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Nursing school level 4 > Final deck #2 > Flashcards

Final deck #2 Flashcards

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1
Q

COPD characterized by

A

airflow limitation, breathlessness, and exacerbation.

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2
Q

COPD disease process is based mainly off of what concept

A

inflammation

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3
Q

process of COPD

A

inhaling noxious particles which releases inflammatory mediators. this causes damage to the tissue of the lungs and an increase in mucus. The lungs become more and more injured which leads to structural remodeling and an increase in scar tissue. the result is either pulmonary fibrosis or damage/destruction (emphysema)

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4
Q

emphysema

A

damaged alveoli in which they trap air

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5
Q

characteristic of chronic bronchitis

A

chronic, productive cough for more than 3 months over consecutive 2 years. it is inflammation of bronchi r/t chronic exposure

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6
Q

what labs do you want for COPD

A

WBC and sputum cultures- PNA or infection
Hgb/Hct - may be increased due to chronic low level of O2
ABGs - hypoxic
electrolytes - Na/K, BUN, glucose
trops - if MI caused acute exacerbation
BNP - if HF caused acute exacerbation
D-dimer - if PE caused acute exacerbation

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7
Q

COPD diagnostics for acute exacerbation

A

CXR - to determine PNA
echocardiogram - determines cor pulmonale
12 lead ECG - if from an MI
spiral CT - if from PE

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8
Q

COPD diagnostics for chronic phase

A

pulmonary function test - determines COPD progression

echocardiogram - determines cor pulmonale

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9
Q

ABG findings in exacerbation of COPD`

A

low PaO2 and SaO2
high PaCO2
normal or low PH
high HCO3

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10
Q

COPD meds for maintenance

A

anticholinergic agents (ipratropium)- long acting, steroid with LABA (Advair or Symbicort)

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11
Q

COPD meds for acute exacerbation

A

short acting beta 2 agonist (albuterol), antibiotic, steroid

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12
Q

caution with beta blockers with COPD pts, why?

A

it can cause the bronchioles to constrict

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13
Q

pharmacological support for smoking cessation

A

Nicotine supplements, bupropion (wellbutrin, zyban), varenicline (chantix)

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14
Q

pulmonary hypertension

A

Chronic progressive disease of small pulmonary arteries (PA) leading to increase pressure in the arteries and vascular remodeling. This can lead to backflow into the right ventricle which puts extra work on it and can lead to failure.

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15
Q

1 cause of pulmonary hypertension

A

COPD

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16
Q

diagnostic studies for pulmonary HTN

A

right cardiac Cath, 12 lead ECG, CT scan

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17
Q

clinical manifestations of cor pulmonale

A

Symptoms are subtle and masked by symptoms of the pulmonary condition, but should see exertional dyspnea, tachypnea, cough, fatigue
Also: RV hypertrophy, increased intensity of S2, chronic hypoxemia

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18
Q

meds for PH and cor pulmonale

A

calcium channel blocker, vasodilators, endothelial receptor antagonist, viagra, oxygen, diuretics, anticoagulants, inotropic agents

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19
Q

endothelial receptor antagonist

A

↓ PA pressures, ↑ cardiac output

for PH and cor pulmonale

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20
Q

Virchow Triad for PE

A

Venous stasis
Vascular endothelium injury
Hypercoagulability

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21
Q

labs for pulmonary embolism

A

ABGs - oxygenation
D-Dimer - clotting in the body
BNP - cardiac ventricular stretch
troponin - how big it is

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22
Q

Massive PE

A

Acute PE w/ sustained SPB <90 for greater than 15 mins
Need for inotropes (no other reason)
Signs of shock
10% of these patients die within the first hour

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23
Q

Submassive PE

A

Acute PE w/ RV dysfunction

Myocardial necrosis present

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24
Q

Thrombolytics

A

Fibrolytics (AKA Alteplase or tPA)

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25
Q

Vitamin-K antagonist

A

warfarin - is main therapy with PE bridged w/ parenteral anti-coagulants but needs frequent monitoring of INR

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26
Q

low molecular weight heparin example

A

enoxaparin sodium - no lab needed

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27
Q

Heparin lab

A

PTT (goal is 50-90)

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28
Q

pneumothorax

A

air in the pleural space resulting in partial collapse of lung - pressure goes from negative to positive

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29
Q

clinical manifestations of large pneumothorax

A

absent breath sounds. Respiratory Distress (shallow, rapid resps, dyspnea, air hunger, O2 desaturation); Chest pain, Cough with or without hemoptysis

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30
Q

spontaneous pneumo can happen in

A

also called a closed pnuemo can occur after rupture of blebs in COPD pt or in tall/thin male with marphans

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31
Q

Tension Pneumothorax

A

Rapid accumulation of air in pleural space without the ability to escape. (medical emergency) - respiratory and circulatory collapse

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32
Q

how much blood is too much during a hemothorax

A

250-300 ml of blood (unit of blood)

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33
Q

flail chest

A

life-threatening medical condition that occurs when a segment of the rib cage breaks due to trauma and becomes detached from the rest of the chest wall.

