Exam 3 Flashcards

1
Q

One good sign of an infection

A
Elevated WBC (11,000-25,000)
3,500/5,000-10,000 (normal)
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2
Q

Leukemia WBC range

A

WBC 100,000-400,000

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3
Q

Eosinophils and basophils

A

Allergies and inflammation

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4
Q

Neutrophils

A

Fight infection

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5
Q

Lymphocyte

A

A lymphocyte is a type of white blood cell in the vertebrate immune system. Lymphocytes include natural killer cells, T cells, and B cells

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6
Q

Serous fluid

A

Watery, like plasma

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7
Q

Fibrinous fluid

A

Clotted

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8
Q

Serosanguious fluid

A

Clear pink, blood tinged

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9
Q

Sanguinous

A

Bloody

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10
Q

Shift to the left** of cells

A

*

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11
Q

Purulent

A

Pus (suppurative)

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12
Q

Serious, fibrinous, serosanguinous, sanguinous, purulent drainage are sisngs of

A

Local manifestations

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13
Q

ESR (erythrocyte sedimentation rate)

A

The erythrocyte sedimentation rate is the rate at which red blood cells in anticoagulated whole blood descend in a standardized tube over a period of one hour. It is a common hematology test, and is a non-specific measure of inflammation.
Stimulates angiogenesis

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14
Q

Chronic inflammation can cause

A

Cancer

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15
Q

Purpose of an inflammatory response

A

To prepare the injured area for healing

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16
Q

3 inflammatory responses:

A
  1. Leukocytes (neutrophils & macrophages) to
    remove debris and provide growth factors
  2. Nutrients (proteins, glucose, vitamins) to
    provide the building blocks for cells
  3. Clotting factors and platelets to limit damage
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17
Q

T/F every disease has some type of inflammation

A

True

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18
Q

3 plasma protein systems:

A
  1. Clotting cascade: prevents further bleeding
  2. Kinin cascade: produces bradykinin, causing pain, vasodilation, vascular permeability
  3. Complement cascade: stimulates opsonins,chemotactic factors, and anaphylatoxins which degrade Mast cells to release histamine, a potent vasodilator.
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19
Q

Vascular response to inflammation (4 steps)

A

Histamine and bradykinin stimulate vasodilation
and increased permeability, resulting in:
1. Increased blood flow to the area, causing redness
(rubor) and heat (calor)
2. Leakage of protein rich plasma into the
interstitial spaces, causing swelling (tumor)
3. Bradykinin also causes pain (dolor)
4. Cells are unable to function

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20
Q

Cellular response of inflammation (4 steps)

A

Chemotactic factors attract neutrophils to:
1. Marginate: move to the capillary walls
2. Emigrate: squeeze through capillary pores
3. Migrate: through chemotaxis to the injury
4. Phagocytosis facilitated by opsonization
(acts to facilitate adherence of WBC’s to
bacteria)

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21
Q

5 cardinal signs of inflammation

A
  1. redness
  2. swelling
  3. loss of function
  4. pain
  5. heat
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22
Q

3 systemic signs of inflammation

A
  1. Fever: caused by specific cytokines
    (endogenous pyrogens)
  2. Leukocytosis: increase in WBC’s (>11,000)
    and in infection, a “left shift” ratio
  3. Increase in plasma proteins as measured by ESR (erythrocyte sedimentation rate)
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23
Q

3 reasons chronic inflammation occurs and 3 results of it:

A
May occur due to:
1. Chronic infection or contamination
2. Continuous exposure to irritants
3. Immune system abnormalities
May result in:
1. Granuloma formation
2. Giant cell formation
3. Cancers in genetically susceptible individuals
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24
Q

3 stages of wound healing

A
  1. Inflammation: usually lasts 1-2 days
  2. Proliferation and New Tissue Formation:
    2-8 weeks until maximum strength achieved.
    May involve regeneration and resolution, or
    repair with scar tissue but loss of function
  3. Remodeling and Maturation: up to 2 years
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25
Q

3 stages of wound healing

A

Hemostasis is first- wound being closed by clotting
1. Inflammation: usually lasts 1-2 days
2. Proliferation and New Tissue Formation:
2-8 weeks until maximum strength achieved.
May involve regeneration and resolution, or
repair with scar tissue but loss of function
3. Remodeling and Maturation: up to 2 years

