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Quiz 5 Flashcards

Anticoagulants

1
Q

Role of Thrombin and the development of the clot

A
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2
Q

General diffference between intrinsic/extrinsic pathway

A

Online: The main difference between the intrinsic and extrinsic pathways in blood coagulation lies in their initiation:
- the intrinsic pathway is activated by factors within the blood itself,
- while the extrinsic pathway is activated by tissue factor released from damaged tissues outside the blood.

Both pathways ultimately converge on the common pathway, where factor X is activated, leading to clot formation

aPTT- intrinsic
PT- Extrinsic

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3
Q

How does ASA work as an anti-platelet?

A

-Decreases aggregation and formation of the platelet clot (Blocks Cox-1)
-Inhibits prostaglandin production

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4
Q

Asprin (ASA) Indications (who needs it)

A

CAD/CVA/PAD
prevention
* Maintains AV grafts
* Post MI
* Post Stent placement
* Other vascular disease

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5
Q

Aspirin Drug interactions

A

Oral anticoagulants, Heparin,
Methotrexate, oral DM
meds, and Insulin – can
increase the risk of toxicity
when taken with ASA
* Steroids may decrease the
ASA effect and cause ulcers
* ACE and Beta Blockers
* NSAIDS

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6
Q

How is Clopidogrel a different type of medication? Who takes this medication?

A

Also an anti-platelet but it INHIBITS platelet aggregation via P2Y12

-It keeps platelets in your blood from attaching to each other and making blood clots

-Used for post stent/Post MI/Post stroke patients

Starts to work in 24-48
hours but not see full effect
for 4-6 days

*Used for patients who need the combined therapy of asparin

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7
Q

Nursing considerations for pt on anti-platelets
Who should not be on anti-platelets

A

Should be stopped at least 2-5 days before surgery
Must take everyday unless told otherwise
Only provider can stop medication

DO NOT GIVE-
* Known bleeding disorder
* * Active bleeding
* * Closed head injuries
* * CVA until prove no bleed
* * Pregnancy (risk benefit)
* * Lactation

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8
Q

Who can discontinue anti-platelet therapy?

A

A Qualified healthcare provider

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9
Q

How does warfarin work?

A

Inhibits the production of Vit K

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10
Q

Who might take warfarin?/ Why does warfarin have so many drug interactions?

A

Used in atrial fibrillation, Valvular heart disease, CVA, DVT and PE prevention, post joint replacement (People at risk of blood clot)
- Due to the drug being highly protein-bound

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11
Q

What is the lab test which monitors warfarin therapy and what is the desired level?

A

PT/INR
Want INR at 2 to 3
For mechanical heart valve = 2.5 to 3.5

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12
Q

When is Warfarin started and administered? How many days until therapeutic levels are
achieved?

A

Takes 4-7 days for take effect

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13
Q

What is the antidote for warfarin? List all potential options

A

Phytonadione (Vitamin K)

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14
Q

Nursing considerations for warfarin? How long does it take to clear the body?

A

-Takes 4-7 days to take effect
-Should be taken in the evening
-Requires frequent lab monitoring (PT/INR)
-Narrow therapeutic range
-Works slowely compared to heparin

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15
Q

How do Factor Xa inhibitors work? (DOAC)

A

-Prevent factor Xs from changing prothrombin to thrombin. They bind directly to factor Xa

Common factor Xa inhibitors include rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Savaysa).

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16
Q

Why is dabigatran (pradaxa) different from the others?
What are special nursing considerations (patient teaching) for dabigatran?

A

it directly blocks thrombin, the enzyme responsible for clot formation, whereas the others are direct factor Xa inhibitors.

Twice daily dosing

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17
Q

Dabigatran (pradaxa):
Antidote?
Which patient group should take with caution/have reduced dose?

A

-Praxbind
-Must reduce in renal failure

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18
Q

Common Coagulation tests

A

PTT (prothrombin time)
International Normalized Ratio (INR)
Activated partial thromboplastin time (aPTT)

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19
Q

Why is this drug class (Factor Xa drugs) different than warfarin?
Which patients should NOT receive this medication?

