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Adult Health I > Adult Health Exam I > Flashcards

Adult Health Exam I Flashcards

1
Q

red blood cell count

A
  • normal = men: 4.5-5.5/women: 4.1-5.1
  • increase d/t = disease, hypoxia, any increased need for oxygen
  • decrease d/t = abnormal loss of erthyrocytes, lack of hormones to stimulate red blood cell production
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2
Q

Hemoglobin

A
  • composed of the pigment heme which contains iron heme and a protein globin
  • normal= men: 13-17/women: 12-16
  • increases d/t = polycythemia and hemoconcentration
    decreases d/t = anemia, hemorrhage, hemodilution
  • Hemoglobin is not affected by hydration
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3
Q

Hematocrit

A
  • proportion of RBCs in the blood
  • normal = men: 37-51%/women: 33-46%
  • increases d/t = dehydration, bone marrow disease
  • decreases d/t = anemia, pregnancy, over-hydration, recent blood loss
  • hematocrit is affected by hydration status
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4
Q

Platelet

A
  • fragments of cytoplasm which aggregate and release a substance that begins the coagulation cascade
  • normal = 150,000 - 450,000
  • increase d/t = tumors, lesions, malignant neoplasm
  • decrease d/t = can be idiopathic, d/t viral infections, lupus, anemias, chemo drugs, radiation, spleen, heparin
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5
Q

white blood cells

A
  • total white blood cell count = absolute count of WBCs per mm^3
  • differential of % of each of the 5 types of WBC
  • normal = 4,500 - 11,100
  • increases seen with infection or severe stress or some versions of cancer
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6
Q

Neutrophils

A
  • 2 types: bands or stabs and segmented neutrophils
  • both rise as a defense against infection
  • neutropenia is a results of certain infections
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7
Q

eosinophils

A
  • associated with antigen-antibody reactions
  • rise related allergies
  • decline in states of elevated adrenal steroids
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8
Q

basophils

A
  • rare type of wbc
  • rise d/t cancer
  • decline during allergic reactions
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9
Q

lymphocytes

A
  • T&B cells, natural killer cells
  • rise in viral infections
  • chronic bacterial infections
  • decline in HIV/AIDs
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10
Q

monocytes

A
  • present in tissues as macrophages
  • act as phagocytes in some chronic inflammatory diseases and will be elevated in those cases
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11
Q

Blood Urea Nitrogen (BUN)

A
  • urea nitrogen in the blood, can reflect hydration status or renal function when looked at in conjunction with creatinine
  • normal = 8-21 mg/dL
  • increase d/t = seen in kidney damage, decreased renal perfusion caused by poor circulation to kidneys & severe dehydration d/t lack of volume to excrete waste products
  • decrease d/t = over hydration
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12
Q

Creatinine

A
  • waste product of creatinine phosphate from muscle
  • morning values matter d/t physical activity
  • normal = 0.5-1.2 mg/dL
  • increase d/t = poor kidney function, dehydration, nephron damage
  • decrease d/t = muscle atrophy, aging, liver disease, protein restricted diet and pregnancy
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13
Q

Glucose

A
  • normal = 70-110 mg/dL
  • increase d/t = diabetes, stress, glucocorticoids, growth, pregnancy, epinephrine
  • decrease d/t = organic disease, pancreatic tumor, ETOH, lack of cortisone
  • if blood sugar is above about 160-190 mg/dL glucose will spill into urine
  • venous blood sugars are 10-15% higher than finger stick
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14
Q

Prothrombin aka clotting factor 2

A
  • a plasma protein produced by liver
  • vitamin K is required for the production of prothrombin by liver and is often used when a patient has a elevated PT/INR
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15
Q

Prothrombin time (PT)

A
  • expressed as time in seconds (normal: 11.2-13.2 seconds)
  • increased d/t = medications (heparin, eliquist, xarelto, prodaxa), liver, vitamin K deficiency
  • decreased d/t = thrombophlebitis, malignant tumor
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16
Q