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26
Q

3 types of wound healing

A
  1. First Intention: must be clean; able to
    approximate wound edges; fastest; preferred
  2. Second Intention: used in contaminated wounds;
    large amount of tissue lost; very slow; large scar
  3. Third Intention: rarely used to close large
    wounds that are clean enough. Example: skin
    grafting
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27
Q

3 types of wound healing

A
  1. First Intention: must be clean; able to
    approximate wound edges; fastest; preferred
  2. Second Intention: used in contaminated wounds;
    large amount of tissue lost; very slow; large scar
  3. Third Intention: rarely used to close large
    wounds that are clean enough. Example: skin grafting
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28
Q

Adherence

A

Wound staying together

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29
Q

Wound vacuum

A

for 2nd intentiton

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30
Q

Wound healing process

A
  1. Macrophages: dissolve clots; clear debris; add
    a. TGF-B, transforming growth factor-beta to
    stimulate collagen precursor procollagen
    b. VEGF, vascular endothelial growth factor
    stimulates angiogenesis
    c. MMPs, Matrix metalloproteinases, remodel collagen and fibrin2. Collagen lattice forms
  2. Granulation tissue fills in wound
  3. Hypertrophic scar tissue overfills wound
  4. Cicatrization (maturation) of wound
    may take 1-2 years. Collagen contracts
    & scar becomes lighter and smoother
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31
Q

Non-union

A

failure of adherence

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32
Q

Dehiscence

A

wound edges separate, exposing underlying tissues

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33
Q

Evisceration

A

underlying viscera are exposed

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34
Q

Abscess

A

A walled pocket of infection

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35
Q

Sinus tract

A

A narrow tunnel forming

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36
Q

Cellulitis

A

A bacterial infection that enters the skin, affected skin appears swollen and red and may be hot and tender. edema is a big risk factor with cellulitis

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37
Q

Necrosis

A

Death of tissues/ cells

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38
Q

Gangrene

A

Type of tissue death caused by a lack of blood supply

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39
Q

Fistula

A

An abnormal connection between two body parts, such as an organ or blood vessel and another structure.

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40
Q

Excess fibrin or dysfunctional collagen
synthesis may result in abnormalities such
as: (5)

A
  1. fistula formation
  2. adhesions
  3. contractures
  4. strictures
  5. keloids
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41
Q

Patients that have the hardest time healing from wounds

A

Diabetics

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42
Q

Systemic markers of vascular inflammation

A

Homocysteine level: elevated in reduced
levels of folate, B vitamins, and riboflavin.
Inhibits anticoagulation cascade and
increases endothelial damage in arteries.
• C-Reactive Protein: increases to neutralize
inflammatory chemicals
• Infectious agents: often found in plaques
• Endothelial dysfunction: lack of NO

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43
Q

Granulation tissue

A

New connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process. Granulation tissue typically grows from the base of a wound and is able to fill wounds of almost any size. Bleeds easily

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44
Q

Define CHF and the mortality rate in 5 years

A
A complex syndrome resulting from
any cardiac dysfunction that results
in low cardiac output (CO) and
symptoms of pulmonary or systemic
fluid congestion. In adults, the
mortality rate is 50% within 5 years.
It is considered an end-stage disease.
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45
Q

Risk factors of CHF

A

Age: generally seniors
• High cholesterol, HTN, DM, obesity
• Pre-existing heart conditions, CAD, MI
• Valve problem or other mechanical issue
• Fluid overload conditions: renal disease
• Alcoholism, liver disease

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46
Q

Cicatrization

A

scar formation at the site of a healing wound

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47
Q

Causes of CHF

A
  1. Coronary Artery Disease/atherosclerosis
  2. Hypertension/myocardial hypertrophy
  3. Myocardial Infarction
  4. Heart Valve Disease
  5. Pericardial restriction/pericarditis
  6. Fluid overload conditions
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48
Q

Hypertrophic cardiomyopathy

A

Hypertrophic: walls are thickened,
reducing ventricular volume.
• Causes: HTN, CAD, valve stenosis,
remodeling

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49
Q

Dilated cardiomyopathy

A

Dilated: walls are weakened and bulge
out, reducing contractility
• Causes: MI with extensive scar, valve
regurgitation

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50
Q

Fluid overload condition

A

CHF

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51
Q

Decrease cardiac output causes: (3 things)

A

Reduced blood flow to kidneys,
stimulating the RAAS and fluid retention
• Less stimulation to baroreceptors in aortic
arch, stimulating hypothalmus to increase
thirst and ADH production
• Stress response stimulates catecholamines,increasing HR and O2 demand of heart

