Adult Health Exam I Flashcards
(98 cards)
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
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
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
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
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
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
7
Q
eosinophils
A
- associated with antigen-antibody reactions
- rise related allergies
- decline in states of elevated adrenal steroids
8
Q
basophils
A
- rare type of wbc
- rise d/t cancer
- decline during allergic reactions
9
Q
lymphocytes
A
- T&B cells, natural killer cells
- rise in viral infections
- chronic bacterial infections
- decline in HIV/AIDs
10
Q
monocytes
A
- present in tissues as macrophages
- act as phagocytes in some chronic inflammatory diseases and will be elevated in those cases
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
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
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
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
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
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
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
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
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
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
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
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
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
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
25
How do we measure I&O?
- 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
26
Assessment for fluid overload
- 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
27
assessment for fluid deficiency
- 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
28
Interventions for fluid balance
- 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
29
Lab value assessment for fluid baalnce
- lab reports reflect only serum levels
- may not reflect the status of electrolytes in individual cells
- examine the latest lab data and note trends
30
Hypernatremia (Na+ >145mEq/L) Causes
- 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
31
Clinical manifestations of hypernatremia
- 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
32
Treatment of hypernatremia
- should be corrected slowly to reduce the risk of brain swelling
- water replacement -- oral replacement, IV fluids
- nursing interventions
33
Hyponatremia (Na+ <135 mEq/L) Causes
- occurs during water gain = syndrome inappropriate anti diuretic hormone, congestive heart failure, increased intake
- occurs during sodium loss = GI losses, renal losses, skin losses
34
Clinical Manifestations of Hyponatremia
- 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
35
Treatment of hyponatremia
- 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
36
Hyperkalemia K+ > 5.0
- common causes = excess K+ intake, shift of K+ out of cells (metabolic acidosis), failure to eliminate K+ (kidney disease)
37
Clinical manifestations of hyperkalemia
- 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
38
Treatment of hyperkalemia
- IV = calcium gluconate, sodium bicarbonate, dextrose and regular insulin (moves K+ inside the cell, maintain blood sugar)
- PO = sodium polystyrene sulfonate
39
Interventions for hyperkalemia
- mild hyperkalemia = monitor telemetry, eliminate oral and parenteral K+, encourage fluids and monitor I&O
- moderate to severe hyperkalemia = dialysis and medications
40
hypokalemia (K+ <3.5 mEq/L)
- K+ is not well conserved in the body
- causes = K+ loss from diuretics, shift of K+ into cells, lack of K+ intake
41
Clinical manifestations of hypokalemia
- 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
Interventions for hypokalemia
- increasing dietary K+ intake
- PO/IV potassium
- monitoring of telemetry
- I&O measurement
- vital signs
- safety
43
hypokalemia treatment
- oral replacement for k+
- oral potassium chloride
- IV potassium, never push potassium
44
nursing considerations for PO K+ administration
- 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
Hypercalcemia (>10.2 mg/dL)
- 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
Clinical manifestations of hypercalcemia
- 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
Treatment of hypercalcemia
- 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
Hypocalcemia (<8.6mg/dL) causes
- CKD
- elevated phosphorus
- primary hypoparathyroidism
- vitamin D deficiency
- acute pancreatitis
- tumor lysis syndrome
- malnutrition
49
clinical manifestations of hypocalcemia
- 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
treatment of hypocalcemia
- 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
hyperphosphatemia (>4.5 mg/dL)
- causes = renal failure, chemotherapy, hypoparathyroidism
- clinical manifestations = same as hypocalcemia
52
interventions of hyperphosphatemia
- dietary restrictions
- correction of hypocalcemia
- adequate of hydration
- VS and I&O
- cardiac monitoring
- skin assessment
53
Hypophosphatemia (<2.5mg/dL)
- causes = malabsorption of malnutrition, ETOH abuse, antiacid abuse, hyperparathyroidism
- clinical manifestations = same as hypercalcemia
54
treatment of hypophosphatemia
- phosphate salts - potassium phosphate
- neuromuscular assessments
- respiratory monitoring
- cardiac monitoring
- adequate hydration
- VS I&O
- safety
- increase activity
- administer supplements
55
magnesium
- appears only in small amounts in serum
- essential for neuromuscular function
- changes affect other ions
56
hypermagnesemia (>2.6 mg/dL)
- 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
treatment of hypermagnesemia
- 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
hypomagnesemia (<1.6 mg/dL)
- seen in patients with: diarrhea, vomiting, chronic alcoholism, prolonged malnutrition, diuresis medications, hyperglycemia
- clinical manifestations: resembles hypocalcemia, cardiac arrhythmias, neuromuscular irritability
59
treatment of hypomagnesemia
- IV magnesium sulfate
- magnesium gluconate PO
- monitoring therapy
- telemetry, I&O, DTRs, seizure precautions
- teaching about foods to include in diet
60
Intravenous solutions
- least invasive to most invasive attempts to reverse fluid and electrolyte balances
- oral fluid replacement, IV fluid replacement
- know the cause
61
findings that contribute to the selection of IV solutions
- assessment of electrolyte values
- elevated hematocrit
- serum/urine osmolarity
- urine specific gravity
- electrolytes
62
decisions about IV solutions are based on
- need to reverse imbalances
- maintenance while PO is restricted: NPO, unconscious patients
- administration of life saving treatments
- corrective loss
63
tonicity
- tension that osmotic pressure size
- isotonic = cells will stay the same
- hypotonic = cells will swell
- hypertonic = cells will shrink
64
isotonic solutions
- 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
hypertonic solutions
- 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
hypotonic solution
- 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
other fluids used
- 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
what is diabetes?
