulating volume, due to sodium retention.

Question 437

BNP

Answer 437

(brain natriuretic peptide) originating from ventricular cells released in response to the elevated atrial pressure result-ing from the increased circulating volume, due to sodium retention.

Question 438

hypernatremia (cause)

Answer 438

increased output or decreased intake of water, increased sodium consumption dehydration, diarrhea, burns, heat stroke diabetes insipidus, isotonic fluid vol. deficit, lack of ADH

Question 439

hypernatremia (s/s)

Answer 439

thirst, fever, dry membranes, hypoten-sion, tachycardia, low jugular venous pressure, and restlessness

Question 440

hypernatremia (Tx)

Answer 440

injection of hypotonic or isotonic fluids diabetes inspidius: desmopressin acetate proper intake output manage. seizure precaution

Question 441

hyponatremia (cause)

Answer 441

loss of fluids (vomit, diarrhea, diuretics), inadequate excretion renal dysfunction (Addison), SIADH, diabetic ketoacidosis

Question 442

hyponatremia (s/s)

Answer 442

neurologic: lethargy, headache, confusion, seizures, and coma possible hypovolemia contributes to symptoms of hypotension, tachycardia, and a deceased urine output

Question 443

hyponatremia (Tx)

Answer 443

Correcting the underlying etiology of the hyponatremia is as important as returning the sodium concentration to within the normal range hypertonic fluids, if mild increase dietary intake,

Question 444

hyperchloremia (cause)

Answer 444

metabolic acidosis (most common), water loss, dehydration, head injury that causes endocrine abnormalities, hypernatremia, severe diarrhea, respiratory alkalosis, and hyperparathyroidism

Question 445

hyperchloremia (s/s)

Answer 445

resemble those of hypernatremia, presenting like dehydration

Question 446

hyperchloremia (Tx)

Answer 446

IV hypotonic fluids, lactated Ringer, sodium bicarbonate, diuretic in line with hypernatremia

Question 447

hypochloremia (cause)

Answer 447

fluid loss (vomiting and/or diarrhea or nasogastric suctioning), elevated bicarbonate level, as in alkalosis, burns

Question 448

hypochloremia (s/s)

Answer 448

Acute fluid volume excess = cerebral edema (confusion and convulsions) headache, weakness, nausea, tetany (muscle spasms), weight gain

Question 449

hypochloremia (Tx)

Answer 449

isotonic or hypertonic fluids, monitor of intake output

Question 450

hyperkalemia (cause)

Answer 450

oversupplementation, renal fail (decreased excretion, tissue trauma and breakdown, hypoxia, acidosis, and insulin deficiency)

Question 451

hyperkalemia (s/s)

Answer 451

muscle weakness, paralysis, and dysrhythmias

Question 452

hyperkalemia (Tx)

Answer 452

intravenous calcium gluconate (counter cariac arrest), Intake and output management, dietary education

Question 453

hypokalemia (cause)

Answer 453

GI loss through suctioning, laxatives, incomplete K replacement

Question 454

hypokalemia (s/s)

Answer 454

elevated blood sugar and elevated serum cortisol elevated BNP, BUN, and creatinine flattened T wave, U wave develop-ment, and cardiac arrest in severe

Question 455

hyperaldosteronism

Answer 455

(cushing disease)

Question 456

hypokalemia (Tx)

Answer 456

correcting underlying disease. , supplementation

Question 457

hypercalcemia (cause)

Answer 457

malignancy, hyperparathyroidism that increases PTH lev-els, immobilization, thiazide diuretics, thyrotoxicosis, and excessive ingestion of calcium and/or vitamin D

Question 458

hypercalcemia (s/s)

Answer 458

Cardiac, musculoskeletal, and neuromuscular effects: fatigue, weakness, lethargy, and possibly nausea

Question 459

hypercalcemia (Tx)

Answer 459

intramuscular calcitonin (serum calcium >17mg/dL), in most PT, IV fluid to dilute serum and enhance renal excretion, corticosteroids

Question 460

hypocalcemia (cause)

Answer 460

renal failure, para-thyroid gland removal, hypoparathyroidism, hypomagnesemia, hyperphosphatemia, hypoalbuminemia, vitamin D deficiency, pancreatitis, alkalosis

Question 461

hypocalcemia (s/s)

Answer 461

Tingling, spasms, tetany, and possibly convulsions, Chvostek, Trousseau, intestinal cramp

Question 462

hypocalcemia (Tx)

Answer 462

IV calcium gluconate & calcium chloride, Vit D supp. dietary education

Question 463

hyperphosphatemia (cause)

Answer 463

both primary and acute care is chronic renal failure other: respiratory acidosis, metabolic acidosis, hypocalcemia

Question 464

hyperphosphatemia (s/s)

