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NURS300 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

ACID-BASE BALANCE: what is the normal pH range for blood in our arteries?

A

7.35-7.45

below 7.35 is acidic and above 7.45 is alkalotic

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2
Q

ACID-BASE BALANCE: acidosis

A

pH <7.35
high concentration of hydrogen ions
low concentration of bicarbonate

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3
Q

ACID-BASE BALANCE: alkalosis

A

pH >7.45
low concentration of hydrogen ions
high concentration of bicarbonate

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4
Q

ACID-BASE BALANCE: ABG’s normal values

A 
pH= 7.35-7.45
paCO2= 35-45 mm Hg
paO2= 80-100 mm Hg
HCO3= 22*26 meq/L
O2 saturation= > 95%
* pH, paCO2, HCO3 are the main components to acid-base balance
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5
Q

ACID-BASE BALANCE: chemical buffer system

A

one of the main regulators of acid-base balance
normal ratio: 20 bicarbonate: 1 carbonic acid
- CO2 + H2O = H2CO3 = H+ + HCO3
a disturbance in the ratio will cause an acid-base imbalance

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6
Q

ACID-BASE BALANCE: lungs

A

one of the main regulators of acid-base balance
has an immediate affect on acid-base balance
its surface is used to diffuse CO2
they remove CO2 from the body [via hyperventilation] in response to increases in H+ concentration

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7
Q

ACID-BASE BALANCE: kidneys

A

one of the main regulators of acid-base balance
has a slow effect on acid-base balance but it is more powerful and efficient than the lungs
it functions to regulate HCO3

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8
Q

ACID-BASE BALANCE: metabolic acidosis

A

marked by a decrease in pH w/ a HCO3- deficit or H+ excess
causes: CRF, ketoacidosis, diarrhea
s/s: headache, confusion, hyperpnea [r/t lungs compensating for acidic env’t., N/V
tx: correct underlying problem, IV bicarbonate [esp. for pt. w/ diarrhea], observe for hyperkalemia

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9
Q

ACID-BASE BALANCE: why does hyperkalemia occur in metabolic acidosis?

A

when a pt. has this type of acid-base disturbance they have an increased amount of hydrogen atoms inside the body
the body compensates for this high number by pushing some of the atoms into cells, cells which contain K+ in addition to other components
the body is able to get rid of the hydrogen ions from the blood but the result is an increase of K+ in the blood

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10
Q

ACID-BASE BALANCE: metabolic alkalosis

A

marked by an increased pH w/ an excess of HCO3- or loss of H+
causes: vomiting, gastric suction, antacids [b/c of its high bicarbonate content]
s/s: dizziness, irritability, tingling of digits, decrease in RR [r/t body holding on to CO2 to be converted into acid]
tx: reverse underlying disorder, increase Cl- to absorb Na+ resulting in excretion of HCO3-, observe for hypokalemia

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11
Q

ACID-BASE BALANCE: respiratory acidosis

A

marked by an excess of carbonic acid or CO2
causes: cardiac/respiratory arrest, COPD, overdose of sedatives
s/s: mental changes, headache, feeling of fullness in head, dizziness, coma
- all are indicative of high CO2 levels in the brain, or CO2 narcosis
tx: improve ventilation, administer bicarbonate [if pt. has a decreased pH]

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12
Q

ACID-BASE BALANCE: respiratory alkalosis

A

marked by a decrease in carbonic acid or CO2
causes: hyperventilation, aftermath of severe exercise, anxiety
s/s: “hyperventilation syndrome”
- palpitations, light-headedness, sweating, dry mouth, N/V, epigastric pain
tx: eliminate cause, control breathing, breath into closed system

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13
Q

ACID-BASE BALANCE: uncompensated ABG

A

there is no imbalance in either CO2 or bicarbonate
there is an alteration in pH
compensation is going to occur in the body [either via the lungs or the kidneys] but it has not occurred yet

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14
Q

ACID-BASE BALANCE: partially compensated

A

there is an imbalance in either CO2 or bicarbonate
the body has undergone an alteration in pH but the body has not kicked in its compensating mechanisms to balance out this alteration in acid-base

