1
Q
True or False: fat has more water than muscle
A
False
2
Q
As we age, our bodies water content increases or decreases? Why?
A
Decreases - we lose muscle mass and typically gain more fat
3
Q
What are two body changes affected by a loss in water content?
A
- decreased kidney function
- decreased thirst perception
4
Q
What is % split between fluids and solids in your body?
A
60% fluids
40% solids
5
Q
How many L of water in a 70kg man?
A
42L
6
Q
insensible fluid loss
A
cannot be measured - invisible vaporization from lungs and skin
7
Q
describe insensible vs sensible perspiration
A
insensible - evaporation of water from skin before is detected as moisture, passive and continuous way for body to regulate temp
sensible - visible sweat = water + electrolytes (primary cooling method)
8
Q
True or False: sensible losses are measurable whereas insensible losses are immeasurable
A
True
9
Q
Breakdown of fluid loss - where and how much/day?
A
GI tract - 100mL
Lungs - 300mL
Skin - 600mL
Kidneys - 1500mL
10
Q
breakdown of fluid gained - where and how much/day?
A
metabolic water - 200mL
ingested foods - 700mL
ingested liquids - 1600mL
11
Q
Where in our bodies does the exchange of fluid, nutrients, oxygen and waste occur?
A
capillary beds
12
Q
What are the four factors affecting fluid movement between the capillaries and the interstitial space?
A
- capillary hydrostatic pressure
- plasma oncotic pressure
- interstitial hydrostatic pressure
- interstitial oncotic pressure
13
Q
the force of fluid in a compartment pushing against a cell membrane or vessel wall.
A
hydrostatic pressure
14
Q
at the capillaries, the major force that pushes water out of the vascular system and into the interstitial space
A
hydrostatic pressure
15
Q
pulling force exerted by albumin (plasna colloid) in the capillaries
A
plasma oncotic pressure
16
Q
What 2 forces move water out of capillaries? What about into capillaries?
A
Out of capillaries - capillary hydrostatic pressure and interstitial oncotic pressure
Into capillaries - plasma oncotic pressure and interstitial hydrostatic pressure
17
Q
Where is capillary hydrostatic pressure higher than plasma osmotic pressure? What does that lead to?
A
on the arterial end of the capillary (40mmHg CHP; 25 mmHg POP)
Leads to water moving out of cap into IS
18
Q
Where is the plasma oncotic pressure higher than the capillary hydrostatic pressure? What does that lead to?
A
on the venous end (25mmHg POP; 10mmHg CHP)
Leads to water moving back into the blood stream
19
Q
What is edema and what four changes in the body can cause it?
A
Accumulation of fluid in the interstitial space
Occurs if:
1. venous hydrostatic pressure increases
2. plasma oncotic pressure decreases
3. interstitial oncotic pressure increases
4. Obstruction of lymphatic outflow
20
Q
What is the typical pressure, both hydrostatic and oncotic, in the IS?
A
1 mmHg
21
Q
What are 2 examples of things that can raise a patient’s venous hydrostatic pressure?
A
IV fluids, heart failure
22
Q
What can cause plasma oncotic pressure to decrease?
A
Low # of plasma proteins
23
Q
What can raise the interstitial oncotic pressure?
A
accumulation of proteins in the interstitial space
24
Q
What are 6 s/sx of edema?
A
- Peripheral swelling/edema
- high BP
- polyuria
- weight gain
- crackles in lungs
- dyspnea
25
What is involved in assessment for edema?
1. Extremities (in mm)
2. Lungs (crackles) and heart (S3 heart sound)
3. blood pressure
4. Is/Os
5. urine color (lighter) and quantity (more)
6. urine specific gravity (<1.010)
7. labs
26
What is it called when fluid accumulates in non-functional areas between cells?
Third spacing
27
What are causes of third spacing?
1. liver disease
2. damage to BVs - trauma, burns, sepsis
28
What are 3 s/sx of third spacing?
1. hypotension
2. edema
3. decreased urine output
29
What are three treatment options for edema?
