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NURS 232 > midterm #1 > Flashcards

midterm #1 Flashcards

1
Q

systemic inflammatory response system
(SIRS)

A
  • response by a variety including: infection, ischemia, infarction, injury
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2
Q

SIRS is characterized by 2 of the following

A
  • fever
  • edema
  • hypotension
  • tachycardia
  • impaired oxygenation
  • increased WBC count
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3
Q

septic shock

A

a subset of sepsis; greater risk of mortality than w/ sepsis alone
- persistent hypotension -> tissue hypoxia -> tissue death
SBP <90 MAP <65

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4
Q

SIRS criteria

A
  • HR >90 bpm
  • RR >20
  • temp >38 or <36
  • WBC >12.0 or <4.0x10^9/L
  • altered LOC (GCS)
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5
Q

when is an adult at risk for developing SEPSIS?

A

if they have a suspected or confirmed source of infection
symptoms:
- OA, pts w/ chronic conditions
(DM, HF, CKD)
- immunosuppressed pts

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6
Q

SEPSIS
- 4 key interventions

A

1 ) labs & diagnostics
- cultures and lactate
2 ) broad spectrum abx
3 ) IV bolus
4 ) monitoring (VS)

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7
Q

SEPSIS
- monitoring and assessment

A

VS: SpO2 Q1h x6h -> Q4h x12h
GCS Q1h x6hr
monitor urine output -> 25cc/hr
- minimum urine output 25-30 mL/h

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8
Q

SEPSIS
- call MD for…

A

RR <10 or >30
O2 sat <90%
P <40 or >140
systolic BP <90 mmHg
sudden change in LOC
urine output <100mL in 4h
OR
hypotension is not resolving even w/ IV bolus fluids

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9
Q

Type 1 (S/S)

A

polyuria
polydipsia (thirst)
polyphagia
cachexic

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10
Q

Type 1
pathophysiology

A

DM is a metabolic disorder
B-cells regulate insulin
alpha-cells regulate glucagon

↑glucose → ↑insulin & ↓glucagon
↓glucose → ↓insulin & ↑glucagon

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11
Q

pathophysiology of type 1

A

lack of insulin secretion
destruction of B-cells

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12
Q

pathophysiology of type 2

A

insulin resistance
desensitization of B cells to hyperglycemia

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13
Q

diagnosis of type 1 & 2

A

A1C <6.5%
FBG >7mmol/L
RBG >11.1 mmol/L

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14
Q

goals of care of DM

A

1 ) reduce sx
2 ) prevent/ manage acute sx
3 ) delay onset + progression chronic complications
4 ) obtain ideal body weight

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15
Q

ABCDESSS of diabetes care

A

A1C targets (<6.5)
BP targets
Cholesterol targets
Drugs for CV and cardiorenal prot.
Exercise goals and healthy heating
Screening for complication - chronic
Smoking cessation
Self management

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16
Q

sick day management for DM

A

hold SADMANS
Sulfonylureas & other secretagogues
ACE inhibitors
Diuretics, direct renin-rehibitors
Metformin
Angiotensin receptor blockers
Non-steroidal anti-inflammatory drugs
SGLT2 inhibitors

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17
Q

DKA

A

hyperglycemia & dehydration
fats metabolized in absence of insulin -> ketosis & acidosis
1 ) illness, infection (stages of stress)
2 ) inadequate insulin dosage or omission
3 ) undiagnosed T1 or poor self management

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18
Q

S/S of DKA

A

> 14 mmol/L
polyuria, polydipsia
ketones in blood and urine
dehydration, lethargy, weakness, orthostatic hypotension, N/V

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19
Q

HHS

A

enough insulin to prevent DKA but not enough to prevent severe hyperglycemia
- osmotic diuresis, ECF depletion
S/S >34 mmol/L
somnolence, coma, seizures, hemiparesis, aphasia

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20
Q

chronic complications (DM)

A

macro:
CAD (atherosclerosis)
hypertension, stroke, PVD
micro:
retinopathy
neuropathy
neuropathy
- sensory: extremities
- autonomic: internally
infections

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21
Q

CAD: atherosclerosis

A

c-reactive protein CRP inflammation
progression of atherosclerosis
a. fatty streak
b. fibrous plaque
c. complicated lesion

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22
Q

CAD risk factors

A

non-mod:
age
M>F
ethnicity
family hx
genetics
mod:
hypertension
elevated serum lipids
physical inactivity

smoking cessation
meds
DM management
diet

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23
Q

chronic stable angina

A

reversible (temporary) myocardial ischemia = angina
primary reason for insufficient blood flow = atherosclerosis

