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exam 2 medsurg Flashcards

1
Q

pH definition

A

strength of hydrogen ions in a solution

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2
Q

normal blood pH

A

7.35-7.45

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3
Q

acidic pH

A

has more H+

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4
Q

base pH

A

has more OH- hydroxyl ions

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5
Q

pH resulting in death

A

7 or less and 7.8 or more

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6
Q

the most common acid

A

carbonic acid H2CO3

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7
Q

regulates CO2

A

lungs

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8
Q

waste products of carb, fat, protein metabolism

A

acids

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9
Q

most common base

A

bicarbonate HCO3

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10
Q

regulate bicarbonate in ECF

A

kidneys

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11
Q

waste product of glucose

A

CO2

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12
Q

carbonic acid

A

the form in which CO2 is transported in the blood

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13
Q

first line of defense, takes seconds

A

chemical. The bicarbonate buffer system is includes bicarbonate (HCO3) and carbonic acid (H2CO3) are constantly regulated by the respiratory and urinary system. These two components increase and decrease depending on the need of the body.
Protein buffer system: hemoglobin promotes movement of chloride across the RBC in exchange for bicarbonate.

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14
Q

second line of defense, takes minutes

A

respiratory. breathing rids body of CO2. Co2 is carried in the body in the form of carbonic acid and bicarbonate. During body metabolism, CO2 is produced which reacts with H2O to form carbonic acid resulting in decreasing pH (as acidity increases). Where as in the lungs, carbonic acid breaks into CO2 and H2O and increased exhalation of CO2 results in increasing pH (acidity decreases)

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15
Q

third line of defense, takes 24-48 hours

A

renal, strongest mechanism. When there high levels of hydrogen ions in the body, the kidneys (a) secrete hydrogen ions and reabsorb sodium ions; (b) ammonia a by product of protein metabolism combines with hydrogen ions to form ammonium ions (NH4+) which is excreted in the urine in exchange of sodium reabsorption into blood. When there are low levels of hydrogen ions in the body, kidneys retain hydrogen ions to form bicarbonate.

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16
Q

pH high

A

alkalosis

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17
Q

pH low

A

acidosis

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18
Q

metabolic acidosis

A

ph <7.35. bicarb <22 mEq/L. often renal failure

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19
Q

metabolic acidosis clinical manifestations

A

headache, confusion, hypotension, dysrhythmia, increased respirations.

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20
Q

metabolic acidosis treatment

A

underlying cause, bicarbonate

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21
Q

metabolic alkalosis

A

ph >7.45. bicarb >26mEq/L. often with hypokalemia

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22
Q

metabolic alkalosis clinical manifestations

A

tachycardia, hypokalemia, respiratory depression

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23
Q

metabolic alkalosis treatment

A

underlying cause, IV NACL to restore fluid volume and allow excretion of excess bicarb

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24
Q

respiratory acidosis

A

ph< 7.35. PaCO2 > 42 mm/Hg. Due to inability to excrete CO2.

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25
Q

respiratory acidosis clinical manifestations

A

sudden increased pulse and RR, HTN, LOC change

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26
Q

respiratory acidosis treatment

A

improve ventilation

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27
Q

respiratory alkalosis

A

pH >7.45. PaCO2 <35 mm/Hg. due to hyperventilation

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28
Q

respiratory alkalosis clinical manifestations

A

lightheadedness, parathesias, loss of consciousness

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29
Q

respiratory alkalosis treatment

A

cause of hyperventilation, paper bag breathing.

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30
Q

acidosis

A

too muc H+ ions in body. too much CO2 in the body results in acidosis.

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31
Q

alkalosis

A

too much bicarbonate. the body has lost CO2 or the pt hyperventilated so much they lost too much CO2

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32
Q

cardiac valves

A

tricuspid, mitral, pulmonic, aortic

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33
Q

Mean arterial pressure

A

must be at lease 60 mm/Hg to maintain adequate blood flow through coronary arteries and perfuse major organs (brain)

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34
Q

cardiac output

A

amount of blood pumped from the left ventricle per minute. heart rate x stroke volume.