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52
Q

Increase fluid retention in CHF causes

A

Increase in preload and afterload

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53
Q

Increased stress hormones/catecholamines vasoconstrict and…

A

Increase afterload, HR and O2 demand increase, causing ischemia

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54
Q

Ischemia reduces

A

Compliance, elasticity, and contractility

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55
Q

In CHF, wall stress is increased causing CO to

A

decrease

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56
Q

S/S of CHF (8)

A
SOB climbing stairs
• SOB lying flat/orthopnea
• SOB with activities
• Increased abdominal girth
• Lower leg edema
• Cough, white sputum
• Increased weight
• Decreased appetite
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57
Q

Assessment findings of CHF

A
• SOB on exertion or at rest
• Lungs may have crackles, esp at bases
• Point of maximal impulse (heart) moved
lower and left, indicating enlargement
• X-rays: cardiac enlargement, pulmonary
congestion.
• Ascites & liver congestion, leg edema,
distended jugular veins
• Decreased urinary output
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58
Q

Left-sided HF s/s

A
  • SOB
  • Orthopnea
  • Low O2 sat
  • Pulmonary crackles
  • S1 or S2 gallop
  • Weak thready pulse
  • Probably low BP
  • left backs up into the lungs
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59
Q

Right-sided HF s/s

A
  • weight gain
  • leg edema
  • ascites/liver enlargement
  • jugular vein distension
  • right backs up to the rest of the bpdy
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60
Q

Diagnostic testing of CHF

A
Echocardiogram/Stress Test/Stress Echo
• Chest X-ray: heart and lungs
• Blood tests: BNP and ANP
• Kidney function: BUN, creatinine
• Liver function: LFT’s
• Cardiac Angiography/catheterization
• Right-sided heart catheterization: Swan-
Ganz catheter (ICU only)
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61
Q

Diagnostic criteria of CHF

A
  1. Ejection fraction less than 40%
  2. Atrial Natriuretic Peptide greater than 77 pg/mL
  3. Brain Natriuretic Peptide greater than 100 pg/mL
  4. S&S of fatigue, SOB, edema, activity intolerance
  5. S&S at rest indicate increased disease burden
  6. Structural heart disease: decreased wall motion,
    coronary artery blockage on angiogram
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62
Q

AHA classification system

A
• Stage A: High risk/ no abnormalities
(example: DM/CAD/HTN)
• Stage B: Abnormalities/no S & S
• Stage C: Abnormalities with S & S
• Stage D: advance abnormalities and S
& S at rest on maximum med therapy
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63
Q

Staging of CHF

A
• Stage 1: SOB with
brisk walk/stairs
• Stage 2: OK at rest.
HR or SOB when
walking or stairs.
• Stage 3: HR up,
tired, daily activity
is an effort.
• Stage 4: HR up,
SOB at rest, fatigue,
anxiety, palpitations
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64
Q

S/S Pulmonary Edema

A

Falling O2 sat, confusion, jugular vein distension, infarct, S3 gallop, tachycardia, enlarged spleen and liver, decreased urine output, weak pulse, cool or most skin, skin pale, grey, or cyanotic, dyspnea, orthopnea, crackles, wheeze, cough

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65
Q

CHF treatments

A

CHF medications are used to:
1. Improve cardiac efficiency by strengthening
contractions and slowing rate: glycosides
2. Reduce peripheral vascular resistance:
vasodilators
3. Reduce fluid retention: diuretics
Other treatments include:
1. Exercise: strengthens myocardium & vasodilates
2. Surgery: Bypass or valve repair as needed

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66
Q

Mechanical treatments for CHF

A
• Cardiac Resynchronization and
Implantable Cardioverter-Defibrilators
• Balloon Pumps: temporary
• L-VAD: left ventricular assist devices
• Heart transplantation
• LV remodeling surgery
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67
Q

T/F: CHF is an end-stage disease

A

True

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68
Q

Atrophic scar

A

A smaller than normal scar that’s atrophied

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69
Q

Hypertrophic scar

A

A bigger, thicker hypertrophied scar, not as thick as a keloid

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70
Q

Ways to prevent CHF

A
Prevent CHF by controlling risk factors:
• Blood pressure (HTN: meds/diet/exercise)
• Blood sugar (DM: meds/diet/exercise)
• Blood cholesterol (meds/diet/exercise)
• Weight: keep normal
• Exercise: keep it up! Resistance training,
walking, isometrics
• Diet: DASH diet (Dietary Approaches to
Stop Hypertension), Mediterranean diet
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71
Q

Define renal failure

A

Renal failure is a condition in which
the kidneys fail to remove metabolic
end products from the blood and
regulate the fluid, electrolyte, and pH
balance of the extracellular fluids. It is
on the list of top 10 causes of mortality
in the United States.