- a chronic multisystem disease that results in hyperglycemia from abnormal insulin production, impaired insulin, or both
69
type one diabetes
- 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
type two diabetes
- 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
Short duration: rapid acting insulin
- lispro and aspart
- onset = 10-30 minutes
- peak = 30 minutes - 3 hours
- duration = 3-5 hours
72
short duration: slower acting insulin
- regular (humulin)
- onset = 30-60 minutes
- peak = 2-5 hours
- duration = 5-8 hours
73
intermediate duration insulin
- NPH
- onset = 1.5-4 hours
- peak = 4-12 hours
- duration = 12-18 hours
74
long duration insulin
- determir, lantus, glargine
- onset = 0.8-4 hours
- no peak
duration = 16-24 hours
75
sulfonylureas
- glipizide, glyburide, glimepiride, amaryl
- increase insulin production from pancreas
76
Meglitinides
- prandin, starlix
- stimulates rapid/short release of insulin
77
Biguanides
- metformin, glucophage
- decreased glucose production, enhance insulin sensitivity at tissue level, improving glucose production to cells
78
Thiazolideinediones
- Actos and avandia
- improve insulin sensitivity, transport, and utilization at target tissues
79
Hyperglycemia
- headache
- polyuria
- fatigue
- weakness
- nausea
- vomiting
- polydipsia
- polyphagia
80
hypoglycemia
- cold and clammy skin
- numbness
- tingling
- tremors
- mood changes
- fainting/dizziness
- seizures
- tachycardia
- slurred speech
- hunger
- unsteady gait
81
treatment of hypoglycemia
- check blood sugar frequently
- 15g of fast acting sugar -- candy, orange juice
- 15-20g of carbohydrates
- IV dextrose and glucagon
82
diabetic ketoacidosis
- 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
Cascade of events d/t insulin deficiency and acidosis
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
causes of dka
- illness or infection
- inadequate insulin
- changes in diet and exercise
- poor management of diabetes
85
signs and symptoms of dka
- polyuria
- polydipsia
- polyphagia
- dry mouth
- kuzmal respirations -- deep and quick
- fruity breath -- exhaling ketones
- tachycardia
- hypotension
- lethargy
- weak
- confusion
- nausea vomiting
86
primary electrolyte lost in dka
- potassium d/t treatment of insulin
87
hyperosmolar hyperglycemic nonkeotic syndrome
- severely hyperglycemia; pancreas produces enough insulin to prevent DKA, but not enough to prevent hyperglycemia, dehydration, osmotic diuresis
88
hypovolemia leads to
- hypotension -- tissue anoxia, increased lactic acid
- decreased renal perfusion -- decreased urination
- increased blood viscosity -- blood clots
89
causes of hhnk
- infection -- sepsis/UTI
- poorly controlled T1 diabetes
- dehydration d/t impaired thirst
- decreased mental capacity
90
symptoms of hhnk
- aphasia, hemipuresis
- lethargy
- seizures
- dehydration
91
assessments for dka and hhnk
- telemetry (d/t fluctuations in K+)
- blood sugar
- vitals
- intake and output
- level of consciousness
- airway,breathing,circulation
- health history
92
labs for dka
- blood glucose (over 250)
- urine glucose (positive)
- blood pH (acidic)
- K+ levels (low)
- BUN/creatinine (high)
- bicarb (low, less than 15)
93
treatment for DKA and hhnk
- ensure airway
- IV fluids
- Insulin drip
- dextrose once BS is under 250
- Potassium drip
94
labs for hhnk
- blood glucose (over 600)
- urinalysis (no ketones)
- BUN/creatinine (high)
- Na+ and K+ (low)
- pH (low)
- Bicarb (high, greater than 20)
95
patient teaching for dka/hhnk
- proper insulin dosage
- signs and symptoms of hyperglycemia
- exercise and meal planning
- adequate hydration
96
special considerations dka and hhnk
- symptoms mimic stroke
- increased blood sugar
97
social determinants of dka and hhnk
- financial status
- insurance
- support system
- ability for self care
- homelessness
- transportation
98
nursing diagnosis for dka and hhnk
- ineffective self management of illness
- risk for infection
- risk for fluid volume deficit
- imbalanced nutrition