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35
Q

heart rate

A

the number of times the ventricles contract in one minute

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36
Q

cardiac index

A

cardiac output / body surface area

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37
Q

Cardiac index normal range

A

2.7-3.2 L/min/m

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38
Q

Cardiac index normal range

A

2.7-3.2 L/min/m

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39
Q

cardiovascular system assessment

A

patient history, nutritional history, family history and genetic risk, current health problems (pain, discomfort, dyspnea, DOE, orthopnea, PND, fatigue, palpitations, edema, syncope, extremity pain)

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40
Q

2.2 LB

A

1 KG= 1 L of H2O

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41
Q

cardiovascular system physical assessment

A

general appearance, skin, extremities, blood pressure

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42
Q

precordium

A

assessment- inspect, palpate, percuss, auscultation- normal heart sounds, paradoxical splitting, gallops and murmurs, pericardial friction rub

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43
Q

serum markers of myocardial damage

A

troponin- T and I, creatinin kinase (CK), myoglobin, serum lipids (total cholesterol <200 mg/DL, triglyceride <150 mg/DL, HDL >40 mg/DL, LDL <70 mg/DL), homocysteine, highly sensitive C-reactive protein

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44
Q

the leading cause of death in US for men and women of all racial and ethnic groups

A

coronary artery disease

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45
Q

the most prevalent cardiovascular disease in adults

A

coronary artery disease

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46
Q

coronary artery disease

A

broad term that includes chronic stable angina and acute coronary syndromes. It affects the arteries that provide blood, oxygen, and nutrients to the myocardium.

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47
Q

coronary artery disease

A

broad term that includes chronic stable angina and acute coronary syndromes. It affects the arteries that provide blood, oxygen, and nutrients to the myocardium.

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48
Q

ischemia

A

blood flow is partially blocked. insufficient oxygen is supplied to meet the requirements of the myocardium. usually followed by infarction.

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49
Q

infarction

A

follows ischemia. necrosis or tissue death of myocardium. irreversible damage.

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50
Q

infarction

A

follows ischemia. necrosis or tissue death of myocardium. irreversible damage.

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51
Q

blockages

A

narrowing of the coronary vessels reduce blood flow to the myocardium

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52
Q

CAD contributing factors

A

high LDL and total cholesterol. Low HDL. triglycerides >150. hypertension. elevated C-reactive protein and fibrinogen level. metabolic syndrome- insulin resistance, central obesity

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53
Q

CAD prevention

A

control cholesterol abnormalities (diet, physical activity, medication), smoking cessation, manage hypertension, control diabetes.

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54
Q

angina

A

chest pain that results from the imbalance between oxygen supply and demand

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55
Q

2 types of angina

A

stable and unstable

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56
Q

chronic stable angina

A

chest discomfort that occurs with moderate to prolonged exertion in a pattern that is familiar to the patient. can occur over several months.

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57
Q

chronic stable angina results in

A

slight limitation of activity and is usually associated with a thickened fixed atherosclerotic plaque.

58
Q

chronic stable angina relieved by

A

nitroglycerine or rest and is often managed with drug therapy. rarely does CSA require aggressive treatment.

59
Q

angina clinical manifestations

A

tightness, choking, or heavy sedation, substernal :radiates to neck, jaw, shoulders, back or arms (usually left), anxiety, dyspnea, SOB, dizziness, N/V, pain less than 15 minutes.

60
Q

unstable angina

A

characterized by increased frequency and severity and is not relieved by rest and NTG. requires medical intervention.

61
Q

angina treatment

A

decrease myocardial oxygen demand and increase oxygen supply, oxygen, reduce and control risk factors (lipids), monitor for heart failure, Chart 40-1

62
Q

angina medications

A

nitroglycerine, beta-adrenergic blocking agents, calcium channel blocking agents, antiplatelet and anticoagulant meds (aspirin, heparin

63
Q

garlic supplements

A

small effect on reduction

64
Q

nitro

A

a nitrate often produces collateral blood flow to the heart and dilates the coronary artieries. It decreases the oxygen demand of the mycocardium by causes peripheral vasodilation (hence fall in BP).
Pain relief should begin in 1-2 mins and clearly evident in 3- 5 mins. If the patient’s systolic BP drops below 100 or 25 mmHg than norm, lower the head of the bed.

65
Q

aspirin

A

inhibits platelet aggregation and decreases the likelihood of thrombosis

66
Q

glyco

A

prevents fibrinogen to attach to activated platelets at the site of the thrombus

67
Q

congestive heart failure

A

the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. indicates myocardial disease- a problem with the contraction of the heart of filling of the heart.

68
Q

causes of left sided heart failure

A

hypertension, CAD, vascular disease (mitral or aortic), indicates LHF: poor cardiac output and pulmonary congestion.