Ex. Eliquis/Xarelto

A

-Do not take with Clopidogrel
-Must reduce in renal failure

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20
Q

What is the antidote for the DOAC class of medications?
Which of these medications are once daily dosing and which are twice daily dosing?

A

Andexanet (For eliquis/xarelto)
Praxbind (for pradaxa)

Pradaxa-is twice daily

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21
Q

DOAC patient education

A

Patient Education:
* Meds must stay in original
bottle, don’t place in pill box
* Pills should not be crushed
* Don’t stop taking for GI
issues, unless there is black,
tarry stools
* Hold before having surgery
* Don’t take with Clopidogrel
* Watch for drug interactions
* Must reduce dose in renal
failure
* Caution in abrupt stopping
* Antidote: Praxbind
(idarucizumab) is for
Dabigatran only

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22
Q

Why might warfarin be a better choice for some patients than the DOAC class?

A

Less expensive

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23
Q

How does heparin work?

A

Anti-thrombin inhibitor- interferes with conversion of thrombin to prothrombin

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24
Q

How long does heparin take to work and how long does it take to clear the body after it is turned off?

A

online: Heparin works quickly, with IV heparin taking effect within minutes, and subcutaneous heparin within 1-2 hours. The anticoagulant effect of therapeutic doses of heparin is mostly eliminated within 3-4 hours after stopping continuous IV administration, with a half-life of about 60-90 minutes.