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72
Q

Pre-renal failure

A

Reduced blood flow to the kidneys (CHF, HT, shock, clots, stenosis)

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73
Q

Intra-renal failure

A

damage to the nephrons (meds, infections, DM, cancer, PKD, dyes, metals)

74
Q

Post-renal failure

A

obstruction of the ureters or urethra (renal calculi, BPH, bladder or prostate cancer that blocks urine)

75
Q

Etiologies of renal failure

A

Pre-renal failure, intra-renal failure, post-renal failure

76
Q

Acute renal failure

A

happens suddenly, may resolve

  • onset phase
  • oliguric (anuric) phase: 8-14 days or more
  • diuretic phase
  • recovery phase: may take up to a year
77
Q

Chronic renal failure

A

Happens gradually over a long time, no recovery, 80% damage before s/s may be evident

78
Q

Causes of acute renal failure: prerenal

A

Prerenal: sudden and severe drop in blood pressure (shock) or interruption of blood flow to the kidneys from severe injury or illness

79
Q

Causes of acute renal failure: intrarenal

A

direct damage to the kidneys by inflammation or reduced blood supply

80
Q

Causes of acute renal failure: postrenal

A

sudden obstruction of urine flow due to enlarged prostate. kidney stones, bladder tumor or injury

81
Q

Causes of chronic renal failure

A
Diabetes
HTN
Glomerulonephritis
Cystic disease
Urologic diseases
82
Q

Renal failure BUN level

A

Above 8-20 mg/dL

83
Q

Renal failure creatinine level

A

above 0.6-1.2 mg/dL

84
Q

Normal calcium level

A

9 -10.6 mg/ dl (total)

4.5 -5.6 mg/dl (ionized)

85
Q

Food sources of calcium

A

dairy products, green leafy vegetables

86
Q

Where is calcium stored and excreted?

A

stored in bone, excreted by kidney

87
Q

Hormonal regulation of calcium

A

parathyroid hormone raises serum levels of calcium by pulling it from bone,- calcitonin (produced by the thyroid gland) lowers serum Ca levels by storing it in bone.

88
Q

Main function of calcium

A

bone, development, blood clotting, smooth muscular contraction

89
Q

Target organ of calcium

A

skeletal muscles

90
Q

What vitamin is necessary for calcium absoprtion

A

Vitamin D

91
Q

What % of calcium is absorbed

A

About 50%

92
Q

What percentage of calcium serum is bound fo albumin

A
  • 40% in serum bound to albumin. If albumin levels are low, total Ca level will be low, too.
93
Q

What calcium level is more accurate?

A

Free or ionized

94
Q

Acidosis will ____ serum calcium and alkalosis will ____ it

A

increase, decrease

95
Q

Excess calcium causes

A

Paraneoplastic syndrome

96
Q

When phosphates are low, calcium is _____

A

high

97
Q

Causes of hypocalcemia

A
Impaired ability to mobilize calcium from bone, ie. hypoparathyroidism.
	Abnormal calcium binding
-	decreased serum albumin
-	decreased pH
-	increased free fatty acids
-	rapid infusion of citrated blood
-	acute pancreatitis
Abnormal losses
-	renal failure
Inadequate vitamin D
-	impaired absorption
-	renal failure
-	liver disease
98
Q

S/S hypocalcemia

A
Laboratory values: below 8.5 mg/dl
	Increased nerve excitability
-	paresthesias, numbness and tingling
-	skeletal muscle cramps
-	abdominal spasms and cramps
-	hyperactive reflexes
-	carpopedal spasm
-	****tetany***
-	laryngeal spasm
-	positive Chvostek's sign
-	positive Trousseau's sign
-	
Cardiovascular manifestations
-	hypotension
-	cardiac insufficiency
-	failure to respond to drugs that act via calcium-mediated mechanisms
99
Q