International Normalized Ratio (INR)

A
  • used because PT can differ based on reagent used
  • normal = 1.0 -1.4
  • therapeutic range = 2-3
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17
Q

Partial Thromboplastin Time

A
  • two purposes = clot factor, monitor heparin therapy
  • normal = 22.1 -34.1 seconds for activated, 60-90 seconds for non-activated
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18
Q

Urinalysis normals

A
  • specific gravity – urine concentration, 1.001-1.035
  • RBCs and WBCs – indicate infection or injury, none to few
  • Leukocyte esterase – negative
  • protein – negative
  • glucose – negative
  • pH – 5-9
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19
Q

UA component for diagnosis of UTI

A
  • pH is alkaline
  • sediment = urine is centrifuged and examined for RBC and WBC, normal is none to few
  • bacteria = only a few is usually contamination, many indicate infection
  • leukocyte esterase = enzyme that if present is indicative of a UTI but can also show inflammation or kidney disease
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20
Q

fluid and electrolyte imbalances

A
  • can be caused by illness or disease – heart failure, burns
  • can be a result of therapeutic measures – diuretics, IV fluids
  • usually more than one imbalance is occurring in a clinical setting
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21
Q

Insensible loss of fluid

A
  • invisible vaporization – lungs and skin (sweat)
  • electrolytes can also be lost
  • approximately 600-900ml/day is lost
  • daily weight to track fluid amount
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22
Q

GI tract regulating fluids

A
  • oral intake accounts for most water
  • small amounts of H20 eliminated by GI tract in feces
  • vomit, diarrhea, NG suction can lead to significant fluid and electrolyte imbalances
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23
Q

Extracellular hypervolemia

A
  • extracellular fluid volume excess
  • excessive intake of fluids
  • related to heart and renal failure
  • interstitial to plasma fluid shift
  • treatment = remove fluid without changing electrolyte composition or osmolality of ECF
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24
Q

Extracellular hypovolemia

A
  • ECF volume deficit
  • d/t diarrhea, fistula drainage, hemorrhage, inadequate intake, plasma to interstitial fluid shift
  • treatment = IV fluids, oral intake
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25
Q

How do we measure I&O?

A
  • intake = PO fluids, IV fluids, tube feeding
  • output = urine, liquid stool, vomit, drainage, sweat, respiration
  • measured every 8 hours, daily weights
  • urine output for an adult = 30 ml
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26
Q

Assessment for fluid overload

A
  • vital signs = increased HR, increased BP, dysrhythmias
  • respiratory status = crackles, shallow rapid respiration
  • hydration status = edema, pale/cool skin, enlarged liver, ascites
  • neuro = level of alertness, confusion, restlessness, muscle weakness/spasms, visual changes, and a headache
  • possible causes of fluid overload = over hydration, heart and renal failure
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27
Q

assessment for fluid deficiency

A
  • vital signs = tachycardia, weak pulse, dysrhythmias
  • respiratory status = tachypnea, dyspnea
  • hydration status = skin turgor, intake and output, moisture in mucous membranes of mouth, nose and eyelids, decreased bowel sounds/constipation, thirst
  • neuro = altered level of alertness, dizziness/syncope, muscle weakness, restlessness
  • possible causes = vomit, diarrhea, trauma, poor intake, exercise, fluid shifts, polyuria, burns, diuretics, drains
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28
Q

Interventions for fluid balance

A
  • monitor I&O, weight
  • manage causes
  • medications – antiemetic, antipyretic, antidiarrheal, antibiotic
  • replacement of fluids (IV and PO) and electrolytes
  • seizure precautions d/t electrolyte imbalance
  • prevent skin breakdown
  • ensure safety
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29
Q

Lab value assessment for fluid baalnce

A
  • lab reports reflect only serum levels
  • may not reflect the status of electrolytes in individual cells
  • examine the latest lab data and note trends
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30
Q