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25
What lab value is used to monitor heparin therapy?
Monitored by aPTT usually 1.5-2.5 times baseline control Pt should normalize 2-6 hours after heparin is stopped
26
How is heparin dosed? Antidote?
Starts by administering an IV bolus dose, followed by continuous dripL Bolus usually 5000units Followed by 1000-1300units/hour Or 80u/kg (can be less) bolus and then 18u/kg/hour Antidote: Protamine sulfate | ALWAYS CHECK DOSE WITH ANOTHER NURSE
27
A patients’ aPTT after 6 hour is 45 seconds. What action should the nurse take?
-Measures time is takes for plsma to clot when exposed to a reagent -30-45 seconds -Intrinsic pathway -A prolonged APTT can be an indicator of bleeding disorders like hemophilia or von Willebrand disease. -The APTT test is commonly used to monitor the effectiveness of heparin, a blood thinner, and ensure that the patient's blood clotting time is within the therapeutic range.
28
What is the difference between unfractionated heparin and low molecular weight heparin? Why would someone receieve one over the other?
* Inhibit thrombus and clot formation by blocking factors Xa * Routes: SQ * Should not be mixed with other medications; multiple interactions * Safe to use during pregnancy, but is considered 2nd line therapy * Adverse Effects: Bleeding, Heparin-Induced Thrombocytopenia, Hypersensitivity Narrow therapeutic range : Requires lab monitoring Want PTT in therapeutic range= 46-70 If aPTT > 70, call the physician LOW MOLECULAR WEIGHT HEPARIN: Commonly used for DVT prophylaxis, MIs Drugs: Enoxaparin (Lovenox) Dalteparin (Fragmin) Route: SQ only Administer 2 inches from the umbilicus; No rubbing/No aspiration Okay to use during pregnancy, considered 1st line Does not require lab monitoring
29
How long does it take for enoxaparin (lovanox) to reach a steady state?
Online - about 2 days
30
anticoagulant Alternatives for Heparin-induced thrombocytopenia
Argatroban Lepirudin
31
What are special considerations which need to be taken when administering enoxaparin?
inject into "love handles" Alternate between sites Do not inject air bubble prior to injection Do Not just injection site after
32
why would tPA be administerd? What are the criteria or contraindications which must be met before administration?
Stroke! Only given IF within 3-4 hours of onset of symptoms. Only give through a peripheral IV, not a central line (so you can compress the site) NO injections No SQ, or IM No ABGs (blood gas) Monitor vital signs and neurologic status If possible CVA, must do head CT before administering Place patient on bleeding precautions
33
Contraindication for tPA
Uncontrolled BP (185/110) * History of Hemorrhagic Stroke, aneurysm, or AV malformations * Heparin in the last 48 hours * Current oral anticoagulant * DOAC use * Surgery within 3 months * Platelet count <100,000
34
Urinary Tract Infections- general info
Second most common type of infection Occurs in Women more than males Accounts for About 50% of all hospital-acquired infections
34
WHAT SHOULD THE NURSE DO IF A PATIENT TAKES AN EXTRA DOSE OF ANY OF THE ANTI-COAGULANTS?
Check for signs of bleeding vital signs labs
35
Common cause of hospital acquired infection?
Accounts for about 50% of all hospital acquired infections Catheter Acquired UTI (CAUTI)
36
UTI Classifications
Lower - Bladder and structures below the bladder Upper -Kidneys -Ureters
37
Example of Lower Urinary tracts infection
Cystitis
38
Example of Upper Urinary tracts infection
Pyelonephritis
39
Most uncomplicated Lower UTI are caused by which bacteria? Where does it usually enter through?
E. Coli? Urethra
40
Washout phenomenon
occurs when urine washes out the bacteria in the urethra during urination
41
Complicated UTI bacteria
Staphylococcus saprophyticus Klebsiella pneumoniae Proteus mirablis Pseudomonas species
42
Causes of UTI: Obstruction
Anatomic: - Stones, BPH, Pregnancy Functional: - Infrequent voiding etc.
43
Causes of UTI: Reflux
Ureterovesical Reflux: -Cough or squatting can cause urine to move back from the bladder into the urethra and then back into the bladder Vesicoureteral Reflex: - Occurs at the level of the bladder and ureter
44
Who is at risk of UTI
Sexually active women Post menopausal women Pregnancy Bladder cancer Renal stones (Calculi) Men with prostate abnormalities (no circumsicion) Anal intercourse Older adults Others at Risk Catherization Instrumentation Diabetes Use of antibiotics