Causes of hypercalcemia

A
Excessive gains
-	increased intestinal absorption
-	excessive vitamin D
-	excessive calcium in diet
-	milk-alkali syndrome
Increased bone resorption
-	immobility
-	increased levels of parathyroid hormone
-	malignant neoplasms
-	thiazide diuretics
  	Inadequate losses
-	hyperthyroidism
100
Q

S/S hypercalcemia

A
Signs and Symptoms
	Laboratory values: serum Ca above 10.5
	Neuromuscular:
-	muscle weakness and atrophy
-	ataxia, loss of muscle tone
-	lethargy 
-	stupor and coma
-	personality and behavioral changes
Bone loss
-	deep bone pain
-	pathological fractures (without trauma)
Renal
-	renal insufficiency
-	polyuria
-	flank pain
-	signs of kidney stones
-	increased loss of K and Na
Cardiovascular
-	hypertension
-	shortened QT interval, AV block
Gastrointestinal
-	anorexia
-	nausea
-	vomiting
-	constipation
101
Q

Serum calcium of hypercalcemia

A

Above 10.5 mg/dl

102
Q

Serum calcium of hypocalcemia

A

Below 8.5 mg/dl

103
Q

Normal magnesium range

A

1.8-3.0 meq/l

104
Q

Food sources of magnesium

A

vegetables, nuts

105
Q

What organ regulates magnesium

A

Kidneys

106
Q

Main function of magnesium

A

maintains intracellular K. Also functions in enzyme reactions and protein and DNA synthesis.

107
Q

Target organ of magnesium

A

Heart

108
Q

% of magnesium in bone, cells and serum

A

50% in bone, 49% in cells, 1% in serum

109
Q

what electrolyte diursese’s with water

A

magnesium

110
Q

Causes of hypomagnesemia

A
Causes of Hypomagnesemia:
	Impaired intake or absorption
-	Alcoholism
-	Malabsorption
-	Small-bowel bypass surgery
-	Malnutrition or starvation
-	Parenteral Hyperalimentation with inadequate Mg
-	High dietary intake of calcium without concomitant increase in Mg
Increased losses
-	diabetic ketoacidosis
-	diuretic therapy
-	hyperparathyroidism
-	hyperaldosteronism
-	magnesium-wasting renal disease
111
Q

S/S Hypomagnesemia

A
Laboratory findings: Mg less than 1.8 meq/l
	Neuromuscular hyperirritability
-	Personality change
-	athetoid or choreiform movements
-	positive Babinski's sign
-	nystagmus
-	tetany
-	positive Chvostek's or Trousseau's signs
Cardiovascular Manifestations
-	tachycardia
-	hypertension
-	ventricular arrhythmias
112
Q

Causes of hypermagnesemia

A
Excess intake, usually in antacid form
	Adrenal insufficiency, low aldosterone
	Renal failure (most common)
113
Q

S/S Hypermagnesemia

A
Laboratory Values: greater than 3.0 meq/l.
	Neuromuscular
-	skeletal smooth muscle contraction
-	excess nerve function
-	loss of deep tendon reflexes
-	muscular weakness
Gastrointestinal: nausea and vomiting
Cardiovascular:
-	hypotension
-	bradycardia
Respiratory distress
114
Q

What electrolyte regulates water balance

A

Sodium

115
Q

What electrolyte deals with acid/base regulation

A

Potassium (K)

116
Q

what four electrolytes are essential for neuromuscular activity

A

sodium, potassium, calcium, chloride

117
Q

4 functions of electrolytes

A

 regulate water balance (mostly sodium)
 acid/base regulation (potassium)
 contribute to enzyme reactions
 essential for neuromuscular activity (sodium, potassium, calcium, chloride)

118
Q

Define electrolyte

A

: a substance that dissociates in solution to form charged particles, or ions

119
Q

Define anion and cation

A

 cations: positively charged particles

 anions: negatively charged particles

120
Q

Electrolytes are found mostly in

A

cells

121
Q

Serum levels may not accurately reflect

A

intracellular levels. (ex: 28 times more K in cells)

122
Q

Normal sodium

A

135-147 meq/l

123
Q

Minimum RDA of sodium vs how much Americans average

A

500mg/day

Americans average 6-15 g/day

124
Q

Regulation of sodium

A

Kidneys

125
Q

Where is sodium lost from

A

GI tract, skin

126
Q

Hormonal regulation of kidneys

A

aldosterone increase retains sodium and therefore water as well. Angiotensin II, ACTH, and cortisol increase the production of aldosterone