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24
Q

unstable angina

A

new and onset
occurs at rest
worsening pattern
chest pain isn’t sustained

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25
Q

clinical manifestations of ACS

A

pain
obj: anxiety, fear, restlessness, cool, clammy skin, diaphoretic, pale/grey, tachy/ bradycardia, dysrhythmias, BP change
goals of care:
1 ) ensure they’re resting
2 ) adding O2
3 ) nitroglycerin
4 ) morphine or analgesic for pain

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26
Q

diagnostic study for ACS

A

12-lead ECG, chest x-ray, echo, exercise stress test
serial troponins
fasting lipid profile: HDL to LDL

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27
Q

unstable angina/ NSTEMI

A

ECG
serial troponins
stress test
urgent angiogram/-plasty

28
Q

STEMI

A

ECG
serial troponins
emergent angioplasty and stenting

29
Q

meds for CAD

A

restrict lipoprotein production
“statin” drugs

30
Q

systolic HF -> HFrEF

A

EF<40%
impaired contractile function
increased afterload or hypertension
mechanical abnormalities

inability of heart to pump blood effectively

31
Q

diastolic -> HFpEF

A

LV hypertrophy
myocardial ischemic
valvular disease
cardio myopathy

inability of V to relax and fill during diastole
- decreased SV and CO

32
Q

compensatory mechanism
- increased SNS stimulation

A

1st but least effective
increased epinephrine and NE -> increased HR, myocardial contractility, peripheral vascular constriction

33
Q

compensatory mechanism
- neurohormonal responses

A

activating renin-angiotensin-aldosterone mechanism > vasoconstriction and leads to an increase in aldosterone secretion
-> retention Na + H2O
increase preload
helpful at first but becomes excessive -> systemic venous congestion & peripheral edema

34
Q

compensatory mechanism
- cardiac decompensation

A

compensatory mech. no longer maintain adequate CO + insufficient tissue perfusion results

35
Q

compensatory mechanism
- ventricular remolding

A

cardiac myocytes > large abnormal cells
increased ventricular mass, changes in ventricular shape, impaired contractility bigger but less effective pump

36
Q

compensatory mechanism
- ventricular dilation

A

enlargement of heart chambers due to elevated pressure over time
- decreased elasticity in the muscle fibers leads to decreased CO

37
Q

compensatory mechanism
- ventricular hypertrophy

A

increased muscle mass and cardiac wall thickness due to overwork and stress

38
Q

Lt. sided HF

A

pulmonary edema
severe dyspnea >30
improve LV function by:
1 ) ↓ intravascular volume - diuretics
2 ) ↓venous return (preload) - positioning
3 ) ↓ afterload - managing BP
4 ) improving gas exchange & oxygenation - byPAP
5 ) improving cardiac function - inotropes, infusion, ICU
6 ) reducing anxiety - pain/ perception

O2 administration
self-management teaching
regular exercise & activity /daily weight

39
Q

medications for HF
- diuretics

A

loop, thiazide
- reduces preload by ↓ intravascular pressure volume

40
Q

meds for HF
- ACE inhibitors

A

ramipril and enalapril
1st line therapy
vasodilator (↓BP), ↓ systemic vascular resistance (afterload), CO

41
Q

meds for HF
- B-adrenergic blockers

A

↓ cardiac O2 demand ↓HR + ↓BP

42
Q

meds for HF
- vasodilators

A

nitrates
reduces afterload by dilating peripheral blood vessels
↑ myocardial O2 supply by dilating cardiac blood vessels
1st line meds for managing chest pain

43
Q

meds for HF
- digitalis

A

↑ CO ( ↓HR -> ↑ ventricular filling and contractility)
apical pulse >60

44
Q

nursing diagnosis for HF (I)

A

inadequate CO

45
Q

nursing diagnosis for HF (II)

A

reduced gas exchange

46
Q

strokes incidence + risk factors

A

non-mod:
- age >65
- gender, race, family hx
mod:
- smoking, alcohol
- obesity, inactivity
- high cholesterol
- illicit drug use
- oral contraceptives, HRT
contributes:
- DM
- hypertension
- heart ( afibb.)
- disease/ CAD

47
Q

strokes
- factors that affect blood flow

A
  • systemic BP
  • high BP
  • CO
  • blood viscosity
48
Q

strokes
- etiology + pathophysiology

A

thrombosis, embolism, hemorrhage
= cerebral ischemia

check notes for diagram lol

49
Q

strokes
- clinical manifestations

A

BE FAST
motor function
communication:
- expressive aphasia -> Broca’s
- receptive aphasia
- amnesic aphasia
- global aphasia
affect
intellectual function
spatial-perceptual alterations (rt.)
elimination (incontinence)