45
All UTI in men are considered..?
Complicated
46
Clincal manifestations of Uncomplicated UTI: (5)
Dysuria Frequency Urgency Hematuria Suprapubic pain
47
Clincal manifestations of complicated UTI:
May be asymptomatic or present with septic shock Fever, chills, nausea, vomiting Back pain/flank pain
48
Urosepsis
spread of infection from urinary tract to bloodstream
49
Older adult sympomts of UTI:
Symptoms can vary: Incontinence Foul smelling concentrated urine Fatigue Confusion Dementia Hallucinations
50
UTI In Children:
After 3 months old, more prevalent in girls. -Frequently involved upper urinary tract
51
Interstitial Cycstitis
* Pain (Pelvic/Perineal) * Urgency * Feeling of bladder fullness/pressure * Women>Men * Exact cause unknown Rule out: Infection Endometriosis Urodynamic Testing
52
Urinary Testing: Specific Gravity
What: Amount of solutes in urine Normal: No true normal but approximately 1.010 Considerations: Extremes of either side can indicate pathology
53
Urinary Testing: pH
What: Acid-base Normal: 6.5-7 in the AM 7.5-8 in the PM Considerations: Can be affected by food etc
54
Urinary Testing: WBCS (leukocytes)
What: Enzyme given off by WBC Normal: Negative *Present in all patients with UTIS
55
Urinary Testing: Nitrites
What: Enzyme released by Enterobacteriaceae Normal: Negative *Can be neagtive and still have UTI
56
Urinary Testing: Blood
What: Can be micro and macrocytic Normal: Negative *Can see in trauma, hemolysis, UTI, malignancy
57
Urinary Testing: Protein
What: Measuring Albumin Normal: Netagive Considerations: Renal disease, Pregnancy, Inflammation
58
Urinary Testing: Glucose
What: Renal threshold to eliminate excess glucose Normal: Negative
59
Urinary Testing: Ketones
What: Measures metabolites of fat metabolism Normal: Negative *Insulin insufficiency, starvation, vomiting
60
Urinary Testing: Biliruben
Normal: Negative *Liver disease obstruction
61
Urinary Testing: Urobilinogen
Normal: Negative *Liver disease, hemolysis, mono, cirrhosis
62
Urinary Testing: Casts
What: Coagulated protein by kidney cells Normal: Negative Hyaline (0-5) in healthy people ceullar not normal *Hyaline are clear. Can have cellular RBC or WBC
63
Urinary Testing: Cystals
What: Wastes solutes. Based on pH and urine temp Normal: None but some are ok
64
Management of UTIs: General
Pharmacologic thearpy Pt education Acute UTI: 3-7 day course of antibiotic, if uncomplicated Chronic or relapse UTI: Up to 2 week course of antibiotics
65
Management of UTI's: Medications
Cephalexin Ciprofloxacin Levofloxacin Ampicillin Amoxicillin Bactrim
66
UTI medications: Fluoroquinolones
(Ciprofloxacin or Levofloxacin) are not routinely recommended due to their side effects and increasing bacterial resistance
67
Patient education: UTI
Drink plenty of fluids daily Void before and after sexual intercourse Avoid douching Take Antibiotics as prescribed Avoid tight/restrictive clothing Shower, don’t bath Personal Hygiene
68
Normal renal functions (9)
* Excretion of waste prodcts and urine * Regulation of BP * RBC production- erythropoietin * Breakdown of drugs * Metabolism of hormones * Regulation of Electrolytes and acid-base balance * Synthesis of Vit D * Fluid Balance * Balance of pH of blood stream
69
Nephrons
Adults tend to lose approximately 10% of their nephrons for each decade beginning at 40 ## Footnote by age 70- nephrons will be down 30mL/min=95mL/min
70
Glomerular Filtration | how much /day
GFR: average adult 125mL/minute or 180L/day
71
How does the kidney conccentrate urine (3 factors)
* Oslomarity of interstitial fluis * Anti diuretic hormone * Action of ADH on the cells in the collecting tubules of the kidney
72
Elimination functions of the kidney
Removal of: - Water - waste products - excess electrolytes - unwanted substances
73
Renal Disorder Categories (3)
Prerenal, Intrarenal, Post renal
74
Prerenal disorders | What is it
Decrease in blood flow and perfusion
75
Intrarenal disorders | what is it
Secondary to actual injuries to the kidney itself
76
Post Renal disorders | what is it
Related to the obstruction of urine outflow from the kidneys
77
Pre-renal disorders
* Hypotension * Shock * Diarrhea/Vomiting (severe) * Bleeding/hemorrhage * Diuretics * diabetes insipidis * Burns * Heart Failure/MI * Cirrhosis * Sepsis
78
Intra-renal disorders