127
Q

Main function of sodium

A

Fluid retention

128
Q

Target organ of sodium

A

Brain

129
Q

Hyponatremia (sodium deficit) causes

A
	Excessive Sodium Losses
-	sweating 
-	gastrointestinal losses
-	diuresis
	    Sodium Dilution
-	excess sodium-free IV's
-	psychogenic polydipsia
-	repeated tap water enemas
	    Renal disease that impairs water elimination
	    Increased ADH Levels
-	trauma, stress, pain
-	SIADH
-	Use of medications that increase ADH
130
Q

S/S hyponatremia

A
	Laboratory Values
-	serum sodium below 137 meq/l
-	decreased serum osmolality
-	dilution of other blood components, esp. chloride, hematocrit, and BUN
	    Increased Water Content of Brain and Nerves
-	headache
-	mental depression
-	personality changes
-	confusion
-	apprehension and feeling of impending doom
-	lethargy and weakness
-	stupor, convulsions, coma
	Gastrointestinal Disturbances
-	anorexia, nausea and vomiting
-	abdominal cramps
-	diarrhea
	Increased Intracellular Fluid
-	Fingerprinting over sternum
131
Q

Hypernatremia causes

A
  • excessive oral intake (sodium bicarbonate)
  • rapid or excessive IV solutions with sodium chloride or sodium bicarbonate
     Decreased extracellular water (concentration)
     Increased water losses
  • adrenal cortical hormone excess
  • diabetes insipidus
  • tracheobronchitis
  • watery diarrhea
  • hypertonic tube feedings
     Decreased water intake
  • unconsciousness or inability to swallow
  • impaired thirst mechanism
  • NPO for therapeutic reasons
132
Q

S/S hypernatremia

A
	Laboratory Findings
-	serum sodium above 147 meq/l
-	increased serum osmolality
	    Thirst
	 Urine Output
-	oliguria or anuria
-	high specific gravity
	     Intracellular Dehydration
-	mucous membranes dry and sticky, skin dry and flushed
-	subcutaneous tissue firm and rubbery
-	central nervous system: agitation, restlessness, decreased reflexes, maniacal behavior, convulsions and coma
-	Increased body temperature
-	Decreased vascular volume with tachycardia, decreased blood pressure, weak and thready pulse
133
Q

because Na and Cl are most often bound together, signs and symptoms are…

A

generally similar

134
Q

Normal phosphate range

A

2.5-4.5 mg/dl, infants up to 7.0

135
Q

Sources of phosphates

A

dairy products, green leafy vegetables (same as calcium)

136
Q

Regulation of phosphates

A

kidneys

137
Q

Hormonal regulation of phosphates

A

opposite of calcium. Parathyroid hormone lowers levels, calcitonin would raise them.

138
Q

Main functions of phosphates

A

acid/base balance, ATP for energy, manufacture of blood components (WBC’s, RBC, platelets).

139
Q

Target organs of phosphates

A

neuromuscular function, blood

140
Q

Calcium and phosphate are

A

reciprocal

141
Q

when calcium is up, it drives phosphate

A

into the bone

Ca x PO4 = 36

142
Q

S/S hypocalcemia are similar to

A

HYPERphosphatemia, and vice versa

143
Q

Hypophosphatemia causes

A
Increased loss from the GI tract
-	antacids (aluminum and calcium bind with phosphates)
-	severe diarrhea
-	lack of vitamin D
Increased renal excretion
-	alkalosis
-	hyperparathyroidism
-	diabetic ketoacidosis
-	renal tubular defects
Decreased intake - malnutrition
Alcoholism
Increased movement into the cell
-	intravenous hyperalimentation
-	recovery from malnutrition
-	administration of insulin for ketoacidosis
144
Q

S/S hypophosphatemia

A
Laboratory values: below 3.0 in adults or 4.0 in children.
Altered neural function
-	intention tremor
-	ataxia
-	parasthesias 
-	hyporeflecia
-	confusion
-	stupor 
-	coma
-	seizures
Altered musculoskeletal function
-	muscle weakness
-	joint stiffness
-	bone pain
-	osteomalacia
Gastrointestinal symptoms
-	anorexia
-	dysphagia
Hematologic disorders
-	hemolytic anemia
-	platelet dysfunction with bleeding disorders
-	impaired function of white blood cells
145
Q

Causes of hyperphosphatemia

A

Excess intake
- long-term use of laxatives or enemas containing phosphate.
- excess administration in parenteral fluid.
- treatment of cancers with chemotherapy that releases large amounts of phosphate into the bloodstream
Inadequate loss: acute or chronic renal failure

146
Q

S/S hyperphosphatemia

A

Similar to low calcium levels, especially muscle cramps, twitches, and tetany.
Calcification of soft tissues in lungs, kidneys, joints.