69
Q

causes of right sided heart failure

A

left ventricle failure, right ventricular myocardial infarction, pulmonary hypertension

70
Q

causes of high output failure

A

increased metabolic needs, septicemia, high fever, anemia, hyperthyroidism

71
Q

left sided failure clinical manifestations

A

LV can not pump blood effectively, decreased cardiac output and elevated pulmonary venous pressure. weakness, low oxygen, confusion, pulmonary congestion, breathlessness, oliguria, tachycardia, palpitations, weak peripheral pulses, cool extremities

72
Q

right sided failure clinical manifestations

A

RV cannot eject sufficient amounts of blood. fluid is retained and pressure builds up in the venous system. peripheral edema, jugular vein distention, swollen hands and feet, anorexia, nausea, weight gain, polyuria at night, advanced stage- ascites and increased abd girth.

73
Q

CHF diagnostics

A

CXR (hazy lung fields, cardiomegaly), echocardiogram (heart enlargement, ineffective ventricular contraction), BUN, elevated creatinine (from renal dysfunction), lipid panel, increased liver enzymes.

74
Q

CHF treatment

A

bedrest to decrease work of heart, frequent rest periods, elevated HOB (high fowlers), oxygen, diet (may restrict fluids, Na+), diuretics, anticoagulants (ASA, coumadin), vasodilators (nitrates, calcium channel blockers).

75
Q

valvular disorders

A

mitral valve prolapse, mitral regurgitation, mitral stenosis, aortic regurgitation, aortic stenosis

76
Q

stenosis

A

narrowing of valve opening

77
Q

insufficiency

A

inability of valve to close compleltely

78
Q

mitral valve prolapse characteristics

A

one or both leaflets enlarge and protrude into LA during systole. usually benign (but may progress to mitral insufficiency. cause unknown. more common in young women. may have anxiety problems.

79
Q

mitral valve prolapse clinical manifestations

A

chest pain (different from angina, not with exertion, is prolonged and not easily relieved), palpitations, dizziness, fatigue, anxiety (like panic attack).

80
Q

mitral valve prolapse treatment

A

medications-antibiotics, anticoagulants, antianxiety, antiarrhythmic. avoid caffeine. relaxation techniques. for chest pain0 lie flat with legs elevated against wall for 3-5 mins.

81
Q

mitral stenosis

A

mitral valve leaflets become thickened and fibrotic. commissure if formed. affects women 20-40 years old. caused primarily by rheumatic fever.

82
Q

mitral stenosis clinical manifestations

A

dyspnea, fatigue, cough, chest pain, activity intolerance.
Late: pulmonary edema
Extremely loud S1.
heart murmur- described as sounding like rumbling underground train.

83
Q

mitral valve treatment

A

similar to CHF
medications : anticoagulants, antibiotics, antiarrhythmics.
surgery: mitral commissurotamy, mitral valve replacement, balloon valvuloplasty.

84
Q

mitral insufficiency

A

often occompanies mitral stenosis. LA and LV enlarged as result of backflow of blood. LV enlarges in attempt to maintain cardiac output. Left side of heart fails and S/S of mitral stenosis develop.
High pitched murmur.

85
Q

mitral insufficiency treatment

A

medications: vasodilators to decrease afterload and regurgitation, digitalis, diuretics, prophylactic antibiotics.
decreased activity
surgery: annuloplasty, mitral valve replacement

86
Q

aortic stenosis

A

flow of oxygenated blood through aortic valve is impeded, causing enlarged LV, powerful LA contraction.

87
Q

aortic stenosis risk factors

A

aortic valve is most commonly diseased in the elderly, esp. men.
rheumatic fever
longer lifespan
drug abuse

88
Q

aortic stenosis clinical manifestations

A 
no s/s until valve opening decreases to 1/3 normal size.
exertional dyspnea
angina, syncope
displaced PMI- to the left
late: fatigue, orthopnea
89
Q

aortic stenosis treatment

A

prophylactic antibiotics for dental and invasive procedures.
for heart failure: digoxin, diuretics, low Na+ diet, activity restriction
surgery: balloon valvuloplasty, aortic valve replacement

90
Q

aortic insufficiency patho

A

regurgitation of blood into LV causes LV to hypertrophy. LV failure and myocardial ischemia occur. Eventually, right sided failure.