1. movement
2. diuretics
3. stopping fluids
30
What is the difference between dehydration and hypovolemia?
dehydration - loss of H2O that is greater than H2O gain
hypovolemia - loss of H2O and sodium
31
Describe how the body works on the kidneys to correct dehydration
1. osmoreceptors in the hypothalamus stimulate thirst and release of anti-diuretic hormone (ADH) from the posterior pituitary gland
2. ADH acts on collecting ducts and distal tubule to allow body to reabsorb more water back into blood stream
32
What are three ways ADH increases BP and water retention by the body?
1. increases water reabsorption in kidneys by insertion of aquaporins in collecting ducts
2. sweat loss slows via sweat glands
3. arterioles constrict
33
ADH is released when blood osmolality increases or decreases?
increases
34
What are three causes of dehydration?
1. increased blood osmolality (more solutes in blood)
2. Excessive fluid loss
3. Low/lack of ADH (vasopressin) production
35
How do we assess for dehydration?
1. Check skin turgor (tenting)
2. Check mucous membranes, should be moist
3. Is/Os (not taking enough in, low output <30mL/hr)
4. urine color (darker) and frequency - oliguria
5. urine specific gravity >1.025
6. labs
36
What are 7 s/sx of dehydration?
1. poor skin turgor
2. dry mucous membranes
3. thirst
4. oliguria
5. hypotension
6. tachycardia
7. weight loss
37
How often do we typically assess output in our patients?
Every 6-8 hours
38
What is the purpose of a diuretic med?
to inhibit water and sodium from being reabsorbed back into the body from the nephron - allows water and Na to remain in the urine
39
What are the three primary functions of the kidney?
1. maintenance of fluid balance
2. maintenance of acid-base balance
3. excretion of metabolic wastes
40
What are three secondary functions of the kidneys?
1. Produces erythropoietin, a hormone that tells the bone marrow to make more RBCs
2. Produces renin - helps control BP and Na/K levels
3. Converts storage form of vitamin D to active form, calcitriol
41
stems from the renal artery and breaks up into capillaries that make up the glomerulus
afferent arterioles
42
Where the glomerulus capillaries unite, which splits into the peritubular capillaries that surround the nephron tubules and empty into the renal vein
efferent arteriole
43
passage of a substance from capillaries into the nephron
tubular secretion
44
Where in the nephron is 25% of filtered sodium reabsorbed and what type of diuretic acts here?
Ascending loop of Henle
45
What hormone works in the DCT and collecting ducts to facilitate reabsorption of water back into the body?
ADH
46
What hormone acts on the DCT to promte reabsorption of sodium and water in exchange for excretion of K?
aldosterone
47
What are the 4 basic renal processes?
1. Filtration
2. Secretion
3. Reabsorption
4. Excretion
48
end diastolic pressure/filling pressure - BV of ventricles during diastole
preload (stretch)
49
pressure the ventricles must work against to open the pulmonary and aortic valves so blood can leave the heart (the peripheral vascular resistance)
afterload (squeeze)
50
True or False: increased preload = increased cardiac workload
False - increased afterload = increased cardiac workload
51
What are three causes of increased preload?
1. hypervolemia
2. regurgitation of heart valves (leaky)
3. heart failure
52
What are two causes of increased afterload?
1. Hypertension
2. Vasoconstriction
53
Loop diuretic:
1. Prototypical drug
2. Site
3. Mechanism
4. Indications
5. AEs
6. NIs
1. Furosemide (Lasix)
2. Ascending loop of Henle
3. Inhibits reabsorption of Na, Cl and H20 and dilates BVs
4. HF (edema), liver disease, kidney disease (even late stage), HTN but not first line of defense
5. hypokalemia, hyperglycemia, dehydration, electrolyte depletion, hypotension, cardiac dysrhythmias
6. monitor daily weight, Is and Os, K+
54
What is the Black Box warning for Furosemide?
Can cause extreme diuresis and electrolyte depletion if too much is given
55
Thiazide diuretics
1. Prototypical drug
2. Site
3. Mechanism
4. Indications
5. AEs
6. NIs
1. Hydrochlorothiazide
2. DCT
3. Inhibits reabsorption of Na, K and Cl
4. mild HF, HTN, liver disease
5. Hypokalemia, hyponatremia, hyperglycemia
6. Encourage K+ foods, monitor BP and electrolytes
56
True or False: aldosterone is secreted by the adrenal gland and has the effect of raising BP and TBV.