147
Q

Define acid

A

an electrolyte that ionizes in water to form hydrogen ions (H+) and anions. The anion is called the conjugate base of the acid.

148
Q

Define base

A

a substance that can bind hydrogen ions. An alkali is a substance that contains a base.

149
Q

Define pH

A

the percentage of hydrogen ions in a solution.

150
Q

Normal blood pH/ where does death occur

A

7.4 with a range of 7.35 - 7.45. Death usually occurs below 6.8 or above 7.8

151
Q

Volatile acids

A

can be excreted from the body as a gas. Example: CO2 + H20 = H2CO3 (carbonic acid) = H+ & HCO3- (bicarbonate)

152
Q

nonvotaile acids

A

or fixed acids, cannot be made into a gas and must be excreted as a liquid by the kidneys. Example: lactic acid, ketones, phosphoric acid, sulfuric acid. The typical American diet causes an overload of fixed acids.

153
Q

Excreting acids

A

The LUNGS excrete volatile acids. The KIDNEYS excrete nonvolatile acids and retain bicarbonate as a buffer for acids.

154
Q

Causes of respiratory acidosis

A

HYPOVENTILATION
• COPD (chronic obstructive pulmonary disease)
• pneumonia, atelectasis
• barbituate or sedative overdose
• Guillain-Barre Syndrome, ALS, or other neuromuscular weakening diseases
• skeletal deformities and injuries to ribcage

155
Q

Lab values of respiratory acidosis

A
  • pH below 7.35
  • CO2 above 45 mmHg.
  • HCO3 normal at 24  test question
  • urine pH less than 6
156
Q

Manifestations of respiratory acidosis

A
  • Neurological: drowsy, disoriented, coma
  • Cardiovascular: hypotension, tachycardia
  • Respiratory: shallow, tachypnea or bradypnea depending on cause.
  • Muscular: weakness
157
Q

Nursing application of treating a person in respiratory acidosis

A

GRAB AMBU BAG AND START GIVING OXYGEN, PT MIGHT NEED TO BE INTUBAED

158
Q

Causes of respiratory alkalosis

A
HYPERVENTILATION
•	anxiety
•	encephalitis
•	fever
•	mechanical over-ventilation
159
Q

Lab values of respiratory alkalosis

A
  • pH above 7.45
  • CO2 below 35 mmHG
  • HCOs normal 24 mEq/L
  • urine pH greater than 7
160
Q

Manifestations of respiratory alkalosis

A
  • Neurological: lethargic, confused, may have numbness or tingling of extremities
  • Muscular: tetany, hyperreflexia
  • Respiratory: hyperventilation
161
Q

What to do if a patient is having an anxiety attack

A

alk them through box breathing (spase breathing) breathing in 4 breaths and out 4 breaths

162
Q

Causes of metabolic acidosis

A
	Excess production of acids
•	diabetic ketoacidosis
•	lactic acidosis
•	starvation with lactic acidosis
	    Inadequate loss of acids
•	uremia
•	renal tubular acidosis
	    Excess loss of base: severe diarrhea (pts with c. diff are also at risk)
163
Q

lab findings in metabolic acidosis

A
  • pH less than 7.35
  • CO2 less than 35 mm HG  Kussmal’s a mechanism for metabolic acidosis, sweet smelling breath
  • HCO3 - less than 24 mEq/L
  • urine pH less than 6
164
Q

Manifestations of metabolic acidosis

A
  • Neurological: disoriented, weak, coma
  • Gastrointestinal: nausea, vomiting, diarrhea, abdominal pain, dehydration
  • Respiratory: hyperventilation
165
Q

Metabolic alkalosis causes

A
*RARE*Loss of acids
•	severe vomiting
•	excess gastric suctioning
•	diuretic therapy
	    Base or buffer imbalance
•	potassium deficit (causes relative Na excess)
•	excess NaHCO3 intake
166
Q