91
Q

aortic insufficiency causes

A

rheumatic fever, infections (syphilis, endocarditis), chronic hypertension, calcification, blunt chest trauma

92
Q

aortic insufficiency clinical manifestations

A

may be asymptomatic
early s/s: signs of CHF, chest pain
widening pulse pressure

93
Q

aortic insufficiency treatment

A

medications: prophylactic antibiotics, digoxin, diuretics

aortic valve replacement

94
Q

mechanical valves

A

do not deteriorate or become infected as easily, but are thrombogenic and require life-long anticoagulant therapy.

95
Q

tissue (biologic) valves

A

xenograft (heterograph): pig or cow valve.
homograft (allograft): human valve
autograph: pt’s own valve

96
Q

infectious diseases of the heart

A

Any of the layers of the heart may be affected by an infectious process.
Diseases are named by the layer of the heart that is affected.
Diagnosis is made by patient symptoms and echocardiogram.
Blood cultures may be used to identify the infectious agent and to monitor therapy.
Treatment is with appropriate antimicrobial therapy. Patients require teaching to complete the course of appropriate antimicrobial therapy, and require teaching for infection prevention and health promotion.

97
Q

pericarditis

A

inflammation of sac surrounding heart. may be acute (virus, fungi, bacteria, chemotherapy, MI, chest trauma or surgery)
may be chronic (TB, radiation, metastasis, connective tissue disorders

98
Q

pericarditis clinical manifestations

A

precordial chest pain is hallmark symptom. aggrevated moving and deep breathing. dyspnea, fever, chills, pericardial friction rub, heart sounds: difficult to hear, if effusion present.

99
Q

pericarditis diagnostics

A

elevated wbc, ST segment ^ on EKG, echocardiogram- wide gap between epicardium and pericardium. CXR- enlarged heart.

100
Q

pericarditis treatment

A

rest, pericardiocentesis, pericardial window, meds (analgesics, antipyretics, NSAIDS), manage pain.

101
Q

thrombophlebitis

A

AKA phlebitis, thrombophlebitis, deep vein thrombosis

102
Q

thrombophlebitis veins most affected

A

superficial- saphenous

deep- femoral, poplital, small calf veins

103
Q

thrombophlebitis risk factors

A

bedrest, general surgery for those over 40, leg trauma, obesity, previous venous insufficiency, oral contraceptives, malignancy and chemotherapy

104
Q

thrombophlebitis clinical manifestations

A

positive homan’s sign, calf pain, inflammation (warm, tender, swollen) as result of congestion distal to clot, others (may vary).

105
Q

thrombophlebitis diagnosis

A

H & P, venogram (use of dye), doppler ultrasound

106
Q

thrombophlebitis treatment

A

bedrest, elevate extremity, warm, moist soaks, ted hose, thrombocytic therapy, anticoagulants (Heparin first (PTT), then coumadin (PT)), never massage or rub, watch for signs of bleeding, prevent recurrence.

107
Q

vascular system assessment

A 
characteristics of arterial and venous insufficiency,
chest pain, 
changes in skin and appearance,
pulses,
aging changes
108
Q

atherosclerosis

A

formation of plaque within arterial walls.
wall stiffens, thickens and decreases in diameter.
lipids, calcium, thrombi adhere to damaged wall.
over time, fat and fibrin harden.
decreased blood flow.
causes hypertension, impaired tissue perfusion and aneurysms.

109
Q

atherosclerosis risk factors

A

diabetes mellitus, smoking, hypertension, sedentary lifestyle, african american or hispanic, low HDL and high LDL

110
Q

atherosclerosis clinical manifestations

A

hypertension, extremities cold/cool with diminished or absent pulses, prolonged capillary filing/ bruit of large arteries, decreased intensity and audibility of a pulse

111
Q

atherosclerosis diagnostics

A

total serum cholesterol levels, HDL-LDL, triglycerides, homocysteine

112
Q

atherosclerosis treatment

A

diet therapy, smoking cessation, exercise, drug therapy, gene therapy

113
Q

PVD and PAD risk factors

A

tobacco use, hyperlipidemia, HTN, DM, obesity, stress, sedentary lifestyle, age, gender, genetics,
PVD: Virchow’s triad, hip surgery

114
Q

PVD clinical manifestations

A

classic: calf/ groin tenderness, unilateral leg swelling.
aching, cramping pain in LE at rest, pulses present but hard to palpate, edema and calf thickness, induration- warmth, purplr/blue color extremity, thick rough skin