Hypernatremia (Na+ >145mEq/L) Causes

A
  • occurs during water loss = insensible loss, inadequate h20 intake, vomit, diarrhea, decreased renal response, to ADH, diuresis, fluid shift to extracellular space
  • occurs during sodium gain = medication administration, primary hyperaldosteronism, sodium intake w/o water, overdose with hypertonic solution
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31
Q

Clinical manifestations of hypernatremia

A
  • neurological = restlessness, agitation, twitching, lethargy, seizures, coma, weakness
  • cardiovascular = postural hypotension, increased pulse, peripheral and pulmonary edema, increased blood pressure
  • integumentary = flushed, dry skin, dry swollen tongue, extreme thirst
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32
Q

Treatment of hypernatremia

A
  • should be corrected slowly to reduce the risk of brain swelling
  • water replacement – oral replacement, IV fluids
  • nursing interventions
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33
Q

Hyponatremia (Na+ <135 mEq/L) Causes

A
  • occurs during water gain = syndrome inappropriate anti diuretic hormone, congestive heart failure, increased intake
  • occurs during sodium loss = GI losses, renal losses, skin losses
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34
Q

Clinical Manifestations of Hyponatremia

A
  • water gain = headache, apathy, weakness, confusion, nausea, vomiting, weight gain, increased blood pressure, muscle spasms, seizures, coma
  • sodium loss = increased irritability, apprehension, confusion, postural hypotension, tachycardia, nausea, vomiting, weight loss, tremors, seizures, coma
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35
Q

Treatment of hyponatremia

A
  • cellular swelling related to cerebral edema, first manifested in the CNS
  • can cause irreversible neuro damage if Na+ drops rapidly
  • can attempt to increase serum sodium by 4-6 mEq/L over the first 1-2 hours
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36
Q

Hyperkalemia K+ > 5.0

A
  • common causes = excess K+ intake, shift of K+ out of cells (metabolic acidosis), failure to eliminate K+ (kidney disease)
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37
Q

Clinical manifestations of hyperkalemia

A
  • irritability or anxiety
  • abdominal cramping
  • diarrhea
  • muscle weakness in lower extremities
  • paresthesias – numbness and tingling
  • cardiac changes – irregular pulse, cardiac arrest if sudden onset
  • EKG changes – peak T waves, prolonged PR, loss of P and widening of the QRS
    arrhythmias such as ventricular fibrillation
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38
Q

Treatment of hyperkalemia

A
  • IV = calcium gluconate, sodium bicarbonate, dextrose and regular insulin (moves K+ inside the cell, maintain blood sugar)
  • PO = sodium polystyrene sulfonate
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39
Q

Interventions for hyperkalemia

A
  • mild hyperkalemia = monitor telemetry, eliminate oral and parenteral K+, encourage fluids and monitor I&O
  • moderate to severe hyperkalemia = dialysis and medications
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40
Q

hypokalemia (K+ <3.5 mEq/L)

A
  • K+ is not well conserved in the body
  • causes = K+ loss from diuretics, shift of K+ into cells, lack of K+ intake
41
Q

Clinical manifestations of hypokalemia

A
  • fatigue, muscle weakness, leg cramps
  • nausea, vomiting
  • decreased reflexes, soft flabby muscles
  • polyuria
  • hyperglycemia
  • cardiac changes = bradycardia, ST depression, flattened T waves, presence of U wave, ventricular arrhythmias, ventricular tachycardia, ventricular fibrillation
42
Q

Interventions for hypokalemia

A
  • increasing dietary K+ intake
  • PO/IV potassium
  • monitoring of telemetry
  • I&O measurement
  • vital signs
  • safety
43
Q

hypokalemia treatment

A
  • oral replacement for k+
  • oral potassium chloride
  • IV potassium, never push potassium
44
Q

nursing considerations for PO K+ administration

A
  • may irritate stomach, throat, and mouth
  • if extended release, do not crush or chew
  • causes nausea/vomiting
  • take with food or after meals to decrease GI upset
45
Q