Answer 464

correlate with hypocalcemia, both Chvostek & Trousseau, decreased BP and arrhythmias in extreme

Question 465

hyperphosphatemia (Tx)

Answer 465

restriction of diet, Vit D to increase calcium absorbtion = dropping serum phosphorus

Question 466

Hypophosphatemia (cause)

Answer 466

malnu-trition, alcohol withdrawal, heat stroke, respiratory alkalosis, hepatic encephalopathy, major burns, hyperparathyroidism, diarrhea, Vit D deficiency

Question 467

Hypophosphatemia (s/s)

Answer 467

similar to hypercalcemia, RBC and thrombo dysfunc, neuromuscular dys-function, altered mental status, convulsions, excessive bone resorption, and possible respiratory failure

Question 468

Hypophosphatemia (Tx)

Answer 468

oral phosphorus, IV managed with caution

Question 469

Hypermagnesemia (cause)

Answer 469

renal failure, laxatives, burns, trauma, shock, lithium toxicity

Question 470

Hypermagnesemia (s/s)

Answer 470

(danger to cardio ) bradyarrhythmias, tall T wave, widened QRS, prolonged QT interval, atrioventricular blocks, and finally cardiac arrest Hypotension, shallow respirations, decreased deep tendon reflexes, and decreased level of consciousness

Question 471

Hypermagnesemia (Tx)

Answer 471

restriction of any Mg., Intravenous calcium gluconate to reverse neuromuscular systems,

Question 472

Hypomagnesemia (cause)

Answer 472

(most common) excessive alcohol intake hypocalcemia, hypokalemia, decreased albumin level, decreased dietary intake, decreased absorption in the small intestine, GI losses, acute pancreatitis, starva-tion, diuretic therapy, and diabetic ketoacidosis

Question 473

Hypomagnesemia (s/s)

Answer 473

premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, and torsades de pointes (very fast HR) changes in mental status and personality along with nystagmus (eyes make repetitive uncontrol move) and hypertension

Question 474

Hypomagnesemia (Tx)

Answer 474

intravenous magnesium sulfate and usually oral magnesium, supplementation can cause diarrhea, intake output management seizure precautions

Question 475

gene

Answer 475

segment of DNA that codes for prod. of certain protein like a sentence

Question 476

genome

Answer 476

like a book

Question 477

chromosome

Answer 477

double helix is combined with proteins called histones and is compacted to form structures like a chapter

Question 478

genetics

Answer 478

study of gens ans their impact on inheritence and single-gene/chromosomal disorder

Question 479

genomics

Answer 479

study of structure, function, analysis of human genome

Question 480

epigenetics

Answer 480

external mod of DNA that affect gene expression

Question 481

epigenomics

Answer 481

study of chem. compounds that instruct the genomw where and when to be expressed

Question 482

nucleotides

Answer 482

each gene is made of a sequence of these 3 components: phosphate, a deoxyribose, and one of four nitrogenous bases, ATGC

Question 483

alleles

Answer 483

alternative forms of an individual gene

Question 484

Barr body

Answer 484

inactivated X chromosome in each cell

Question 485

central dogma

Answer 485

process of DNA to RNA to protein

Question 486

how many chromosomes in each cell of the body

Answer 486

46

Question 487

mitosis

Answer 487

process of cell division used to create identical copies of a cell

Question 488

gonadal cells contain

Answer 488

23 chromosomes, total

Question 489

meiosis

Answer 489

cell division of sex cells so each cell has one of each chromosome pair begins with a cell w/ 46 chrom. (diploid cell) = 2 sets of cell divisions = 4 daughter cells (haploid cells)

Question 490

somatic cells

Answer 490

this is where mitosis occurs; everything that not a sperm or egg

Question 491

transcription

Answer 491

process of reading a gene, RNA is formed from DNA

Question 492

mRNA

Answer 492

template for protein synthesis

Question 493

tRNA

Answer 493

carries appropriate amino acids to the template mRNA during protein formation

Question 494

rRNA

Answer 494

make ribosomes

Question 495

transcription factors

Answer 495

(regulatory proteins) in order for transcription to begin, these must bind to the promoter region at the beginning of the gene

Question 496

splicing

Answer 496

mRNA transcript needs to go through this process ro become a mature message

Question 497

exons & introns

Answer 497

are the useful part, introns split each exon and are throwaways when splicing begins

Question 498

translation

Answer 498

process of protein synthesis with mRNA directing assembly of a string of amino acids to create a protein product

Question 499

codon

Answer 499

3 nucleotides grouped together; 64 possible codons, only 20 amino acids; more than one codon to each amino acid

Question 500

mutation

Answer 500

grammatical error in gene, varying in severity

Question 501

point mutation

Answer 501

a change in one nucleotide

Question 502

silent mutation

Answer 502

if amino acid is not changed by a point mutation

Question 503

missense mutation

Answer 503

casues a change in amino acid

Question 504

nonsense mutation

Answer 504

little or no protein prod. and almost always results in serious clinical consequences