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34
Q

sign of flail chest

A

paradoxical movement - breathing reverses this pattern, which means that during inspiration, the chest contracts, and during expiration, it expands.

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35
Q

s/s of cardiac tamponade

A

muffled, distant heart tones, decrease BP, jugular vein distention, and increase Central venous pressure

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36
Q

treatment of cardiac tamponade

A

it is a medical emergency and a pericardiocentesis or surgical repair needs to occur

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37
Q

causes of hypoxemic respiratory failure

A

V/Q mismatch, shunt, diffusion limitation, alveolar hypoventilation

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38
Q

causes of hypercapnic respiratory failure

A

abnormal chest wall movement, CNS issue, airways and alveoli

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39
Q

perfusion without ventilation

A

shunt v/q=0

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40
Q

normal v/q

A

=0.8

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41
Q

ventilation without perfusion

A

dead space v/q = infinity (pulmonary embolism)

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42
Q

specific Manifestations of Hypoxemic Respiratory Failure

A

Dyspnea, tachypnea, Prolonged I:E time (1:3); nasal flaring, intercostal muscle retraction, use of accessory muscles, abnormal chest wall movement, CYANOSIS (LATE)

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43
Q

nonspecific Manifestations of Hypoxemic Respiratory Failure

A

TACHYCARDIA and HTN (EARLY)- heart compensating, agitation, disorientation, restlessness, delirium, confusion, change in LOC, cool/clammy skin, fatigue, inability to speak in complete sentences, COMA, DYSRTHYMIAS, HoTN (all LATE)

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44
Q

ARDS is characterized by

A 
Severe dyspnea/Tachypnea
Hypoxia/Hypoxemia
Decreased lung compliance
Alveolar Collapse
Diffuse pulmonary infiltrates
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45
Q

phases of ARDs

A

exudative phase, reparative or proliferative phase, and fibrotic or chronic/late phase

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46
Q

ABGs with ARDS

A

initial - hypoxemia and respiratory alkalosis secondary to hyperventilation. then respiratory acidosis and O2 keeps decreasing despite the amount of O2 they are receiving

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47
Q

what occurs after a burn

A

Local and systemic inflammatory reaction

An immediate shift of intravascular fluid into the surrounding interstitial space

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48
Q

two types of burn injury classification

A
  1. Lund-Browder chart (more accurate)
    - Percentages = 100%
  2. Rule of Nines (adults)
    - Head & neck 9%
    - Arms 9% each
    - Ant trunk 18%
    - Post trunk 18%
    - Legs 18% each
    - Perineum 1%
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49
Q

which burn injury classification is more accurate

A

lund-browder chart

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50
Q

Superficial Partial thickness burn

A

epidermis to dermis
more painful then deep partial thickness and full thickness
Sunburn

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51
Q

Deep partial thickness burn

A

deep dermis including sweat & oil glands)

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52
Q

Full thickness burn

A

All layers of the skin & beyond including bone & muscles

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53
Q

best way to evaluate valve function or dysfunction

A

Transthoracic echocardiogram

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54
Q

Gold standard for evaluating the severity of MV stenosis

A

Trans-mitral gradient (measured by echocardiogram)

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55
Q

1 cause of MV stenosis

A

congenital heart disease

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56
Q

MV Treatments Stenosis, Regurgitation, Prolapse

A

avoid caffeine and stimulants, Cath lab, mitral valve replacement

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57
Q

cause of AV stenosis

A

Calcification (#1)

Bicuspid AV that calcifies (seen at age 40 to 50)

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58
Q

acute AV regurgitation is a

A

life threatening emergency

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59
Q

AV Regurgitation Clinical Manifestations

A 
CARDIOVASCULAR COLLAPSE
Abrupt onset of PROFOUND DYSPNEA
Angina…more subtle than in AV stenosis
Diastolic murmur
Hypotension
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60
Q

TV stenosis cause

A

Almost always in patients with IV drug use (infective endocarditis)
rheumatic heart disease…patients might also have MV or AV stenosis

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61
Q

TV stenosis treatment

A

valve replacement

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62
Q

infective endocarditis clinical manifestations

A 
Acute: Non specific: symptoms are flu like
Fever in >90% 
New/changing systolic murmur
Sub-acute: more generalized symptoms
Ha, back pains, body ache
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63
Q

Treatment for IE

A

Treat the causative agent may need valve replacement

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64
Q

pericarditis

A

inflammation of the sac

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65
Q

hall mark finding of pericarditis

A

Pericardial friction rub
also Severe angina, sharp & pleuritic in nature
Worse w/ deep breathing

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66
Q

complications of pericarditis

A

Pericardial effusion: accumulation of excess fluid in the pericardium. Can be rapid or slow.
Cardiac tamponade: effusion increases in volume, compresses the heart.