Hypercalcemia (>10.2 mg/dL)

A
  • can be caused by breast and lung cancer and multiple myeloma
  • other causes are vitamin D overdose, prolonged, immobility and rarely increase Ca+ intake
46
Q

Clinical manifestations of hypercalcemia

A
  • lethargy, fatigue, confusion, coma
  • personality changes and decreased memory
  • muscle weakness and decreased reflexes
  • anorexia, nausea, vomiting, constipation
  • EKG changes = shortened ST segment and QT interval and ventricular arrhythmias
47
Q

Treatment of hypercalcemia

A
  • excretion in urine with loop diuretic along with hydration using isotonic IV solutions
  • oral intake of 3-4L a day to promote excretion and decrease risk of kidney stones
  • neuro assessments, safety checks, telemetry monitoring, increase weight bearing activities
  • lower dietary levels of Ca2+
48
Q

Hypocalcemia (<8.6mg/dL) causes

A
  • CKD
  • elevated phosphorus
  • primary hypoparathyroidism
  • vitamin D deficiency
  • acute pancreatitis
  • tumor lysis syndrome
  • malnutrition
49
Q

clinical manifestations of hypocalcemia

A
  • easy fatiguability, depression, confusion
  • hyperreflexia and muscle cramps
  • Chvostek’s and Trousseau’s sign
  • laryngeal spasm
  • numbness and tingling around mouth and in extremities
  • EKG changes = decreased contractility and elongation of ST segment and OT interval that can result in V tach
50
Q

treatment of hypocalcemia

A
  • oral or IV supplements: IV calcium chloride or gluconate, tums, calcium carbonate, calcitriol
  • diet high in Ca with vitamin D supplements
  • pain and anxiety assessments
  • safety
  • EKG monitoring
  • careful monitoring
51
Q

hyperphosphatemia (>4.5 mg/dL)

A
  • causes = renal failure, chemotherapy, hypoparathyroidism
  • clinical manifestations = same as hypocalcemia
52
Q

interventions of hyperphosphatemia

A
  • dietary restrictions
  • correction of hypocalcemia
  • adequate of hydration
  • VS and I&O
  • cardiac monitoring
  • skin assessment
53
Q

Hypophosphatemia (<2.5mg/dL)

A
  • causes = malabsorption of malnutrition, ETOH abuse, antiacid abuse, hyperparathyroidism
  • clinical manifestations = same as hypercalcemia
54
Q

treatment of hypophosphatemia

A
  • phosphate salts - potassium phosphate
  • neuromuscular assessments
  • respiratory monitoring
  • cardiac monitoring
  • adequate hydration
  • VS I&O
  • safety
  • increase activity
  • administer supplements
55
Q

magnesium

A
  • appears only in small amounts in serum
  • essential for neuromuscular function
  • changes affect other ions
56
Q

hypermagnesemia (>2.6 mg/dL)

A
  • causes = renal failure, excessive intake (IV or PO magnesium), adrenal insufficiency
  • clinical manifestations = lethargy, drowsiness, nausea, vomiting, decreased deep tendon reflexes, somnolence (lethargy), respiratory and cardiac arrest
57
Q

treatment of hypermagnesemia

A
  • IV calcium gluconate
  • encourage PO fluids to excrete through kidneys
  • focus on education
  • cautious use of Mg
  • review OTC medications
  • VS, I&O, telemetry, frequent neuro checks
58
Q

hypomagnesemia (<1.6 mg/dL)

A
  • seen in patients with: diarrhea, vomiting, chronic alcoholism, prolonged malnutrition, diuresis medications, hyperglycemia
  • clinical manifestations: resembles hypocalcemia, cardiac arrhythmias, neuromuscular irritability
59
Q

treatment of hypomagnesemia

A
  • IV magnesium sulfate
  • magnesium gluconate PO
  • monitoring therapy
  • telemetry, I&O, DTRs, seizure precautions
  • teaching about foods to include in diet
60
Q