Question 505

genetic imprinting

Answer 505

differential expression based on the parent from whom the genes are inherited

Question 506

SNP

Answer 506

(single-nucleotide polymorphism) Not all genetic changes among individuals are pathogenic

Question 507

aneuploidy

Answer 507

when the wrong number of chromosomes occurs in pregnancy, the embryo is said tobe affected by

Question 508

chromosome nondisfunction

Answer 508

can cause an embryo to have an extra (trisomy) or missing chromosome (monosomy), which most often can result in an early miscarriage but in some cases can result in a live-born baby

Question 509

mosaicism

Answer 509

the presence of more than one genetic cell line in a person

Question 510

triploidy

Answer 510

embryo with 69 chromosomes

Question 511

down syndrome

Answer 511

trisomy 21

Question 512

penetrance

Answer 512

reduced = not everyone who inherits a mutation will have clini-cal symptoms

Question 513

neurofibromatosis

Answer 513

dominant causes numerous cutaneous lesions

Question 514

pedigree

Answer 514

visualization of several generations genetic disease pattern

Question 515

Marfan

Answer 515

dominant connective tissue disorder that causes pathogenic skeletal, ocular, and cardiac features 38

Question 516

syndrome

Answer 516

refers to a group of signs and symptoms that emerge from a disease state

Question 517

prevelance

Answer 517

the number of individuals of a defined population who already have a disease or condition

Question 518

incidence

Answer 518

number of new cases of a disease or condition within a defined period and defined population

Question 519

public health

Answer 519

science of protecting and improving the health of families and communities through promotion of healthy lifestyles, research for disease and injury pre-vention, and detection and control of infectious diseases

Question 520

mortality

Answer 520

the number of deaths in a given population

Question 521

morbidity

Answer 521

departure from physiologic or psychologic well-being and encompasses disease, injury, and disability

Question 522

EBP

Answer 522

(evidence-based practice)

Question 523

illness

Answer 523

the individual experience that a person has with a disease

Question 524

disorder

Answer 524

disruption of physiologic or psychologic function

Question 525

epidemiology

Answer 525

the study of how disease is distributed in populations and identification of the factors influencing the distribution

Question 526

proto-oncogenes

Answer 526

category of genes: regulate cell proliferation

Question 527

tumor suppressor genes

Answer 527

category of genes: responsible for curbing cell growth

Question 528

preimplantation genetic diagnosis

Answer 528

screening of embryos that are produced through in vitro fertilization for the presence of genetic or chromosome abnormalities

Question 529

cytogenetics

Answer 529

laboratory field involving the character-ization of chromosome structure and number

Question 530

karyotyping

Answer 530

test used to examine the visual appearance of chromo-some structure and number

Question 531

FISH

Answer 531

(Fluorescence in situ hybridization) utilized both for rapid detection of chromosome number and for targeting specific DNA sequences

Question 532

pharmacogenomics

Answer 532

discipline that blends pharmacology with genomic capabilities

Question 533

antisense oligonucleotide

Answer 533

(sequence of complementary nucleotides) is used to directly bind the DNA or RNA to block the aberrant gene product Imantinib

Question 534

transcription factor modulators

Answer 534

selectively increase or decrease transcription levels of certain genes

Question 535

GWAS

Answer 535

(Genome-wide association studies) genomic tests used in both research and clinical practice that were originally designed to identify relationships between common genome variation and particular traits of interest

Question 536

lymphoma

Answer 536

hematolgic malignancies that originate in the lymphatic tissue

Question 537

AML

Answer 537

(Acute myelogenous leukemia) 30% of cases

Question 538

ALL

Answer 538

(Acute lymphocytic leukemia) 2/3 cases likely to be children

Question 539

CML

Answer 539

(Chronic myelogenous leukemia)

Question 540

CLL

Answer 540

(Chronic lymphocytic leukemia)

Question 541

NHL

Answer 541

(Non-Hodgkin lymphoma)

Question 542

Multiple myeloma

Answer 542

a group of B cells (plasma cells), these produce large amounts of antibodies

Question 543

Multiple myeloma (causes)

Answer 543

not well understood obesity, toxin exposure, substance abuse, and genetic influence play a role

Question 544

AML (cause)

Answer 544

unknown, but risk factors (not inherited) (1) chemotherapeutic treatment (2) ionizing radiation (3) long-term exposure to benzenes or other petroleum products (4) smoking those with down syndrome

Question 545

AML (s/s)

Answer 545

depend on degree of pancytopenia (a lower-than-normal number of red and white blood cells and platelets in the blood) weakness and fatigue related to anemia, unresolved fever and fection related to neutrotpenia (inf: pneumonia, UTI, upper respiratory) bleeding issues (ecchymoses, petechiae, menorrhagia)