Lab findings of metabolic alkalosis

A
  • pH above 7.45
  • CO2 above 45 mmHg.
  • HCO3 above 24 mEq./l
  • urine pH above 7
167
Q

Manifestations of metabolic alkalosis

A
  • Neurological: confusion, stupor, coma
  • GI: anorexia, nausea, tremors, cramps
  • MS: tetany
  • Respiratory: hypoventilation
168
Q

Normal values in arterial blood gases

A
Normal Values
pa O2:   above 90%
pa CO2: 40 range 38-43
pH:         7.4 range 7.35-7.45
HCO3:    24 range 22-26
O2 Sat:   93-100%
Hgb:       13-15
CO:         0
169
Q

Steps in blood gas analysis

A
  1. Is the pH acidic or basic?
  2. Is the CO2 elevated (acidic) or decreased (basic)?
  3. Does the CO2 match the pH? If yes, problem is probably respiratory. Confirm by step 4.
  4. Is the O2 normal or decreased? If O2 confirms CO2, problem is probably respiratory.
  5. Is the HCO3 elevated (alkalotic) or decreased (acidotic)? If the HCO3 matches the pH, the problem is probably metabolic.
  6. If the ph is within normal but the CO2 and HCO3 are abnormal, the problem is a chronic one that has been compensated.
170
Q

Normal potassium range

A

3.5 - 5.0 meq/l

171
Q

Minimum RDA of potassium

A

50-100 meq/day

172
Q

Sources of potassium

A

Fruits and vegetables

173
Q

Regulation of potassium is in the

A

kidneys

174
Q

hormonal regulation os potassium

A

aldosterone reduces potassium in the bloodstream. Na and K are exchange ions - when one goes up, the other goes down.

175
Q

main function of potassium

A

smooth electrical conduction to the muscles

176
Q

target organ of potassium

A

heart

177
Q

what percentage of potassium is inside the cells?

A

98%

178
Q

4 special considerations of potassium

A

 Potassium follows water. Diuresis will wash out potassium from the bloodstream.
 K will shift out of cells with acidosis.
 Insulin will also drive K into cells.
 A deficiency of Mg will cause intracellular K depletion regardless of serum K levels.

179
Q

causes of hypokalemia (potassium deficit)

A
Inadequate Intake
-	Inability to eat
-	Diet deficient in potassium
-	Administration of K free IV solutions
Excessive Gastrointestinal Losses
-	Vomiting
-	Diarrhea
-	Nasogastric Suctioning
-	Fistula Drainage
Excessive Renal Losses
-	Diuretic phase of renal failure
-	Diuretic therapy (except K-sparing ones)
-	Increased mineralcorticoid levels
	Cushing's Syndrome
	Primary aldosteronism
 	Glucocorticoid Therapy
Intracellular Shift
-	Treatment for diabetic acidosis
-	Alkalosis, metabolic or respiratory
180
Q

S/S hypokalemia

A
Laboratory Values: Serum K below 3.5
		Skeletal Muscles:
-	tenderness, paresthesias, cramps
-	weakness
-	flabbiness
-	paralysis
Cardiovascular System:
-	Postural hypotension
-	Increased sensitivity to digitalis
-	Arrhythmias and tachycardia
Gastrointestinal Tract:
-	Anorexia
-	Vomiting
-	Abdominal Distention
-	Paralytic Ileus
Respiratory Muscles:
-	Shortness of breath
-	Shallow breathing	
Kidneys:
-	Polyuria
-	Nocturia
-	Low osmolality and low specific gravity
Thirst
Central Nervous System Function
-	Confusion
-	Depression
Acid-Base Balance: metabolic alkalosis
181
Q

Causes of hyperkalemia

A
Excessive Intake or Gain
-	Excessive Oral Intake
-	Excessive or rapid parenteral infusion
-	Tissue trauma, burns, and massive crushing injuries
Inadequate Renal Losses
-	Renal failure
-	Adrenal Insufficiency; Addison's Disease
-	Potassium sparing diuretics
182
Q

S/S hyperkalemia

A
Laboratory values: Serum K above 5.5 meq/l
		Neural and skeletal muscle activity
-	Paresthesias
-	Weakness and dizziness
-	Muscle cramps
Smooth muscle activity of the GI tract
-	Nausea, diarrhea
-	Intestinal colic and GI distress

Cardiac Electrophysiology

  • Peaked T waves, depressed S-T segment
  • Depressed P wave and widening of QRS segment
  • Cardiac Arrest