Intravenous solutions

A
  • least invasive to most invasive attempts to reverse fluid and electrolyte balances
  • oral fluid replacement, IV fluid replacement
  • know the cause
61
Q

findings that contribute to the selection of IV solutions

A
  • assessment of electrolyte values
  • elevated hematocrit
  • serum/urine osmolarity
  • urine specific gravity
  • electrolytes
62
Q

decisions about IV solutions are based on

A
  • need to reverse imbalances
  • maintenance while PO is restricted: NPO, unconscious patients
  • administration of life saving treatments
  • corrective loss
63
Q

tonicity

A
  • tension that osmotic pressure size
  • isotonic = cells will stay the same
  • hypotonic = cells will swell
  • hypertonic = cells will shrink
64
Q

isotonic solutions

A
  • closest to human osmolality
  • expands only ECF with no net gain/loss from ICF
  • ideal for replacement of ECF volume deficit
  • examples: 0.9% normal saline, lactated ringers
65
Q

hypertonic solutions

A
  • raises osmolarity of ECF and expands it
  • used in the treatment of hypovolemia and severe hyponatremia
  • nurses must closely monitor lung sounds and serum sodium
66
Q

hypotonic solution

A
  • provides more water than electrolytes, diluting ECF
  • osmosis moves water from the ECF to the ICF
  • once the equilibrium both compartments are expanded
  • nurse must frequently monitor neuro status
67
Q

other fluids used

A
  • plasma expanders = stay in vascular spaces and increase osmotic pressure
  • colloids = protein solutions
  • dextran = complex synthetic sugar
  • hetastarch = synthetic colloid similar to dextran
  • packed red blood cells
68
Q

what is diabetes?

A
  • a chronic multisystem disease that results in hyperglycemia from abnormal insulin production, impaired insulin, or both
69
Q

type one diabetes

A
  • insulin dependent diabetes mellitus
  • more likely to occur before the age of 40
  • beta cells in the pancreas are destroyed – no insulin
  • signs and symptoms = polyuria, polydipsia, polyphagia, weight loss, fatigue
  • treatment = insulin and health promotion
70
Q

type two diabetes

A
  • non insulin dependent diabetes mellitus
  • adult onset
  • insulin resistance, impaired insulin production, inappropriate glucose production in the liver
  • signs and symptoms = fatigue, recurrent infections, delayed wound healing
  • risk factors = obesity, lack of exercise, genetics, ethnicity, diet, age
  • treatment = diet and exercise
71
Q

Short duration: rapid acting insulin

A
  • lispro and aspart
  • onset = 10-30 minutes
  • peak = 30 minutes - 3 hours
  • duration = 3-5 hours
72
Q

short duration: slower acting insulin

A
  • regular (humulin)
  • onset = 30-60 minutes
  • peak = 2-5 hours
  • duration = 5-8 hours
73
Q

intermediate duration insulin

A
  • NPH
  • onset = 1.5-4 hours
  • peak = 4-12 hours
  • duration = 12-18 hours
74
Q

long duration insulin

A
  • determir, lantus, glargine
  • onset = 0.8-4 hours
  • no peak
    duration = 16-24 hours
75
Q

sulfonylureas

A
  • glipizide, glyburide, glimepiride, amaryl
  • increase insulin production from pancreas
76
Q

Meglitinides

A
  • prandin, starlix
  • stimulates rapid/short release of insulin
77
Q

Biguanides

A
  • metformin, glucophage
  • decreased glucose production, enhance insulin sensitivity at tissue level, improving glucose production to cells
78
Q

Thiazolideinediones

A
  • Actos and avandia
  • improve insulin sensitivity, transport, and utilization at target tissues
79
Q