50
Q

strokes
- diagnostics

A

CT scan = 1st
lumbar puncture RBC in CSF
lab work:
- CBC, platelets, PT, INR, PTT)
- low INR = high risk for stoke
- blood glucose
- renal + hepatic study
- cholesterol
cardiac assessment
- why? embolic stroke from afibb
- ECG
- chest x-ray
- cardiac markers: troponins
- echocardiographs

51
Q

strokes
- collaborative care

A

drug therapy
- antiplatelet > aspirin
- statins > lower cholesterol
- oral anticoagulants > apixaban & dabigatran
nutritional therapy

52
Q

strokes
- acute nursing management

A

goals:
- preserving life
- prevent further brain damage
- reduce disability
assessment:
- ABCs, VS, LOC, A+O (GCS), PERLLA
- neuro assessment for baseline

53
Q

strokes
- ICP

A

S/S of ICP
- N/V > projectile
- headache
- decreasing GCS
- swelling
- cerebral edema
- hemorrhagic stroke
Cushing’s triad:
- ↑ systolic BP, ↓ P, ↓ RR
opposite of Sepsis
- ↓ BP, ↑P, ↑ RR

54
Q

strokes
- nursing interventions

A

promote rest
reduce visual overstimulation
avoid straining while pooping ↑ ICP
medical induced coma
- reduce brain activity & swelling
meds

55
Q

strokes
- rehab

A

first 3-6 months are where the most relearning happens
baseline

56
Q

PVD
- PAD

A

risk factors
- atherosclerosis
- high BP
- smoking
- high cholesterol
- obesity
- DM
- age

57
Q

PVD
- PAD complications 6 P’s

A

Pain
Pallor
Pulselessness
Paresthesia
Paralysis
Perishingly cold

58
Q

PVD
- PAD complications cont.

A

continuous pain at rest
gangrene
limb threatening disease
elevating foot = pain
S/S:
- intermittent claudication
- dependent rubour
- skin change: cool to touch, pallor, increased cap refill, loss of hair, taut and thin skin
- decreased circulation signs

59
Q

PVD
- PAD interventions

A

femoral popliteal bypass
percutaneous transluminal angioplasty (PTA) of the femoral arteries
endarterectomy
amputation = last resort

60
Q

PVD
- nursing management of PAD

A

nutritional therapy:
- low cholesterol
- high fiber
- low glycemic indexic food (DM)
exercise therapy:
- increase blood flow
risk factor modification:
- control BP, weight control
- smoking cessation
- blood glucose control
- similar to stroke
- diet

61
Q

PVD
- SVT and DVT risk factors

A

blood clots > Virchow’s Triad
- stasis: afibb, valve dysfunction, obesity
- hypercoagulability: cancer, smoking, dehydration, ↑clotting fac.

62
Q

PVD
- clinical characteristics of SVT

A
  • palpable, firm
  • cord-like subq veins w/ surrounding area tender, reddened and warm
  • pain / discomfort around area
63
Q

PVD
- clinical characteristics of DVT

A
  • unilateral leg edema
  • extremity pain
  • sense of fullness in thigh or calf
  • warm skin, erythema, cyanotic
  • temp >38
64
Q

PVD
- nursing management

A

intervention:
early & aggressive mobilization
- 4-6x/day
bedrest pt
- changing positions, dorsiflex feet, rotate ankles Q2-4h
compression stockings
sequential compression devices

65
Q

PVD
- anticoagulants + nursing management

A

warfarin (vit K = antidote)
48-72 hr to work
CHECK INR (high = thinner)

thrombin inhibitor (indirect)
- heparin (HIT)
- LMWH (dataperin/ enoxaparin)

thrombin inhibitor (direct)
- hirudin, orgatroben
- directly inhibit thrombin enzyme

66
Q

PVD
- nursing diagnosis

A

ineffective tissue perfusion
1 ) walking, feet down, avoid tight socks/shoes, protective clothing
impaired skin integrity
1 ) turning & repositioning
2 ) prevent damage & injury (roomy shoes)
3 ) check H2O w/ fingers
Acute pain
1 ) effective tissue perfusion: walk
2 ) MEDS
activity tolerance
1 ) staggering exercise program
ineffective therapeutic regimen Mgmt.
1 ) education
2 ) do they know/ understand ??
3 ) can they do it themselves?
- open the bottle

NURS 232 (3 decks)

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