True
57
What class of diuretic/drug name is an aldosterone antagonist?
potassium sparing/spironolactone
58
K+ sparing
1. Prototypical drug
2. Site
3. Mechanism
4. Indications
5. AEs
6. NIs
1. Spironolactone
2. DCT and collecting ducts
3. Aldosterone antagonist: Blocks reabsorption of Na and water; retains K+
4. Hypertension; edema related to liver or kidney disease; can be given with loop to counteract loss of K+
5. hyperkalemia
6. Avoid K+ supplements; monitor arrhyhtmias
7.
59
Osmotic diuretics
1. Prototypical drug
2. Site
3. Mechanism
4. Indications
5. AEs
6. NIs
1. Mannitol
2. whole nephron, but mainly PCT and descending loop of Henle
3. osmotic pressure pulls water in renal tubules; inhibits reabsorption of water and solutes - rapid diuresis
4. intracranial pressure i.e. cerebral edema, glaucoma and generalized edema
5. pulmonary congestion - fluid buildup in lungs
6. Rapid infusion = profound diuresis; monitor electrolytes
60
What are 5 nursing responsibilities related to giving diuretics?
1. Monitor I&O, daily weights and VS
2. Assess electrolytes
3. Educate on K+ diet
4. Take in AM
5. Report dizziness or cramps
61
What are 6 effects of diuretics on geriatric patients?
1. recommend taking in AM
2. can cause dizziness or lightheadedness
3. risk of orthostatic hypotension
4. increase risk of constipation and dehydration
5. lower doses if taking more than one diuretic or HTN med
6. more prone to fluid/electrolyte imbalances
62
What are 5 nursing diagnoses associated with diuretics?
1. deficient fluid volume
2. deficient knowledge r/t diuretic therapy
3. risk for falls, r/t hypotension and dizziness associated with AEs
4. risk of injury
5. risk for urge urinary incontinence
63
Which type of diuretic has a low ceiling, meaning giving more past this dose will not help and only increases chance of AE?
thiazide
64
Fast administration of furosemide can lead to what AE?
ototoxicity - tinnitus and hearing loss
65
What are the three steps of hemostasis?
1. vasoconstriction
2. platelet plug formation
3. clotting cascade
66
What happens to form the platelet plug during hemostasis?
1. blood is exposed to collagen which leads to adhesion by platelets
2. activated platelets secrete stimulators that start the clotting cascade (fibrin mesh)
67
What happens to form the fibrin mesh during hemostasis?
Clotting factors (plasma proteins) are activated through proteins in the blood (intrinsic) and out of the blood (extrinsic) which forms a fibrin mesh and stabilizes the clot
68
What activates platelets in hemostasis?
Exposure to collagen
69
What stimulators do platelets secrete?
ADP, thrombin, thromboxane A2 (TXA2) and prostaglandin H2
70
What are four effects that these proteins have on hemostasis?
1. Further vasoconstrict BVs
2. Change shape of platelets and aggregate them
3. Attract more platelets to the site
4. Stimulate clotting cascade
71
T/F: aspirin and clopidogrel (Plavix) are anti-platelets
True
72
What is the mechanism for ASA?
Prevents formation fo TXA2 so platelets do not clump together
73
Indication, Adverse Effects and Drug-Drug interactions for aspirin
I: stroke and MI prophylaxis
AE: GI bleeds, dyspepsia, Reye's Syndrome
Drug-Drug interactions: may increase risk of bleeding with anticoags and other antiplatelet meds
74
What is Reye's Syndrome?
swelling of the brain and liver after a viral illness in children and teens due to giving aspirin
75
What is the mechanism of action for clopidogrel?
Inhibits ADP, which prevents the signal for platelets to aggregate
76
What is the brandname of clopidogrel?
Plavix
77
When is it effective to give clopidogrel with aspirin?
in patients with cardiovascular disease
78
Which anti-platelet med is PO only?
cloplidogrel
79
Indication and AE for clopidogrel
I: prophylaxis of stroke, TIA, MI and post-MI
AE: bleeding, BBW
80
What is the BBW for clopidogrel?