Hyperglycemia

A
  • headache
  • polyuria
  • fatigue
  • weakness
  • nausea
  • vomiting
  • polydipsia
  • polyphagia
80
Q

hypoglycemia

A
  • cold and clammy skin
  • numbness
  • tingling
  • tremors
  • mood changes
  • fainting/dizziness
  • seizures
  • tachycardia
  • slurred speech
  • hunger
  • unsteady gait
81
Q

treatment of hypoglycemia

A
  • check blood sugar frequently
  • 15g of fast acting sugar – candy, orange juice
  • 15-20g of carbohydrates
  • IV dextrose and glucagon
82
Q

diabetic ketoacidosis

A
  • associated with type I diabetes
  • occurs when there is a severe deficiency of insulin for cells to utilize in producing energy
  • body compensates by breaking down fats
  • ketones are acidic by-product as a result and causes metabolic acidosis
83
Q

Cascade of events d/t insulin deficiency and acidosis

A
  1. production of glucose from amino acids in liver -> hyperglycemia -> adds to osmotic diuresis
  2. severe loss of K+, Na+, Cl, Mg, and P
  3. vomiting that causes dehydration and electrolyte loss
  4. hypovolemia (fluid deficit) -> shock
  5. kidney failure causes retention of ketones and glucose
  6. coma from hyperglycemia, acidosis, and dehydration
84
Q

causes of dka

A
  • illness or infection
  • inadequate insulin
  • changes in diet and exercise
  • poor management of diabetes
85
Q

signs and symptoms of dka

A
  • polyuria
  • polydipsia
  • polyphagia
  • dry mouth
  • kuzmal respirations – deep and quick
  • fruity breath – exhaling ketones
  • tachycardia
  • hypotension
  • lethargy
  • weak
  • confusion
  • nausea vomiting
86
Q

primary electrolyte lost in dka

A
  • potassium d/t treatment of insulin
87
Q

hyperosmolar hyperglycemic nonkeotic syndrome

A
  • severely hyperglycemia; pancreas produces enough insulin to prevent DKA, but not enough to prevent hyperglycemia, dehydration, osmotic diuresis
88
Q

hypovolemia leads to

A
  • hypotension – tissue anoxia, increased lactic acid
  • decreased renal perfusion – decreased urination
  • increased blood viscosity – blood clots
89
Q

causes of hhnk

A
  • infection – sepsis/UTI
  • poorly controlled T1 diabetes
  • dehydration d/t impaired thirst
  • decreased mental capacity
90
Q

symptoms of hhnk

A
  • aphasia, hemipuresis
  • lethargy
  • seizures
  • dehydration
91
Q

assessments for dka and hhnk

A
  • telemetry (d/t fluctuations in K+)
  • blood sugar
  • vitals
  • intake and output
  • level of consciousness
  • airway,breathing,circulation
  • health history
92
Q

labs for dka

A
  • blood glucose (over 250)
  • urine glucose (positive)
  • blood pH (acidic)
  • K+ levels (low)
  • BUN/creatinine (high)
  • bicarb (low, less than 15)
93
Q

treatment for DKA and hhnk

A
  • ensure airway
  • IV fluids
  • Insulin drip
  • dextrose once BS is under 250
  • Potassium drip
94
Q

labs for hhnk

A
  • blood glucose (over 600)
  • urinalysis (no ketones)
  • BUN/creatinine (high)
  • Na+ and K+ (low)
  • pH (low)
  • Bicarb (high, greater than 20)
95
Q

patient teaching for dka/hhnk

A
  • proper insulin dosage
  • signs and symptoms of hyperglycemia
  • exercise and meal planning
  • adequate hydration
96
Q

special considerations dka and hhnk

A
  • symptoms mimic stroke
  • increased blood sugar
97
Q

social determinants of dka and hhnk

A
  • financial status
  • insurance
  • support system
  • ability for self care
  • homelessness
  • transportation
98
Q

nursing diagnosis for dka and hhnk

A
  • ineffective self management of illness
  • risk for infection
  • risk for fluid volume deficit
  • imbalanced nutrition

Adult Health I (4 decks)

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