115
Q

PAD clinical manifestations

A

intermittent claudication, sharp, constant pain, diminished or absent pulses, dependent rubor, extremities pale when elevated, dry shiny skin, cool temp, hair loss, thick nails

116
Q

PVD diagnostics

A

D-dimer, MRI, impedance plethysmography, venous duplex ultrasonography, CT scan

117
Q

PAD diagnostics

A

arteriography, plethysmography, C-reactive protein (CRP- inflammatory marker), D-dimer, homocysteine level (protein indicating thrombin formation)

118
Q

PVD treatment

A

prevention- weight loss, smoking cessation, regular exercise, compression stockings, pneumatic compression devices, leg exercises, alternate up and down of LE, anticoagulant therapy-heparin, surgical management

119
Q

PAD treatment

A

prevention- foot care, exercise program, medications (pentoxifylline [trental], cilostazol [pletal]), use of antiplatelet agents, avoid cold temps, avoid prolonged dependency of LE, surgical management (angioplasty, atherectomy, bypass)

120
Q

Buerger’s Disease

A

Recurring inflammatory process of the small and intermediate vessels of the LE, probably an autoimmune disorder.
Most often occurs in men ages 20-35.
Risk or aggravating factor:tobacco.
Progressive occlusion of vessels results in pain, ischemic changes, ulcerations, gangrene

121
Q

Raynaud’s disease

A

intermittent arterial vasoocclusion, usually of fingertips or toes.
associated with other underlying conditions such as scleroderma.
manifestations: sudden vasoconstriction resulting in color changes, numbness, tingling or burning pain.
episodes are usually brought on by a trigger such as cold or stress.
occurs most frequently in young women.
protect from cold/ other triggers. Avoid injury to hand/fingers.

122
Q

Most common CV problem in US

A

hypertension

123
Q

hypertension risk age

A

30-50, complications increase after age 50

124
Q

hypertension nationality risk

A

2x as many african american’s as whites

125
Q

hypertension

A

persistent systolic elevation >140 and diastolic >90.

severity defined according to diastolic B/P.

126
Q

hypertension (primary or essential) risk factors

A

age>60, alcoholic, salt, caffeine, obesity, hyperlipidemia, smoking, stress, ethnicity.
95% of hypertension is this type

127
Q

secondary hypertension caused by

A

underlying factors such as: kidney disease, arterial disease, pregnancy, drugs- estrogen, glucocorticoids, cyclosporines, erythropoietin

128
Q

hypertension complications

A

MI, PVD, Chronic renal failure, CVA

129
Q

hypertension clinical manifestations

A 
may be none
headaches
lightheaded/dizzy
abd. bruits, tachycardia
sweating, pallor
epistaxis
130
Q

hypertension diagnostics

A

initally B/P in both arms in standing, sitting and lying position- BP above 140/90 on 2 or more occasions.
test to check for complications

131
Q

hypertension treatment

A 
lifestyle modifications is the first step
weight reduction
smoking cessation
sodium restriction
exercise
relaxation techniques
modified alcohol intake
drug therapy
132
Q

hypertension medication

A

diuretics, beta blockers, Ca++ channel blockers, angiotensin converting enzyme (ACE) inhibitors, alpha adrenergic blockers, central adrenergic blockers, rauwolfia derivatives, vasodilators

133
Q

hydrochlorothiazide (diuril), Lasix, Bumex

A

Diuretics

134
Q

Propranalol (Inderal)

A

Beta adrenergic blocker

135
Q

Nifedipine (procardia), Verapanil (Calan)

A

Ca++ channel blocker

136
Q

Captopril (Capoten)

A

Angiotensin converting enzyme (ACE) inhibitor

137
Q

Prazosin (Minipress)

A

Alpha adrenergic blocker

138
Q

Methyldopa (Aldomet)

A

central adrenergic blockers

139
Q

Reserpine (Serpasil)

A

Rauwolfia derivatives

140
Q

Hydralazine (Apresoline)

A

vasodilator

141
Q

hypertension teaching

A

Monitor B/P regularly
Encourage patients to take medications and keep appointments even when feeling well
Consult doctor or pharmacist about OTC drugs
If orthostatic hypotension
rise slowly
avoid prolonged standing
avoid hot baths/showers
Do not stop abruptly or rebound hypertension may occur
Present measures to manage hypertension as health practices beneficial to everyone (not a long list of “don’ts)
Sexual dysfunction is common side effect
Encourage patients to talk to doctor about this

pharm (2 decks)

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