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SI Flashcards

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1
Q

4 Key interventions for sepsisw

A

Lab Diagnositics (Serum lactate and blood culture)
IV Fluids (Bolus isotonic fluid through large IV Port)
Antibiotics (Broad spectruum at first then narrow once result of blood culture are back)
Moniter: VS QH x6 hours, then Q4 for 12 hours

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2
Q

How often do you moniter as a sepsis intervention

A

VS QH x6 hours, then Q4 for 12 hours
And SPO2

LOC (GCS)

Urinary output (Catheter) - at least 25/30mL per hour

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3
Q

T1 vs T2 DM

A

T1: NO insulin; Early start (Non mod risk factors)

T2: SOME insulin production; not enough insulin or it’s ineffective

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4
Q

Diagnosis of DM

A

A1C > 6.5%; FBG> 7mmol/L, RBG > 11.1mmol/L

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5
Q

Recognizing the difference bw T1 vs T2

A

T1; Early onset, often w/ polyuria, polydipsia, polyuria cachexia (Starved) appearance

T2: Late onset normally, P neuropathy, fatigue, decreased cisual acuity, slow wound healing

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6
Q

Treatment for T1DM

A

Insulin

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7
Q

Treatment for T2DM

A

First lifestyle changes, second antihyperglycemic third insulin

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8
Q

Prediabetes

A

Disease process trending towards diabetees (IFTG 6.1-6.9mmol/L)

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9
Q

Secondary DM

A

Those with schizo, Cushings, Cystific Fibrosis etc.

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10
Q

Dyslipidemia

A

Abnormal Cholesterol

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11
Q

Most modifiable risk factor for DM

A

Abdom obesity

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12
Q

Type 2 DM is basically caused by an issue with which process

A

Insufficent insulin
Insulin resitance
Tired pancreas
Liver makes too much glucose hormones

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13
Q

ABCDESSS for DM

A

A1C - ideally less than 7%
BP less 130/80
Choleterol : LDL < 2.0 mmol
Drugs to protect the heart (Statin, ACE inhibitors)
Exercise and diet
Screening
Smoking cessation
Self management

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14
Q

Alpha cells produce

A
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15
Q

How to differntiate bw DKA and HSS

A

DKA happens bc NO insulin in the body (Therefore usually DMT1)
- Very easy to recognize
- Very sudden onset
- Breaks down ketones
- Ketones drop blood pH (Metabolic acidosis)
- Fast breathing (tachypnea)
- Fruity Breath
- Polyuria (Body excreting glucose + Blood volume increase)
- Fluid deficit causing polydipsia

HSS pts has SOME insulin - very high BG
- Slowly symptoms get more severe
- Super dehydrated (Water ism oving out of cells into blood to dilute all the glucose)
- No ketones
- No blood pH changes (NO acidosis)

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16
Q

Know hypoglycemic protocols

A
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17
Q

What to do first when you have a DKA pt

A

Stablize ABCs
Call MD
Check V/S
O2 infusion
Fluids
Correct electrolytes
Check BG QH
Check electrolytes

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18
Q

Macrovascular Complications

A

R/t development. of atherosclerosis on large BVs
- Increase risk for thrombus formation etc.

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19
Q

Microvascular complications pathoology

A

Thickining of cap basement membrane, capillaries harden adn ischemia of the rest

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20
Q

Retinopathy ID/treatment

A

Best treatment is prevention
Do regular eye exames BIY

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21
Q

Nephropathy ID/treatment

A

Good glycemic and BP control, annual screening for microalbuminuria

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22
Q

Neuropathy ID/Treatment

A

Sensory: Distal symmetrical neuropaty: Paresthesia, numgess, tingling

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23
Q

Tx for HHS

A

Slow fluid replacement
Insulin bolus
Electorlytes as needed

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24
Q

Chronic Stable Angina

A

Predictable (It’s happened before)
Same precipitating fcators

Relieved when precipitating factor is releived (Nitro or at rest)

Pain lasts 3-5 minutes
(COnstrictive, squeezing, heavy, choking pain)