* Vasculitis * Venous Occlusion * Pre-eclampsia * Acute Tubular Necrosis * Multiple Myeloma * Hypercalcemia * IV contact dyes * Pyelonephritis * Certain meds: NSAIDS, ACE inhibitors, Heavy metals * Transfusion Reaction * Rhabdomyolysis
79
Post-renal disorders
* Renal Calculi * Enlarged prostate * cancer * diabetes * Functinal obstruction due to drugs * blood clot * Trauma
80
Acute Tubular Necrosis (ATN)
Most common cause of acute kidney injury Damage to renal tubes causing cells to slough into the tubular lumen and lumen becomes blocked -Decrased urine formation Causes: -Post-ischemia (all causes of severe pre-renal disease) -Nephrotoxic *Permanent injury if not reversed | INTRA renal disorder
81
Acute Tubular Necrosis Labs: Creatinine
Creatinine clearance (100-150 cc/min): Less than 5-10cc/min
82
Acute Tubular Necrosis Labs: Urine Sodium
Urine sodium (10-20 meQ/L): >20 med/L
83
Acute Tubular Necrosis Labs: Specific Gravity
Normal: (1.005-1.025) ATN: 1.010 fixed
84
Acute Tubular Necrosis Labs: Urine osmolality
Normal: (200-1200) ATN: Osmotic = 300mOM
85
Acute Tubular Necrosis Labs: Serum BUN/creatinine
(10-20) 10:1 Fixed
86
Acute Tubular Necrosis Labs: Urinalysis
Red/white cells, casts, epithelial cells
87
88
Azotemia Labs: Creatinine
Normal: (100-150( Azo: 15-80cc
89
Azotemia Labs: Urine sodium
>10 meq/L | normal: 10-20
90
Azotemia Labs: Specific gravity
>1.015
91
Azotemia Labs: Urine osmolality
Concentrated >450 | Normal: 200-1200
92
Azotemia Labs: Serum BUN/Creatinine
> 15:1 | 10-20
93
Azotemia Labs: Urinalysis
Normal
94
Phases of Acute Kidney Injury (4)
Initial Oliguria Late Diuretic Recovery
95
AKI: Initial Onset
0-2 days Initial Insult to point when BUN/Crt rise and/or Urine output drops
96
AKI: Oliguria phase
1-2 days to 6-8 weeks Drop in GFR, retention of urea, Potassium, sulfate and creatinine. Decrease Urine output and edema
97
AKI: Late Diuretic phase
2-8 days Begins with a slow, gradual increase in urine output, then high output
98
AKI: Recovery phase
2-4 months Labs return to normal
99
Clinical manifestation/Diagnosis of AKI
-Pt will have oliguria and fluid overload -Build up of nitrogenous waste --Uremia, metabolic acidosis, thrombocytopenia -Edema Labs: Urinalysis Serum electrolytes Bun/crt ABG CBC -Imaging -Renal Biopsy
100
Treatment of AKI
- Return to normal chemical balance, prevent futher complications, restore renal function *Fluid administration diuretics Monitor electrolytes Cardiac monitoring Hemodialysis
101
Indications for Dialysis
Volume overload K+ > 6 meQ/L Metabolic acidosis/serum HC03 >0.15 BUN > 120 mg/dL
102
Chronic Kidney Disease (CKD)
An irreversible, progressive disease Often Asymptomatic initially until disease is far advanced * Kidney damage or a GFR < 60 mL/min/1.73 m2 for 3 months or longer. * Numerous Causes: * *Hypertension, *Diabetes, obesity, glomerulonephritis, SLE, polycystic kidney disease * Loss of functioning nephrons, progressive deterioration of glomerular filtration, ability of tubules to reabsorb, endocrine functions. * As nephrons are destroyed remaining hypertrophy to take on the work.
103
Renal Dysfunction stages (1-5)
Stages 1/2: Often asymptomatic + crt normal -Compensation will occur GFR: normal >90 Stage 3: Decreased function <50% nephrons working. -Lab changes -No longer able to compensate GFR- 30-59 Stage 4: -Renal insufficiency is evident -nephrons dead -Diet restriction of proteins -GFR 15-29 Stage 5: Dialysis/transplant GFR: <15
104
Clinical manifestations of CKD
-Buildup of nitrogenous waste: Encephalopathy/Anemia/Thrombocytopenia -Hyperkalemia - hyPOcalcemia (VitD not activated)....leads to hyperparathyroidism/Bone breakdown - Normochromic/normocytic anemia - low albumin - hyPERphostphatemia
105
Treatment of CKD
Treat underlying cause Monitor labs Smoking cessation Manage hyperglycemia, if diabetic Manage anemia Exercise program Decrease sodium Avoid alcohol Dialysis Kidney transplant
106
Glomerulonephritis | symptoms/complications
Inflammation of the glomerular capillaries Causes about 25-30% of all ESRD cases Can be acute or chronic Most common cause of acute is post-streptococcal glomerulonephritis *Symptoms:* Pink or cola-colored urine, proteinuria, hematuria, hypertension, fluid retention/edema, decrease urine, nausea and vomiting, muscle cramps, fatigue *Complications*: Accumulation of wastes or toxins in the bloodstream., Poor regulation of essential minerals and nutrients, Loss of red blood cells, Loss of blood proteins.
107
Pathology of Glomerulonephritis