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67
Q

leads with pericarditis

A

ST elevation present in all leads

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68
Q

HFrEF

A

Heart Failure with reduced ejection fraction
Systolic Failure…“Failure of systole”
Inability of the heart to pump effectively

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69
Q

hallmark sign of HFrEF

A

Hallmark sign is decreased EF, usually less than 45%

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70
Q

HFpEF

A

Heart Failure with preserved ejection fraction (EF 65% and greater)
Diastolic failure…“Failure of diastole” – failure to fill
Inability of the ventricles to relax and fill during diastole, most commonly r/t hypertension

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71
Q

signs of left sided HF

A

pulmonary congestion and edema - back up of blood into the pulmonary veins

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72
Q

Compensatory Mechanisms in HF

A

Aimed at maintaining CO and BP (helps at first!)
Neurohormonal Response – RAAS
SNS stimulation – catecholamine
Dilation – stretch of ventricles/atrium
Hypertrophy - increase of mass & thickness – diuretics, ACEs, ARBs

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73
Q

Counter-regulatory Mechanisms

A 
ANP, BNP (renal, CV, and hormonal effects)
Nitric Oxide (NO)…vasodilation
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74
Q

what happens during Acute Decompensated Heart Failure

A

Engorgement of the pulmonary vascular system, as this increases, alveolar lining cells disrupted – RBCs leak w/ fluid

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75
Q

s/s of Acute Decompensated Heart Failure

A

Tachypnea, dyspnea and orthopnea (RR>30) – increased pulmonary congestion
Worsening ABGs – ↓ PaO2, possibly ↑ PaCO2 & progressive acidosis
Anxious, pale  cyanotic, clammy, cold skin
Bilateral crackles, possibly wheezes, copious frothy, pink sputum (due increased pressure and RBC crossing the membrane)
Tachycardia – compensating
↑ BP initially – but then drops

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76
Q

meds for Acute decompensated HF

A

Diuretics, Vasodilators, morphine, positive inotropes

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77
Q

positive inotropes

A 
Increases myocardial contractility and CO
Includes dobutamine (preferred), milrinone, and digoxin
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78
Q

meds for chronic HF

A

diuretics, ACE, ARB, vasodilator, Beta blocker, positive inotropes, antiarrythmic, anticoagulant

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79
Q

beta blockers

A

Metoprolol, carvedilol (preferred)- assists with blocking ventricular remodeling during HF
Can help with rate control

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80
Q

managing acute decompensation

A

Assess, Assess, Assess!
High flow O2, consider CPAP or intubation
Cardiac monitor, IV x2, positioning (high folwers)
Daily weights, strict I&Os, Na/H2O diet/fluid restriction

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81
Q

complications of HF

A

pleural effusions, dysrhythmias, thrombus, hepatomegaly, renal failure

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82
Q

women and MI

A

SOB and fatigue are common presenting factors
Present w/ general fatigue, flu like symptoms, n/v or GI upset…
they often don’t think they are having an MI

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83
Q

cause of ACS

A 
Occlusion of coronary artery…#1 cause
   Endothelial damage occurs
   Atherosclerotic plaque disruption “rupture”
   Platelet aggregation
   Thrombus formation
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84
Q

N-STEMI

A

Non-ST-segment-elevation myocardial infarction

will have positive trops

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85
Q

STEMI

A

ST-segment-elevation myocardial infarction
Manifests w/ signs and symptoms of dyspnea, diaphoresis & change in ECG
will have positive trops

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86
Q

troponins

A

show cardiac ischemia!

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87
Q

chest pain work up

A

trop, 12 lead EKG, H&P, cardiac monitor, O2, pain relief, ASA, fibrolytics

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88
Q

STEMI management

A

Get the artery open ASAP, immediate cath lab

Fibrolytics (NO cath lab available)

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89
Q

NSTEMI management

A

ASA, heparin, monitor and Cath lab later

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90
Q

door to needle

A

less than 30 minutes

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91
Q

door to balloon

A

less than 90 minutes

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92
Q

H&P with chest pain

A

Assess pain – PQRST or OLDCARTS

Assess age, race, co-morbidities, risk factors, family history, recent drug use

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93
Q

does a normal ECG rule out ACS/AMI

A

no

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94
Q

primary identifier of STEMI

A

ST segment elevation in 2 or more consecutive leads

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95
Q

what differentiates old MIs from acute process

A

T-wave inversions and pathologic Q-waves develop after an MI

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96
Q

ST elevation

A

infarction

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97
Q

ST depression

A

Ischemia

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98
Q

Lateral leads

A

CIR - I, AVL, V5, V6

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99
Q

anterior leads

A

LAD (left anterior descending artery) - V1, V2, V3

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100
Q

Inferior leads

A

RCA - II, III, AVF

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101
Q

which STEMI carries the worst prognosis

A

anterior - Due to larger infarct size; feeds a majority of the LV
Infarct in the left coronary artery will see septal, anterior and lateral changes…left coronary artery

102
Q

Inferior MI

A

Right Coronary Artery RCA

ST elevation in leads II, III and aVF

103
Q

pharm management with ACS/AMI

A

MONA (aspirin is key), atorvastatin

104
Q

Criteria for stress test:

A

Chest pain present
2 negative Troponins
No significant 12 lead ECG changes (pt may have abnormal but not STEMI)
Need some form of direct evaluation of the heart (prior to discharge)

105
Q

what can decrease the effectiveness of Cardiac Nuclear Stress Tests

A

Theophylline & caffeine decrease the effectiveness of the test
Also beta blockers or drugs that speed up or slow down the heart can effect the test

106
Q

What would make us want to immediately stop a stress test?