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25
Unstable Angina
New in onset Occuring at rest or as a worsening pattern Medical Emergency No tissue death, no ECG chnges
26
NSTEMI
Partial thickness blockage MI leads to thrombus formation Occluded vessel = Where muscel will die Less dramatic manifestation than STEMI
27
STEMI
Full thickness blockage MI Same s/s as NSTEMI but faster onset + Progression Usually look shocky/impending doom Goal: Angiogram in 90 minutes (Only at RCH)
28
Heart attack pain
Heaviness, pressure, squeezing
29
Mneumonic if someone has chest pain
Precipiating Quality of pain Radiate Severity (1-10) Tining (Come and go, happening all the time)
30
If there are signs of a heart attack, what is the next step
Call MD Order ECG
31
After MD has been called, ECG has been done, what nexted
Full CV assessment + VS
32
After assessment, what is the last thing to do
Check labs Looking for treponin changes and ECG changes
33
Side effect of beta blocker
Drops BP
34
Heparin does what
Prevents clots from forming
35
Nitro would be effective if the patient was
Relieved of pain
36
Which ECG change is most importnat?
ST elevation
37
You conduct an assessmnt on a patentient who expereienced STEMI 2 previously, what is a VERY concerning sign
Crackles bilaterally in mid lobe of lungs
38
ASA does what
Dissolves thrombus formation, does not remove plaque
39
Troponin panel tells
How much/fast is the heart dying
40
IV NacCL is given to a MI pt
To increase BP
41
Angina vs MI
Chest pain vs heart attack
42
Pathological basic for clinical manifestations
Ischemia causing pain Backflow of blood into lungs causing crackles
43
Why wouldnt nitro or morphine be given for an MI?
If it is an inferior MI it could cause a sudden drop in BP
44
When is PCI indicatied for a STEMI versus "fibrinolysis"
45
Increased SNS in CHF
Increased HR and myocardial contractiltiy Will not last forever, 1st mech, BUT probably LEAST effective
46
Neurohormonal response to CHF
RAAS system Release of aldosterone to retain NA and H2O thus increasing preload Eventually wil lead to systemic congestion and pripheral edema
47
Cardiac decomp response to CHF
Can't maintain adequate cardiac output therefore insuffiecnt perfusion
48
Ventircular remodelling/hypertorphy repsonse to CHF
Larger, less efective pump Increaed muscle mass r/t increased workload Conutnererulatory ANP and BNP released wh4en too much blood volume in the heart
49
Ventricular Dilation response to CHF
Enlargemengt of the heart chambers and elevated rpressue increase force of contraction Overtime decreased elasticity leading to decreased cardiac output
50
L Sided HF
Backup of blood atrium and pilmonary veins Pulmonare yedema, lung crckles, SOB, paroxysmal dsypnea, cough with frothy blood tinged spututm
51
R Sided CHF
Backwards flow of blood into the right atrium and venous circulation JVD, peripheral edema, spleen and liver enlargement
52
Nursing implications for CHF
Diuretics decrease fluid (venous returen Ace inhibs- decrease vasc ressistance Beta blockers- decrease HR and BP Vsodilators - increases O2 supply to heart Digoxin - increaes CO and contractiituy *toxicity
53
Acute Decompensated HF
The worst Wjhen compensatory mechs failm it will manifest and PE often caused by an MI S/S: SOB etc
54
Nursing implicaitons of nutritional therapy
Na resticitoin, Fluid restiriction Report weight gains
55
ACE inhibs end in
-PRIL
56
What causes a TIA
Caused by a microemboli
57
Symptoms of TIA
Same symptoms of normal stroke, temporary altered LOC lasting LESS than 24hr It is different because it resolves on it's own
58
Thrombotic stroke symptoms
Slow and progresseive, mane not have altered LOC in first 24hr
59
Embolic stroke sympomts
Suden, no chance for collateral circulation to form
60
Often emoblic strokes are r/t which condition
Afib
61
Intracerebral brain patho
Bleeding into the brain that occurs during activity Sudden onset
62
Subarachnoid stroke patho and s/s
Intracranial bleeding into the CSF "silent killer" Projectile vomiting Headache N/V
63
Manifestatoins of stroke depend on whether it is hem or ischemic
No, depends on where the stroke occurs