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15
Q

ACID-BASE BALANCE: completely compensated

A

there is an imbalance in either CO2 or bicarbonate

the pH has reached the normal range but there is still an imbalance in the ABG’s

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16
Q

ACID-BASE BALANCE: R-A-M-S

A

r- respiratory
a- alternate direction of arrows
m- metabolic
s- same direction of arrows

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17
Q

ACID-BASE BALANCE: “arrow method”

A

1: look at the pH
- up: alkalosis
- down: acidosis
2: look at CO2 and HCO3
- determine if values are increased or decreased, place arrows
3: determine compensation
- a normal value in the CO2 or HCO3= uncompensated
- no normal values= partially compensated
- a normal pH w/ abnormal CO2 or HCO3= completely compensated
4: determine type of imbalance
- if all [CO2, HCO3, pH] arrows are in the same direction= metabolic imbalance
- if CO2 and HCO3 arrows are opposite of the pH arrow= respiratory imbalance

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18
Q

BLOOD ADMINISTRATION: who is the universal blood donor?

A

O-

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19
Q

BLOOD ADMINISTRATION: who is the universal blood recipient?

A

AB+

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20
Q

BLOOD ADMINISTRATION: Rh factor

A

it is a powerful antigen that is a component of the Rh blood groups and is made up of numerous complex antigens
Rh+ indicates a person has Rh factor on surface of RBC’s
Rh- indicates a person does not have Rh factor on surface of RBC’S
Rh- person may only be transfused w/ Rh- blood to prevent formation of antibodies to Rh+ blood
Rh+ person may be transfused w/ either Rh- or Rh+ blood

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21
Q

BLOOD ADMINISTRATION: blood typing

A

blood test that determines blood type

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22
Q

BLOOD ADMINISTRATION: cross matching

A

blood test that indicates compatibility b/w blood of donor and recipient

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23
Q

BLOOD ADMINISTRATION: pre-transfusion protocol and nursing care

A

administer blood w/ a 19 gauge or greater IV line
establish patency, or set a new IV, ac requesting blood
use sterile technique
NSS/Y-type IV tubing set-up and primed at bedside
- NSS is the only sol’n. that can be given w/ blood
baseline vitals
check orders
double-check pt. ID and blood product ID data w/ RN or MD
administer blood as soon as it arrives to floor [w/i 2-4 hr.’s]
- after that time frame, blood cells will die
minimal handling of bag
vital signs at start of infusion and 15 minutes into infusion [slowly at first]
- stay w/ pt. b/w vitals

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24
Q

BLOOD ADMINISTRATION: post-transfusion protocol and nursing care

A

vitals/necessary assessments
document findings after transfusion
complete any adverse reaction forms, if needed
monitor lab values

25
Q

BLOOD ADMINISTRATION: how does the H/H alter after a blood transfusion?

A

one unit of packed RBC’s raises the Hct by 3% and the Hmg by 1 g/dL

26
Q

BLOOD ADMINISTRATION: acute hemolytic reaction

A

this is the most dangerous of rx.’s that can occur w/ blood administration and can occur even if the pt. is receiving the right blood type
s/s manifest after 10 mL of blood have reached recipient
the antibodies in the recipient’s plasma attach to antigens on transfused RBC leads to RBC destruction
s/s: LOW BACK PAIN, chills, fever, chest tightness, dyspnea, hypotension, acute kidney injury, vascular collapse, cardiac arrest, and death
tx: discontinue blood and KVO, emergency fluids/drugs/dialysis to maintain renal perfusion/B.P., treat shock, COLLECT URINE [tells us the degree of cell destruction occurring], collect blood specimen

27
Q

BLOOD ADMINISTRATION: anaphylactic reaction

A

it is a sensitivity to donor plasma proteins which can occur after only a few mL’s of blood
s/s: anxiety, urticaria, dyspnea, wheezing, bronchospasm, shock, possible cardiac arrest
tx: antihistamines/corticosteroids [for allergic rx], stop infusion [for anaphylactic rx], monitor closely