Begins with an antigen-antibody reaction Antigen-antibody complex damages structures of the glomeruli which causes nephron dysfunction: * Decreased filtration of blood * Decreased urine production * Hypervolemia * Hypertension
108
Clinical manifestations of Glomerulonephritis
-Oliguria often the first symptom Followed by hematuria, proteinuria -Cola colored urine * Edema often of face and hands * HTN * Elevated anti-strep antibodies(ASO) * Increased Creatinine * Decreased serum albumin * Treat the cause and full recovery is expected.
109
Treatment of Glomerulonephritis ## Footnote Goal of treatment/Medications/Diet modifications/Complication
Goal of treatment is to: Increase urine output Decrease urinary protein Medications: Corticosteroids Antibiotics, if needed Antihypertensives, if needed Antipyretics Diet modifications: Low sodium Low protein Monitor for complications: HTN encephalopathy Heart failure Pulmonary edema
110
Nephrotic Syndrome
Damage to the glomerulus -The filter is damaged and things which should stay in are able to leak out through the pores which become bigger due to the damage -Leads to increased permeability of proteins and other substances in the blood -Diabetic nephropathy most common type but can be due to other causes such as: Lupus or amyloidosis ( top 3 causes account for 90% of all cases) --Also vasculitis, allergies, preeclampsia, HTN, and other infections
111
Clinical manifestations/Diagnosis Nephrotic syndrome
Albuminuria/Proteinuria EDEMA Labs: -Urinalysis (proteinuria/hematuria) -Elevated BUN/CRT -Low serum albumin -Tests of lupus/hep B/C -24 hours urine *renal US and Renal Biopsy
112
Treatment for nephrotic syndrome ## Footnote Diet/Vaccines/Complications
Monitor diet: Low sodium Protein Adequate fluid intake, but avoid fluid overload Vaccines – pneumococcal and influenza ACE inhibitor or ARB Monitor for complications: Hyperlipidemia Thromboembolism
113
Nephritic Syndrome
Produces inflammatory response Related to: -immune complexes and antibody-antigen complexes lodge in capillary. --Immune response develops against the antigens -Inflammatory processes occlude glomerular capillary lumen & damage capillary wall. -Damage allows RBCs to escape into urine. -Alterations due to decrease in GFR, fluid retention and nitrogen waste accumulation. -Also proteinuria, oliguria.
114
Post strep Glomerular Nephritis Vs Nephrotic syndrome
*Post strep G.NephRITIS* Typically seen ages 4-7 Onset: 10-14 days after strep infection Anti-strep titer + Urine- cola colored Heamturia-massive Proteinuria-minimal Hypertension Edema-moderate Hyperkalemia Elevated BUN *NephPHROTIC syndrome* Ages 2-3 years (males) Anti-strep titer NEG Urine- clear Hematuria - microscopic Pretineuria- Massive BP- normal or slightly decreased Hypoalbuminemia Edema-massive K+ normal BUN- normal Hyperlipidemia
115
Diabetes and hypertension: Renal
Diabetes -Thickening of basement membrane -Dysfunction of glomerular podocytes -Remember they cover the urinary side of the glomerular basement membrane. -Inflammation (T cells and macrophages) into glomerulus Hypertension -Vascular changes -Glomerular changes -Damage to basement membrane (podocytes) - damaged -Allows plasma proteins to escape
116
Impact NSAIDS on renal function
* NSAIDs work by inhibiting prostaglandins * Renal prostaglandins protect against decrease renal flow * Prostaglandin inhibition can depress already decreased renal blood flow * Leads to reduction in renal perfusion and decreased GFR
117
Those at risk for NSAID issues: Renal
* Dehydration * Arterial volume depletion due to heart failure, nephrotic syndrome or cirrhosis * Chronic kidney disease (CKD), especially stage 3 or worse (estimated GFR <60 mL/min * Volume depletion from aggressive diuresis, vomiting, or diarrhea * Older age * Severe hypercalcemia with associated renal arteriolar vasoconstriction
118
NSAIDS IN healthy people: renal
* In extreme exercise especially in heat the skin and muscle complete for blood flow * Takes away from the pancreas, GI, liver and kidneys * When exercising at max GRF can be reduced by 30-60% * Add dehydration, heat stress * Add chronic NSAID use * Avoid NSAID use outside of recommended doses * Avoid in those with HTN, HF, DM, and Metabolic syndrome * Avoid in states of dehydration * Increase fluids in athletes. * As anti-inflammatory use for shortest time and try to use acetaminophen as well

NUR 516 (24 decks)

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