Question 546

menorrhagia

Answer 546

heavy bleeding; menstrual bleeding that lasts more than 7 days

Question 547

metrorrhagia

Answer 547

bleeding at irregular intervals, particularly between expected menstrual periods

Question 548

menometrorrhagia

Answer 548

excessive and prolonged uterine bleeding occurring at irregular intervals

Question 549

polymenorrhea

Answer 549

menstrual interval of less than 21 days

Question 550

dysmenorrhea

Answer 550

severe mentral cramping

Question 551

leukocytosis (s/s) w/ AML

Answer 551

(an abnormally elevated white blood cell count) headache, diplopia, cranial nerve palsies, and mental status changes

Question 552

AML (Tx)

Answer 552

Restoring normal hematopoiesis is the goal systemic chemotherapy is the cornerstone (induction and consolidation)

Question 553

AML complete remission is defined as

Answer 553

restoration of normal peripheral blood cell counts, maturation of all cell lines, and fewer than 5% blasts

Question 554

ALL (causes)

Answer 554

can occur ant any age but considered to be particularly childhood malignant features of the leukemic cells: Morphologic (change in shape) cytochemical (change in biochemical properties) cytogenetic (change in genetic properties) immunologic (change in immunologic properties, such as surface proteins)

Question 555

ALL is considered to be a clonal disease

Answer 555

(one in which all malignant cells derive from a single errant cell) via a progeny (initially transformed leukemic cell divides and passes on the alterations in genetic material to descendant cells)

Question 556

ALL (s/s)

Answer 556

fever, bleeding, bone pain, and lymphadenopathy, but persist beyond treatment bone pain is common among children but if they refuse to bear weight uncommon: mediastinal mass which is concurrent with NHL, making it difficult to differentiate

Question 557

ALL (Tx)

Answer 557

eradicate the malignant immature lymphoid cells and restore normal hematopoiesis induction and consolidation, but aimed at CNS (diff from AML)

Question 558

CML (causes)

Answer 558

characterized by overproliferation of mature granulocytes exposure to high-dose radiation consistent with surviving an atomic bomb - direct result of a genetic alteration that results in aberrant cellular proliferation. (diff btwn AML) increased myeloid cell proliferation

Question 559

CML (s/s)

Answer 559

asymptomatic; disease is frequently found during routine blood work thrombocytosis or thrombocytopenia symp: excessive sweating or night sweats, weakness and fatigue, splenomegaly, Acute gouty arthritis

Question 560

CML (Tx)

Answer 560

normalizing the white blood cell count, eliminating immature myeloid cells chemo: hemotologic remission, difficult to achieve cytogenic tyrosine kinase inhibitors: target genetic defect material

Question 561

CLL (cause)

Answer 561

overproduction of B cells prime in older (white) adults, asians have lowest rates split into Rai (US) and Binet (EU) stages trisomy 12 was the most common cytogenetic abnormality, 11,13,14 were 2nd most

Question 562

CLL (s/s)

Answer 562

25% asymp. blood tests; spleno/hepatomegaly fever for 2 weeks w/o inf., night sweat, weight loss

Question 563

CLL (Tx)

Answer 563

no known cure; determined by stage, aimed at restoring normal lymphocyte counts Chemotherapy is given to stop the cancer cells from progressing, and immunotherapy is used to stimulate the body’s own defenses in fighting the disease

Question 564

NHL (cause)

Answer 564

heterogeneous group of malignancies that originate in the lymphatic system rates are higher in older individuals, classified on basis on cell lineage and maturity of malignant cells; rate of cell prolif. indolent/aggressive

Question 565

indolent

Answer 565

(low grade tumor) grow slow and do not result in PT feeling symp.

Question 566

aggressive

Answer 566

(high-grade tumor) grows fast and result in PT feelling symp

Question 567

NHL (s/s)

Answer 567

enlarged lymph nodes is most common extranodal: commonly in GI, abdomin pain, swelling, loss of appetite; red patches A for absent, B for present

Question 568

NHL (Tx)

Answer 568

depends on pathology, stage, and tumor, age comorbidity surgery, chemotherapy, radiation therapy, immunotherapy, stem cell transplant, and waiting

Question 569

Multiple myeloma (cause)

Answer 569

characterized by the proliferation of malignant plasma cells toxin and hazardous chemical exposure, obesity, and possible genetic influence most common genetic: inactivation of tumor-suppressing genes

Question 570

Multiple myeloma (s/s)

Answer 570

Anemia (normocytic or normochromic) is a common bone pain, and renal issues

Question 571

Multiple myeloma (Tx)

Answer 571

combo: radiation and chemotherapy and often involves stem-cell transplantation ferrous supplementation, hydration and biphosphate to str. bone.; braces applied to back and extremities