28
Q

BLOOD ADMINISTRATION: circulatory overload reaction

A

this occurs when blood is administered more rapidly that the circulatory system can not accommodate
s/s: cough, dyspnea, chest tightness, tachycardia, pulmonary edema, HTN, restlessless, JVD
tx: stop infusion and increase HOB, IV NSS to KVO, notify MD

29
Q

BLOOD ADMINISTRATION: sepsis reacction

A

this is due to transfusion of bacterially infected blood components, or when blood sits around too long
s/s: rapid onset chills, high fever N/V/D, marked hypotension, shock
tx: stop blood, NSS to KV, notify MD, send blood bag and tubing to lab [for analysis of organism]

30
Q

BLOOD ADMINISTRATION: TRALI

A

or transfusion-related acute lung injury
it is the possible rx b/w recipient’s leukocytes and donor’s antibodies= pulmonary inflammation and capillary leak= sudden development of non-cardiogenic pulmonary edema
this can occur 2-6 hours pc completion of transfusion
s/s: fever, hypotension, tachypnea, dyspnea, decreased O2 sat., frothy sputum
tx: stop blood, IV KVO, O2. STEROIDS [will decrease the inflammation in the lungs]

31
Q

BLOOD ADMINISTRATION: delayed hemolytic reaction

A

this type of rx is not to be compared to an acute hemolytic rx
this can occur days to week and is usually the least severe of all blood transfusion rx.’s
- despite its lack of emergence, this is an imp. condition to monitor b/c it may be a precursor to a more severe rx in further transfusions
s/s: fever, malaise, gradual decrease in H/H

32
Q

BLOOD ADMINISTRATION: hypocalcemia

A

this occurs due to the preservative used to store blood binds w/ Ca+ to cause a deficiency

33
Q

BLOOD ADMINISTRATION: hyperkalemia

A

all instances have to do w/ cell death

i.e. prolonged storage of blood, cell destruction, improper handling

34
Q

DIABETES MELLITUS: diabetes mellitus

A

it is a multi-system disease r/t abnormal insulin production, impaired insulin utilization or both, which is what determines the type of diabetes a person has
it is the LEADING CAUSE OF HEART DISEASE, cerebral vascular accidents, renal failure, blindness, and non-traumatic limb amputation
theories of causes: genetic, autoimmune, viral, env’t.
- in reality it is multi-factorial
serum glucose is controlled by the emptying rate of the stomach and delivery of nutrient into the small intestines
the pancreas produces and releases insulin in small pulsatile increments during fasting and during increased levels post-prandially to counteract the rise of glucose in the body

35
Q

DIABETES MELLITUS: blood glucose range

A

70-100 mg/dL

36
Q

DIABETES MELLITUS: counter-regulatory hormones

A

glucagon, epinephrine, growth hormone, and cortisol
- all these hormones will raise blood sugar levels, by stimulating glucose production and liver output, and oppose the effects of insulin

37
Q

DIABETES MELLITUS: insulin

A

it is released from the pancreatic beta cells
it promotes transport of glucose from the bloodstream across the cell membrane to the cytoplasm of the cell
- once in the cytoplasm, it can be used for energy
it is impacted by the incretin hormone which is usually only released in response to food intake

38
Q

DIABETES MELLITUS: incretin hormone

A

this is produced in the intestines
it is secreted in response to the presence of food
it increases insulin and decreases glucagon
it slows the rate of gastric emptying which will decrease the possibility of there being spikes in the blood sugar

39
Q

DIABETES MELLITUS: type I diabetes

A

this type is caused by failure of the pancreas due to progressive destruction of its B cells
this category includes 5-10% of diabetics which usually occurs in those < 40 yr.’s of age
causes: genetic [recessive], presence toxins/virus
s/s: Polyuria [increased frequency of urination], Polydipsia [excessive thirst], Polyphagia [excessive hunger], weight loss, diabetic ketoacidosis
tx: exogenous insulin

40
Q

DIABETES MELLITUS: acute onset of type I diabetes

A

the three P’s
polyuria- increased frequency of urination
- the kidneys keep glucose w/i the body, but there is a threshold of how much sugar can be kept inside of the body [250 mg/dL], once that threshold has been exceeded the kidneys begin to filter out the extra amount of glucose
- glucose works ass an osmotic diuretic :. excretion of glucose= excretion of water
polydipsia- excessive thirst
- the polyuria leads to dehydration
- the sx of dehydration is thirst
polyphagia- excessive hunger
- occurs b/c of cellular starvation due to lack of insulin to move glucose w/i the cell which causes starvation