A

Substernal chest pain, ST elevation on ECG or lethal rhythm

107
Q

4 stages of shock

A

initial, compensatory, progressive and refractory

108
Q

Initial stage of shock

A

Begins at cellular level, not clinically apparent
Oxygen to cells impacted by decreased perfusion
decrease cardiac output
Metabolism changing from aerobic to anaerobic

109
Q

Anaerobic Metabolism =

A

lactic acid buildup

110
Q

Compensatory Stage of Shock

A

Activation of compensatory mechanisms
Goal: maintain homeostasis
Neural: ↑ HR, contractility, arterial/venous congestion, shunting of blood to vital organs
Hormonal: activation of RAAS-causes vasocontraction, ADH and ACTH
Drop in BP
Immediate response of baroreceptors activating SNS
increase HR & vasoconstriction (most common)

111
Q

Compensatory stage Clinical manifestations

A 
Oriented x 3 (restless, apprehensive)
Shunting of blood to heart and brain
↑ contractility and HR
↓ BP
↑ renin, aldosterone and ADH
↓ blood flow to lungs
↓ GI blood supply
↓ renal blood flow
112
Q

Progressive Stage

A

Compensatory mechanisms fail
Trying to prevent multiple organ dysfunction syndrome
Continued ↓ in cellular perfusion
↓ cerebral perfusion = ↓ responsiveness
↑ cap permeability
Critical dysfunction first seen in lungs (ARDS)
First signs of MODS

113
Q

Progressive Stage Clinical Manifestations

A

Cardiovascular collapse – ↓ perfusion
Worsening of metabolic acidosis
Renal: ARF,AKI – increased BUN = decreased perfusion to the kidney
GI: Dysfunction – (bleeding, impaired absorption) – obstruction (ileus) , decreased bowel sounds
Liver: ↑ LFTs, altered drug/waste metabolism – decreased perfusion to liver
DIC (Disseminated intravascular coagulation)
Seen more in sepsis
Clotting and bleeding at the same time – seen in shock states

114
Q

Systemic Inflammatory Response Syndrome (SIRS)

A

Generalized inflammation in organs remote from the initial insult

115
Q

DIC

A

Bleeding and Clotting disorder
ALWAYS a complication of another disorder
Massive trauma (hemorrhagic shock)
Sepsis

116
Q

what happens in DIC

A

Pro-inflammatory cytokines activates clotting cascade causing microclots forming in capillaries = widespread microvascular coagulation
Systemic Clotting factors are being used up at microvascular level
No clotting factors left = bleeding everywhere!

117
Q

LABS that will be decrease for DIC

A 
Decreased:
Hgb/Hct - bleeding
Platelets (key…rapid decline) 
Fibrinogen 
aPTT (early DIC)
118
Q

LABS that will be increased for DIC

A

PT/INR
aPTT (late DIC)
D-dimer
Fibrin degradation products

119
Q

Refractory Stage of shock

A

↓ perfusion from peripheral vasoconstriction &↓ CO exacerbate anaerobic metabolism  Low BP
Lactic acid leads to cap permeability and loss of vascular fluid
As decrease perfusion and hypoxic state continues, organs fail
MODS
Profound hypotension & hypoxemia
Ischemic gut, Anuria, progression of DIC
Hypothermia

120
Q

Cardiogenic Shock

A

Impaired ability of ventricle to pump blood forward

121
Q

Cardiogenic Shock manifestations

A

Early presentation similar to decompensated HF
Increased: HR, SVR, pulmonary pressures
Decreased: B/P, cardiac output/index, urine output
Chest pain, tachypnea, crackles, cyanosis, anxiety

122
Q

meds for cardiogenic shock

A

inotropes, vasopressor, diuretics, vasodilators, antidysrhythmic agents

123
Q

Hypovolemic Shock

A

Loss of intravascular fluid volume

124
Q

Hypovolemic Shock manifestations

A

Decreased: B/P, CVP, preload, SV, UO, cap refill; Hgb/Hct
Increased: HR, SVR, RR
Pallor, anxiety, confusion, agitation
Depends on severity of volume depletion - how much and how fast is volume lost

125
Q

Obstructive Shock

A

Physical obstruction impeding the filling/outflow of blood flow occurs resulting in ↓ CO

126
Q

types of distributive shock

A

sepsis and anaphylactic

127
Q

medications for Anaphylactic Shock

A

Epinephrine, Benadryl, Bronchodilators, fluids, Corticosteroids, H2 Blockers

128
Q

Leading cause of inpatient death in non-coronary adult ICUs in the US

A

septic shock

129
Q

septic shock

A

Persisting BP requiring vasopressors to maintain MAP ≥65 and LA >2 despite adequate volume resuscitation. (Surviving Sepsis Campaign)