People with certain genetic variations may be poor metabolizers and not get full effect. Genetic testing recommended.
81
Why do you need to stop taking plavix 5-7 days before surgery?
Duration of action is 5 days because it is bound to proteins the blood.
82
What is the normal range for platelets in a CBC?
150,000-400,000/mcL
83
What is thrombocytopenia?
A low number of platelets in the in blood <150,000
84
At what # is antiplatelet therapy possible discontinued?
<80,000
85
What are 4 nursing implications for antiplatelet meds?
1. avoid IM injections
2. discontinue 5-7 days before surgery
3. abruptly stopping med may increase risk of CV events
4. assess CBC (H/H and platelets)
86
What are 4 patient teaching points for anti-platelets?
1. use electric razors and soft toothbrushes
2. prevent injury
3. report signs of bleeding
4. be aware of food and herbal interactions that can increase risk of bleeding
87
What foods and herbs can increase risk of bleeding while on anti-platelets?
chamomile, feverfew, garlic, ginger, gingko, biloba
88
Difference between thrombus and embolus
thrombus - blood clot
embolism - clot on the move
89
What starts the intrinsic pathway of the clotting cascade?
collagen exposure
90
What initiates the extrinsic pathway of the clotting cascade?
tissue factor (aka thromboplastin)
91
Which pathway is the primary initiator of the clotting cascade?
extrinsic
92
What is primary hemostasis and what is secondary hemostasis?
primary = platelet plug
secondary = clotting cascade
93
What are the 3 anticoagulants we learned about in class?
1. rivaroxaban (Xarelto)
2. apixaban (Eliquis)
3. warfarin (Coumadin)
94
What is the MOA for rivaroxaban (Xarelto) and apixaban (Eliquis)?
1. inihibits oral factor Xa in the clotting cascade which prevents new clots from forming
95
True or False: anticoags can break up already formed clots
False: can prevent new clots from forming and existing clots from growing
96
indication, AE, D-D interactions for rivaroxaban (Xarelto) and apixaban (Eliquis)
I: increased risk of thrombolytic events or past events
AE: bleeding
D-D: other anti-coags, anti-platelets
97
What is the BBW for rivaroxaban and apixaban?
increased risk of clots if stopped abruptly
98
Antidote to rivaroxaban and apixaban
andexanet alpha aka Andexxa
99
What is the mechanism of action for warfarin (Coumadin)?
inactivates vitamin K dependent-clotting factors, II, VII, IX and X
100
What effect does warfarin have on a formed clot?
None, it only prevents clot enlargement
101
Indications for warfarin
prophylaxis and treatment of thromboembolic events
102
What is the onset of action for warfarin and how long does it take to reach therapeutic range?
onset: 36-72 hours
Therapeutic after 3-5 days (also takes this long to return to normal coag levels)
103
What bridge therapy drug is typically given with warfarin?
heparin
104
What are D-D interactions for warfarin?
heparin, NSAIDS, anti-platelets
105
What is the BBW, antidote and mointoring required for warfarin?
BBW/AE: bleeding
Antidote: vitamin K
Monitor PT/INR
106
Once vitamin K is given at warfarin overdose antidote, how long does warfarin resistance last?
Up to 7 days
107
What is Prothrombin time (PT)?
the time it takes for a clot to form in the blood
108
What is the International Normalized Ratio?
a standardized system for representing Prothrombin Time
109
What drug requires monitoring of PT/INR?
warfarin
110
What is the normal range for PT and the therapeutic range? How does this translate to INR?
PT:
normal range: 12-15 seconds
therapeutic range: 1.5-2x baseline
INR:
normal range: 0.8-1.2
therapeutic range: >2-3.5
111
True or False: older adults may have a lower INR threshold for bleeding issues
True
112
Foods with vitamin K
asparagus, broccoli, cabbage, cauliflower, kale
113
What are the drug-food interactions for warfarin?
green tea, gingko, garlic, ginger, cranberry juice, chamomile, licorice (May increase risk of bleeding)
NRAD 201D
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