41
Q

DIABETES MELLITUS: prediabetes

A

or impaired glucose tolerance
this occurs when the beta cells in the pancreas become fatigued from overproduction but dysfunction is mild
s/s: fasting blood glucose levels closer to the upper limit [100 mg/dL]
pt.’s w/ IGT are at risk for contracting DM II
tx: delay or prevent by changing lifestyle [weight loss and regular exercise]

42
Q

DIABETES MELLITUS: type II diabetes

A

the type is caused by the body’s insulin resistance
- the pancreas is releasing insulin but it is either not enough or receptors found on insulin are not binding w/ receptors that bring glucose w/i a cell
this category includes 90% of diabetics which usually occurs in Nat. Ame. and Hispanics
causes: obesity, genetics yet it is multi-factorial
s/s: HHNK [hyperosmolar hyperglycemic non-ketotic state, hyperglycemia, hyperinsulinemia, fatigue, 3P’s, recurrent infections, visual changes, prolonged healing times

43
Q

DIABETES MELLITUS: diagnosing diabetes mellitus

A

fasting plasma glucose
- no caloric intake for past 8 hr.’s
- impaired fasting glucose= 100-126 mg/dL
random glucose
- can be drawn at any time
- >180 on 2 occasions, >200 w/ s/s hyperglycemia
OGTT [2-hr. oral glucose tolerance test]
- multiple blood draw over 2 hr.’s pc a glucose load of 75 g
- >140 & 200= diabetes
HbA1c [glycosylated Hg A1c]
- a blood test that measures the amount of glycosylated Hmg in the blood [glucose attached to Hmg protein], remains aattached for 90 days]
- normal range: 4-7%, goal for diabetic pt.: <6.5%
urine
- tests for protein, ketones, glucose
- done b/c 1 of the complications of diabetes is kidney dysfunction
BUN & creatinine
BMI

44
Q

DIABETES MELLITUS: rapid acting insulin

A

i. e. lispro [humalog], aspart [novolog]
onset: 10-30 min.
peak: 30 min.-3 hr.
duration: 3-5 hr.

45
Q

DIABETES MELLITUS: short-acting insulin

A

i. e. regular [humalin R, novolin R]
onset: 30 min.-1 hr.
peak: 2-5 hr.
duration: 5-8 hr.

46
Q

DIABETES MELLITUS: intermediate-acting diabetes

A

i. e. NPH [humalin N, novolin N
onset: 1.5-4 hr.
peak: 4-12 hr.
duration: 12-18 hr.

47
Q

DIABETES MELLITUS: long-acting insulin

A

i.e.. glargine [lantus], detemir [levemir
this can not be mixed w/ any other form of insulin
onset: 0.8 -4 hr.
peak: no pronounced peak
duration: 24+ hr.

48
Q

DIABETES MELLITUS: pancreas, pancreas-kidney transplantation

A

indications: pt.’s w/ type I diabetes
complications: hypo-hyperglycemia, somoyi/dawn effect, DKA [diabetic ketoacidosis], hyperosmolar hyperglycemic state, lipoystrophy [overuse same of injection site -> hyper-atrophy of subq. tissue]

49
Q

DIABETES MELLITUS: hypoglycemia

A

a blood glucose of < 70 mg/dL
s/s: cold skin, nervousness, tremors, tachycardia, palpitations, diaphoresis, slurred speech, unsteady gait, numbness of periphery, ketones (-) and if left untreated, L.O.C., seizures, coma, and death
tx: CONSCIOUS PT. “rule of 15” [give 15 g quick-acting CHO, wait 15 min.’s, re-check blood sugar and if it is still low, give another 15 g, or if it is higher give complex CHO + protein or fat]; UNCONSCIOUS PT. glucagon 1 mg SC or IM, 50% dextrose IVP, rub sugar on gums