130
Q

3 major pathophysiologic effects of septic shock

A

Vasodilation
Maldistribution of blood flow
Myocardial depression

131
Q

sepsis 1 hour bundle

A

for sepsis

  • measure lactate level
  • rapidly administer 30 mL/kg cystalloid for hypotension or lactate greater than or equal to 4 mmol/L
  • apply vasopressors after fluids - Norepinephrine (Levophed) is first, then others
132
Q

levophed (norepinephrine)

A

common first line pressor for sepsis, cardiogenic shock, or nuerogenic shock. stimulates beta 1 heart receptor which increases HR and CO. and stimulates alpha 1 - increases SVR and BP (vasoconstriction) and beta 2 - protects blood flow to organs

133
Q

phenylephrine (neosynephrine)

A

peripheral pusher - alpha 1- increase SVR and BP but can cause reflex bradycardia

134
Q

vasopressin (ADH)

A

commonly used as an adjunct to norepinephrine - vasoconstriction and increases volume by increasing H20 reabsorption

135
Q

signs of sepsis

A

increase temp, tachypnea, warm and flushed skin, respiratory alkalosis

136
Q

septic shock signs

A

cool and mottles (cold shock is dead shock), respiratory failure, GI bleed or paralytic ileus, myocardial dysfunction

137
Q

The Gold Standard of Treatment for someone having a MI

A

Percutaneous Cardiac Intervention (PCI )

138
Q

what do you need to do before Cardiac Catheterization

A 
Medication Hx &amp; Allergies
assess pulses! 
Check Labs (Which Ones &amp; Why?)
	Pt/Ptt/INR – need to know clotting 
	kidney function labs 
IV assess
pt understands procedure and consent
139
Q

Takotsubo

A

broken heart syndrome - Chest pain, ST elevation, mildly elevate troponins - caused by stress

140
Q

post Cardiac Catheterization

A

MONITOR PULSES. position leg straight, monitor for reclusion- s/s ischemia, thrombosis, bleeding and Trops will go up first then down

141
Q

CORONARY ARTERY BYPASS GRAFT (CABG)

A

A procedure in which the patient’s diseased coronary arteries are bypassed with the patient’s own venous (saphenous vein) or arterial (internal mammary artery [most common]) vessels.

142
Q

who is a CABG for

A

Failed Medical Mgt

Have Left Main or 3 diseased vessels with significant blockage.

143
Q

who is not a candidate for CABG

A

Failed PCI
Newly added criteria
Diabetes Mellitus
Expected longer term benefits/outcomes

144
Q

dopamine

A

(hulk)- squeeze! - vasoconstriction

145
Q

Addison’s Disease

A

Incurable disease controlled w/ hormone replacement

90% of adrenal cortex destroyed

146
Q

Adrenal glands produce

A

cortisol and aldosterone

147
Q

what does cortisol do

A

helps the body respond to stress, maintains BP, balance the effects of insulin…has hundreds of functions

148
Q

Patient Presentation in Addison’s Disease

A

Low BP, dizziness, orthostatic HoTN, hypoglycemia, fatigue, weight loss, hair loss, salt craving

149
Q

acute adrenal failure results in

A

Circulatory collapse and electrolyte imbalance

150
Q

causes acute adrenal failure

A

stress, Adrenal surgery/hemorrhage

151
Q

A patient’s circulatory collapse in an addisonian crisis is often refractory to fluids and vasopressors…. WHY???

A

we give them vasopressors during this crisis but the patient does not respond because they still lack the hormone needed to squeeze (increase their BP)

152
Q

diagnostics in acute adrenal failure

A

ACTH stimulation test, Insulin-induced hypoglycemia test, CT, MRI

153
Q

during acute adrenal failure there is Ongoing cortisol monitoring to monitor efficacy of steroid dosage. when do you take them?

A

Highest early in “morning” (0600 – 0800)

lower in the evening (1600 – 1800)

154
Q

Assist patients to avoid what during acute adrenal failure

A

stress - Physical, Mental, Emotional, Spiritual

155
Q

what do we need to administer during acute adrenal failure

A

Corticosteroid administration

156
Q

education during acute adrenal failure

A

Importance to take cortisol replacement daily
↑ dose at times of stress (fever, flu, surgery, etc)
Double/triple doses!!!!!
Follow up with MD immediately

157
Q

DKA and insulin

A

Insulin Deficiency

158
Q

DKA what happens

A 
Break down of FAT &amp; PROTEIN→Ketones
Rapid onset
Liver continues to produce glucose
Hyperglycemia (> 250)
Osmotic Diuresis
Severe Dehydration
159
Q

HHS and insulin

A 
Insulin Present (Only Type II)
Liver continues to produce glucose
160
Q

HHS what happens

A

Neuro signs may be the first really noted
Slower, insidious onset
Break down of fatty acids minimal because of insulin facilitating glucose transport into cells
NO KETONES
Hyperglycemia (> 600)
Osmotic Diuresis
Severe Dehydration