64
R side stroke
Paralyzed on L side Spatial deficiets Spontaneous, impaired judgement Deny/miniize problems
65
L side stroke
Opposite soide stroke Aphasias Impaired R and L discriminations Knowledge of deficits (depressions) Impaired language and math abillities
66
Is a TIA a stroke?
NO
67
A patient experiencing TIAs is scheduled for a carotid endarterectomy. The nurse explains that this procedure is done to:
To prevent a stroke by removing atherosclerotic plaques blocking cerebral blood flow.
68
When monitoring a patient post-hemorrhagic stroke, which of the following identify that the patient is demonstrating signs of increased ICP
a) Increased Systolic Blood Pressure c) Bradycardia d) Bradypnea
69
In the care of a patient with a post-hemorrhagic stroke, which of the following are applicable interventions in cases of increased ICP due to cerebral edema? Select all that
Administration of Mannitol c) Neurological Assessment as per protocol. d) Elevating HOB > 30°
70
Best intervention for acute peripeheral ischemia
Pt to remain lying supine as to not change pressure on thrombus clot
71
Which topic should the nurse include in patient teaching for a patient with a venous stasis ulcer on the left lower leg?
Which topic should the nurse include in patient teaching for a patient with a venous stasis ulcer on the left lower leg?
72
What type of wound dressing promtoes healing in venous stasis ulcers
Clean but moist environment
73
"I can't get my shoes on at the end of the day." Aligns best with what diagosis
PVD
74
A 45-year-old patient is admitted to the hospital complaining of a new "sharp, tearing" pain to her chest. Based on the quality of her pain, what do you initially suspect?
The patient may be having an aortic dissection
75
Role of K+ and why it shifts
Too much glucose Water moves into bloodstream to dilute When cells are dehydrated they die Releasing potassium into bloodstream
76
Why does hyperkalmeia occur in DKA
H+ ions that are in bloodstream from acidosis are moved into cells to try to decrease acidioty, kicking K+ ions into bloodstream Hyperglycemia causes hyperKalemia Tx (Fluids and insulin) can cause hypokalmeia as it moves back into cells Therefore Potassium might need K+ supplements
77
Which blood tests indicate a positive diagnosis of DKA?
a) Blood test positive for beta hydroxybutyrate c) RBG = 20mmol/L d) K+ = 5.8
78
Cheyne stokes resps
Very shallow spread out
78
Most significant risk factor for DMT2
Abdom obesity
79
The nurse is caring for a patient who is hospitalized with diabetes mellitus. Which of the following laboratory test results would provide information related to the patient's past glucose control?
c) glycated hemoglobin
80
Which of the following laboratory results follows the expected pattern accompanying macrovascular disease as a complication of diabetes?
Increased triglyceride levels (low density lipoprotieins
81
HF simply means
Fluid overload
81
Acute decompensated HF interventions
Often caused by an MI. Happens FAST GET HELP AND ECG. CALL A DOCTOR. IV diuretics and fluid restriction. Fix the cause (if NSTEMI or STEMI). 02 therapy prn, high positioning, deep breathing. Manage BP. Interventions should occur RIGHT NOW.
82
the time She has hen a Exerdered that sining fargement ore al patient displaying flect
ventricular hypertrophy c) Cardiac decompensation
82
For which of the following conditions is percutaneous coronary intervention (PCI) most clearly indicated?
Acute MI
82
Your patient has +2 pitting edema to lower calfs, weight gain, and paroxysmal nocturnal dyspnea. How would you classify their HF?
left and right sided
83
Is flushing a symptom of an MI?
No
84
For your preceptorship, you decide to go work for northern health where you work at the only hospital in a 300 km radius. A patient presents to you with crushing and heavy chest pain. An ECG shows that the patient is having a STEMI.
Give pt TNKase (Clot buster)
85
Intreventions for chest pain
PQRST (Hx is most important) Order ECG Full CV assessment w/ VS Blood test (troponins)

NURS232 (27 decks)

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