50
Q

DIABETES MELLITUS: hyperglycemia

A

a blood glucose of >200 mg/dL
s/s: polyuria, polydipsia, increaased appetite -> decreased appetite, fatigue, blurred vision, headache, N/V, + ketones; if untreated -> DKA [seen in type I] or HHNK [seen in type II]

51
Q

DIABETES MELLITUS: somogyi effect

A

it is a result of decreased blood sugar in the middle of night -> a rebound effect in which an overdose of exogenous insulin induces morning hyperglycemia [via compensatory mechanisms putting out excess glucose]

tx: check blood sugar ~ 3 A.M.
- if the blood sugar is LOW, provide a ac bedtime snack or reduce dose of P.M. insulin

52
Q

DIABETES MELLITUS: dawn phenomenon

A

it is a result of increased blood sugar in the middle of night [caused by excess release of hormones i.e. G.H.]

tx: check blood sugar ~ 3 A.M.
- if the blood sugar is HIGH, provide bedtime snack and increase dose of P.M. insulin

53
Q

DIABETES MELLITUS: DKA

A

or diabetes ketoacidosis
it is a profound deficiency of insulin, w/ blood sugars >300 mg/dL usually seen in type I
s/s: electrolyte imbalances, ketosis, acidosis, dehydration , fruity odor to breath [due to ketones], kussmaul resp.’s [body compensating for the acidity], anorexia, N/V, lethargy, altered mental status; if untreated -> coma and death
tx: IV administration of NSS OF 1/2 NSS [d/o degree of dehydration], regular insulin IV, electrolyte replacement, HCO3- [if pH <7.10], treat underlying cause/complications, place on cardiac monitor [initially to treat hyperkalemia (due to metabolic acidosiss) then hypokalemia (due to insulin administration]

54
Q

DIABETES MELLITUS: HHNK

A

or hyperglycemia hyperosmolar state
a condition where there’s enough production of insulin to prevent DKA [so there are no ketones present] but not enough to prevent osmotic diuresis, hyperglycemia [>400 mg/dL], or ECF depletion and is usually seen in type II
s/s: polyuria, polydepsia [but not polyphagia (cellular starvation) b/c insulin is placing glucose w/i cells but there’s not enough insulin to prevent hyperglycemia] high serum osmolarity -> neurological manifestations [i.e. coma, seizures], stroke like s/s
tx: IV administration of NSS OF 1/2 NSS [d/o degree of dehydration], regular insulin IV, electrolyte replacement, HCO3- [if pH <7.10], treat underlying cause/complication

55
Q

DIABETES MELLITUS: chronic complications associated w/ D.M.

A 
retinopathy/blindness
infections [i.e. gangrene]
kidney disease
cardiovascular disease
neuropathy
arteriosclerosis
myocardial infarctions
valvular disease
cerebral vascular accidents 
erectile dysfunction
cataracts
56
Q

DIABETES MELLITUS: nutritional therapy for pt.’s w/ D.M.

A 
CHO
- minimum of 130 g/day
- include fruits, veggies, whole grains, low-fat milk 
protein
- 15-20% of total kcal
fats
- limit sat. fats to < 7%
alcohol
consumption will interfere w/ the liver's ability to respond to glucagon which will decrease its release of stored glucose
57
Q

DIABETES MELLITUS: exercise for pt.’s w/ D.M.

A

benefits:
- lowers blood glucose by increasing CHO metabolism
- fosters weight reduction and maintenance
- increased insulin sensitivity
- increases high-density lipoprotein levels, decreases LDL
- lowers B.P.
- reduces stress and tension
– exercise can become a stressor [educate pt. to exercise to their capabilities
responsibilities:
- monitor blood sugar ac and pc exercise

58
Q

DIABETES MELLITUS: when does insulin rise/fall?

A

rise in insulin after a meal
- stimulates storage of glucose as glycogen in the liver and muscle [glycogenesis]
- it inhibits conversion of proteins to glucose
- it enhances fat cells to store triglycerides
- it increases protein synthesis
fall in insulin overnight
- released store of glucose from the liver, protein from muscle, and fat from adipose tissue
- GH is released over-night :. insulin is released to balance the blood sugar

NURS300 (4 decks)

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