161
Q

DKA diagnostic criteria

A

pH < 7.30 (Typically) - pH in SEVERE cases can drop below 7.0
Metabolic Acidosis (due to build up of lactic acid) w/ respiratory compensation
Blood glucose greater than 250 mg/dL
+ Ketones in blood and urine
Serum bicarbonate less than 18 mEq/L
aka CO2 on BMP/CMP

162
Q

HHS diagnostic criteria

A 
Blood glucose ˃ 600  mg/dL
NO KETONES!!!!! 
Serum bicarbonate can be ˃ 18 mEq/L
Serum osmolality can ˃ 320 mOsm/kg
pH ˃ 7.30
163
Q

blood sugars in DKA

A

above 250

164
Q

blood sugars HHS

A

above 600

165
Q

what occurs during ketoacidosis?

A

decreased perfusion causes +++ lactic acid release r/t anaerobic metabolism
FAT/PRO breakdown used for fuel
Free fatty acids convert to ketones
Brain cells are especially sensitive to loss of glucose for fuel and inability to use fatty acid fuel. Seen first as ↓ LOC.
overall buildup of ketones results in metabolic acidosis

166
Q

DKA: Clinical manifestations

A

Keys: RAPID ONSET
Polyuria: excessive urination (increased BS pulling water out of cells)
Polydipsia: dehydration, dry mouth, excessive thirst
Polyphagia: excessive hunger (cells are starving)
Others:
GI effects: n/v/abd pain
Neuro effects: Not as profound, ketones allow brain to be fed; can be altered LOC

167
Q

vital signs in DKA

A

Kussmaul respirations: fruity/acetone breath – compensation for metabolic acidosis
Tachycardia/HoTN/Orthostatic HoTN
Fever – why? – possible infection and increase stress response

168
Q

Initial Interventions DKA and HHS

A

ABCs..
Ensure patent airway
Administer oxygen
FLUIDS!!!!…
IV access – hydration!
Begin fluid resuscitation then give them regular insulin
Electrolyte replacement once partial glucose correction

169
Q

when do you know that you should switch to D5 in DKA/HHS treatment?

A

u/o ˃ 0.5ml /kg/hr and B/P normal

170
Q

DI

A

Deficiency of antidiuretic hormone (ADH, vasopressin) results in inability to conserve water

171
Q

SIADH

A

Excessive amounts of ADH secreted from posterior pituitary and other ectopic sources. – body not producing urine

172
Q

commonality between DI and SIADH

A

ADH – key component that we see between the two

173
Q

SIADH causes

A

80% r/t small cell carcinoma

174
Q

risk factors for DI

A

head injury, neurosurgery, tumor

175
Q

what happens in DI

A

Permeability of water is diminished, resulting in excretion of large volumes of hypotonic fluid.

176
Q

what happens in SIADH

A

Water Retention
Hyponatremia (dilutional)
Hypo-osmolality - A continual release of ADH causes water retention from renal tubules and collecting ducts.

177
Q

DI physical exam

A 
Mucous Membranes  - Dry
Skin - Dry, cool skin
Cardiovascular (more acute) - Tachycardia to respond to fluid loss 
Electrolyte Problems (acute) 
weight loss
decreased level of consciousness
faucet pee
178
Q

SIADH physical exam

A 
R/T Hyponatremia - Decreased deep tendon reflexes, confusion, seizures, fatigue, H/A, anorexia, nausea, decreased mental status, seizures, coma.
R/T Fluid Vol. Excess
- Wt. gain w/o edema
- JVD
- Tachycardia
- Tachypnea
- Rales (crackles) 
GI - decreased motility
179
Q

diagnostics of DI

A 
Urinary OutPut- A few liters to 18L/d
Serum Osmo ↑ >290
Serum Na+ ↑ >150
Sp. Gravity < 1.005
Water deprivation study
180
Q

diagnostics of SIADH

A

Serum Na+ ↓ < 130
Urine Na+ ↑
BUN ↓
urinary output low – urine will be concentrated

181
Q

management of DI

A

Surgical:
Hypophysectomy
Medical:
IV Fluids – quarter saline – remember they are holding onto sodium

182
Q

management of SIADH

A 
Surgical:
None
Medical:
Hypertonic Flds.
Demeclocycline (antibiotic) to facilitate free water clearance (side effect)
Sodium restriction
Diuretics due to low plasma osmo
Treat underlying cause.
183
Q

initiating phase AKI

A

This begins at the time of the insult and continues until the signs and symptoms become apparent.
Lasting hours to days.

184
Q

Oliguric Phase AKI

A

Reduction in GFR
Occurs within 1-7 days of causative event
Duration 10-14 days, but can last months
The longer in this phase the poorer the prognosis for recovery of complete renal function.
Urinary Changes, Fluid Vol. Excess, Metabolic Acidosis, Sodium Balance Loss, Potassium Excess

185
Q

diuretic phase AKI

A

Begins with gradual increase in dly UOP secondary to high urea concentration in the urine and the inability of the tubules to concentrate the urine.
Can excrete waste, but not concentrate
Must monitor lytes and hydration levels
Lasts 1-3 weeks
Patients lab values begin to normalize near the end of this phase

186
Q

recovery phase AKI

A

Begins with increasing GFR
BUN and CR levels plateau and then decrease
Improvements occur in first 1-2 weeks of this phase, but renal function may take up to 12 months to stabilize
Outcome influenced by the patient’s overall health, severity of renal failure and the number and type of complications
Some will progress to CRF
Older adults less likely to recover full function
Those who recover achieve clinically normal function without complications.

187
Q

hallmark of rhabdo

A

increase in serum Creatine kinase

188
Q

normal CK

A

45-260 units/L

189
Q

treatment for rhabdo

A 
Removal of Tight Clothing
Fasciotomy or Escharatomy
NS @ to 1000-1500ml/hr to maintain UOP @ 300ml/hr  
diuretic 
dialysis
190
Q

Continuous Renal Replacement Therapy (CRRT)

A

Used for hemodynamically unstable pts.

Artificial kidney support.

191
Q

Heparin Induced Thrombocytopenia (HIT)

A

immune reaction to heparin. lowers platelet count, and causes thromboses

192
Q

acute pyelonephritis manifestations

A

flank pain, fatigue, chills, fever, dysuria

193
Q

nephrotic syndrome marked by:

A

very high levels of protein in the urine, a condition called proteinuria
low levels of protein in the blood
swelling, especially around the eyes, feet, and hands
high cholesterol → high triglycerides

194
Q

what is nephrotic syndrome

A

immune response that leads to damage of the glomeruli and third spacing of fluids (fluid accumulates into the tissues rather than circulating)

195
Q

Anasarca

A

weeping of the skin- protein leaking from skin

196
Q

Diagnosing Nephrotic Syndrome

A

blood and urine samples (Protein)

may order a 24-hour collection of urine

197
Q

risk factors of renal cancer

A

2 X more often in men than women, cigarette smoking most common risk factor.

198
Q

Carcinomas

A

Cancers that begin in the skin or in the tissue that line or cover internal organs

199
Q

Sarcomas

A

Start in the connective tissue including bones, cartilage, tendons, and fibrous tissue

200
Q

Leukemia

A

Bone marrow makes too many white blood cells, and they do not form correctly, but continue to build up in the blood

201
Q

Lymphomas and Myelomas

A

cancer in the lymphatic system – system that filters bodily fluid and fights infection

202
Q

Melanoma

A

Most dangerous type of skin cancer
Risk factors include:
Have fair skin, blue or green eyes, or red or blond hair
Live in sunny climates or at high altitudes

203
Q

Pancreatic Cancer common causes

A

Diabetics
Chronic pancreatitis
Smokers

204
Q

Clinical manifestations of pancreatic cancer:

A

Clinical manifestations
Dark urine & clay stools
Fatigue & weakness
Jaundice

205
Q

TNM staging system

A

T - tumor
N - nodes
M - metastasis
Once staging is complete is does NOT change

206
Q

flare reaction

A

distinguishable from extravasation by lack of pain or swelling, presence of good blood return

207
Q

nadir

A

Point at which the lowest blood-cell count is reached
Usually 7-10 days after treatment
Onset and duration depends on agent used
WBC & platelets are usually 1st to drop
Anemia is seen later

208
Q

life span of a neutrophil

A

7-12 hours

209
Q

life span of platelets

A

7-8 days

210
Q

life span of erythrocytes

A

90-120 days

211
Q

mild neutropenic absolute neutrophil count

A

1000-1500

212
Q

moderate neutropenic absolute neutrophil count

A

500-1000

213
Q

severe neutropenic absolute neutrophil count

A

0-500

214
Q

how to calculate Absolute Neutrophil Count (ANC)

A

ANC = Total WBC × (% Segmented Neutrophils + % Bands)

215
Q

what meds can we give a chemo patient for infection prevention

A

colony-stimulating factors - Neupogen and Neulasta

216
Q

both UC and Crohn’s are characterized by

A

chronic inflammation of the intestine w/ periods of remission & exacerbation

217
Q

UC

A

inflammation beginning in the rectum and spreading up the COLON (only) in a continuous pattern

218
Q

crohns

A

Can affect any part of the GI tract from the lips to the anus
Most often seen in the terminal ileum and colon

219
Q

Hallmark sign of crohns

A

skip lesions: Segments of normal bowel occurring between diseased portions causing classic cobblestone appearance

220
Q

fistulas are seen more in

A

crohns - leaks out all the way to skin

221
Q

nutrition with UC/Crohns

A 
High-calorie, High-protein
Low-residue diet- helps control diarrhea
Vitamin and iron supplements
Elemental diets: Enteral feedings for bowel rest
Parenteral nutrition: during bowel rest
222
Q

drugs for UC/Crohns

A

Aminosalicylates, Antimicrobials, Corticosteroids, Immunosuppressants, Biologic therapy, Antidepressants

223
Q

Solid organs

A

liver, spleen, kidneys and pancreas; bleed profusely

224
Q

Hollow organs

A

stomach, intestines, bladder, gallbladder; peritonitis/sepsis leakage after injury

225
Q

most common cause of blunt abdominal trauma

A

MVCs

226
Q

hollow organs can collapse

A

and absorb force

227
Q

Cullen’s Sign

A

bruising around the umbilicus - Intra-peritoneal hemorrhage

228
Q

Grey Turner’s sign

A

flanks- Retro-peritoneal hemorrhage

229
Q

what is used with ABD trauma in rural areas when CT is not available

A

Diagnostic Peritoneal Lavage DPL - old technique

230
Q

Intra-abdominal pressure (IAP) in a normal adult

A

0-5

elevation in IAP ≥ 12 mmHg = hypertension (IAH)

231
Q

What does abdominal compartment syndrome (ACS) mean for your patient?

A 
50% of IAP is reflected into the thoracic cavity…causing ⇩ CO
Atelectasis, PNA
decrease PaO2 increase PaCO2
decrease GFR; AKI
increase ICP
decrease wound healing

Complication of Abdominal Trauma!!!

232
Q

Gold standard for intra-abdominal indirect intermittent pressures

A

Urinary bladder pressure monitoring

Utilizes a foley catheter for monitoring

233
Q

Most common prognostic systems Acute Pancreatitis

A

Ranson’s Criteria - Estimating the severity of acute pancreatitis

234
Q

Acute pancreatitis causes

A

Most Common (80% of cases):
Gallbladder Disease
Excessive ETOH

235
Q

labs for Acute pancreatitis

A 
Serum lipase 
≥ 3 x the upper limit of normal 
more specific to pancreas
more accurate marker for acute pancreatitis
Amylase (will be increased as well)
Elevations in:
Triglycerides, CRP, glucose, WBCs, bilirubin, LFTs, PT
Urine amylase
Reductions in:
Calcium, magnesium, potassium, albumin
236
Q

Collaborative Management for Acute Pancreatitis

A

Ensure Hemodynamic Stability…remember this is C of your ABCs
Pain & N/V management
Antibiotics: ONLY if SEPSIS or abscess are present
NPO & NG
NG suction: ONLY if patient has persistent vomiting obstruction or gastric distention

237
Q

Classic triad of chronic pancreatitis

A

calcification, steatorrhea, and diabetes

history of heavy ETOH use

238
Q

gold standard for dx for chronic pancreatitis

A

Surgical biopsy of pancreas

239
Q

Anticipate medications for GI bleed

A 
Vasopressors:
- norepinephrine, vasopressin, phenylephrine
Acid Reduction:
- PPIs: pantoprazole sodium (Protonix) IV drip
- Give IV bolus then ~ 8 mg/hr IV 
- NOT Titrated!
Octreotide IV drip (Sandostatin)
- Give an IV bolus then ~ 50 mcg/hr IV
- NOT Titrated!
- ↓ bleeding of varices
May need to give blood products
240
Q

acute liver failure causes

A 
Drugs are #1 cause
#1: Tylenol (acetaminophen), NSAIDs (all types), INH, mushrooms
#2: Hepatitis B &amp; C
241
Q

outcomes for acute liver failure

A

75 - 90% DIE!; 10-25% “SURVIVE”…W/ INTENSIVE CARE!

NEED A LIVER

242
Q

Collaborative CareAcute Liver Failure

A

Lower the AMMONIA LEVEL!
Neomycin, metronidazole, rifaximin or LACTULOSE (gold standard)
Correction of coagulopathies: best through PREVENTION!

243
Q

TIPS

A

Trans jugular intrahepatic porto systemic shunt

Manage complications of portal HTN

244
Q

Bariatric Surgery

A 
to qualify: BMI>40 or >35 with comorbidities
5+ years
Understand risks/benefits
Tried and failed at weight loss
No serious endocrine disorders
245
Q

Restrictive bariatric Surgeries

A

gastric banding - ↓ stomach to 30 mL, feeling fuller faster

246
Q

malabsorption bariatric surgeries

A

Various lengths of the small intestine bypassed ↓ absorption of nutrients
Less food is absorbed – DOES alter digestion

247
Q

Roux-en-Y Gastric bypass

A 
Stomach size is ↓ w/ gastric pouch 
Most common bariatric procedure in US
Considered gold standard
Low complication rates
Excellent patient tolerance
248
Q

Preoperative Concerns with bariatric surgeries

A

Liquid Diet for up to 6 wks preop

Detailed health hx, address comorbidities

249
Q

post op complications in bariatric surgeries

A

Dehiscence or leaking
- First sign is tachycardia
Anemia: malabsorption of Iron and Vit B
Increased risk of Infection

250
Q

Nutritional Goals: after bariatric surgery

A 
PREVENT MALABSORPTION
DUMPING SYNDROME
SPEED HEALING 
Meals:
6 to 8 small @ 30 mL
Don’t skip!!!
High PRO/low FAT/low CHO/low roughage
Fluids: NOT w/ meals; limited to 1000 mL/day

Nursing school level 4 (6 decks)

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