Final deck #2 Flashcards
(250 cards)
1
Q
COPD characterized by
A
airflow limitation, breathlessness, and exacerbation.
2
Q
COPD disease process is based mainly off of what concept
A
inflammation
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)
4
Q
emphysema
A
damaged alveoli in which they trap air
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
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
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
8
Q
COPD diagnostics for chronic phase
A
pulmonary function test - determines COPD progression
echocardiogram - determines cor pulmonale
9
Q
ABG findings in exacerbation of COPD`
A
low PaO2 and SaO2
high PaCO2
normal or low PH
high HCO3
10
Q
COPD meds for maintenance
A
anticholinergic agents (ipratropium)- long acting, steroid with LABA (Advair or Symbicort)
11
Q
COPD meds for acute exacerbation
A
short acting beta 2 agonist (albuterol), antibiotic, steroid
12
Q
caution with beta blockers with COPD pts, why?
A
it can cause the bronchioles to constrict
13
Q
pharmacological support for smoking cessation
A
Nicotine supplements, bupropion (wellbutrin, zyban), varenicline (chantix)
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.
15
Q
1 cause of pulmonary hypertension
A
COPD
16
Q
diagnostic studies for pulmonary HTN
A
right cardiac Cath, 12 lead ECG, CT scan
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
18
Q
meds for PH and cor pulmonale
A
calcium channel blocker, vasodilators, endothelial receptor antagonist, viagra, oxygen, diuretics, anticoagulants, inotropic agents
19
Q
endothelial receptor antagonist
A
↓ PA pressures, ↑ cardiac output
for PH and cor pulmonale
20
Q
Virchow Triad for PE
A
Venous stasis
Vascular endothelium injury
Hypercoagulability
21
Q
labs for pulmonary embolism
A
ABGs - oxygenation
D-Dimer - clotting in the body
BNP - cardiac ventricular stretch
troponin - how big it is
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
23
Q
Submassive PE
A
Acute PE w/ RV dysfunction
Myocardial necrosis present
24
Q
Thrombolytics
A
Fibrolytics (AKA Alteplase or tPA)
25
Vitamin-K antagonist
warfarin - is main therapy with PE bridged w/ parenteral anti-coagulants but needs frequent monitoring of INR
26
low molecular weight heparin example
enoxaparin sodium - no lab needed
27
Heparin lab
PTT (goal is 50-90)
28
pneumothorax
air in the pleural space resulting in partial collapse of lung - pressure goes from negative to positive
29
clinical manifestations of large pneumothorax
absent breath sounds. Respiratory Distress (shallow, rapid resps, dyspnea, air hunger, O2 desaturation); Chest pain, Cough with or without hemoptysis
30
spontaneous pneumo can happen in
also called a closed pnuemo can occur after rupture of blebs in COPD pt or in tall/thin male with marphans
31
Tension Pneumothorax
Rapid accumulation of air in pleural space without the ability to escape. (medical emergency) - respiratory and circulatory collapse
32
how much blood is too much during a hemothorax
250-300 ml of blood (unit of blood)
33
flail chest
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.
34
sign of flail chest
paradoxical movement - breathing reverses this pattern, which means that during inspiration, the chest contracts, and during expiration, it expands.
35
s/s of cardiac tamponade
muffled, distant heart tones, decrease BP, jugular vein distention, and increase Central venous pressure
36
treatment of cardiac tamponade
it is a medical emergency and a pericardiocentesis or surgical repair needs to occur
37
causes of hypoxemic respiratory failure
V/Q mismatch, shunt, diffusion limitation, alveolar hypoventilation
38
causes of hypercapnic respiratory failure
abnormal chest wall movement, CNS issue, airways and alveoli
39
perfusion without ventilation
shunt v/q=0
40
normal v/q
=0.8
41
ventilation without perfusion
dead space v/q = infinity (pulmonary embolism)
42
specific Manifestations of Hypoxemic Respiratory Failure
Dyspnea, tachypnea, Prolonged I:E time (1:3); nasal flaring, intercostal muscle retraction, use of accessory muscles, abnormal chest wall movement, CYANOSIS (LATE)
43
nonspecific Manifestations of Hypoxemic Respiratory Failure
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)
44
ARDS is characterized by
```
Severe dyspnea/Tachypnea
Hypoxia/Hypoxemia
Decreased lung compliance
Alveolar Collapse
Diffuse pulmonary infiltrates
```
45
phases of ARDs
exudative phase, reparative or proliferative phase, and fibrotic or chronic/late phase
46
ABGs with ARDS
initial - hypoxemia and respiratory alkalosis secondary to hyperventilation. then respiratory acidosis and O2 keeps decreasing despite the amount of O2 they are receiving
47
what occurs after a burn
Local and systemic inflammatory reaction
| An immediate shift of intravascular fluid into the surrounding interstitial space
48
two types of burn injury classification
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%
49
which burn injury classification is more accurate
lund-browder chart
50
Superficial Partial thickness burn
epidermis to dermis
more painful then deep partial thickness and full thickness
Sunburn
51
Deep partial thickness burn
deep dermis including sweat & oil glands)
52
Full thickness burn
All layers of the skin & beyond including bone & muscles
53
best way to evaluate valve function or dysfunction
Transthoracic echocardiogram
54
Gold standard for evaluating the severity of MV stenosis
Trans-mitral gradient (measured by echocardiogram)
55
#1 cause of MV stenosis
congenital heart disease
56
MV Treatments Stenosis, Regurgitation, Prolapse
avoid caffeine and stimulants, Cath lab, mitral valve replacement
57
cause of AV stenosis
Calcification (#1)
| Bicuspid AV that calcifies (seen at age 40 to 50)
58
acute AV regurgitation is a
life threatening emergency
59
AV Regurgitation Clinical Manifestations
```
CARDIOVASCULAR COLLAPSE
Abrupt onset of PROFOUND DYSPNEA
Angina…more subtle than in AV stenosis
Diastolic murmur
Hypotension
```
60
TV stenosis cause
Almost always in patients with IV drug use (infective endocarditis)
rheumatic heart disease…patients might also have MV or AV stenosis
61
TV stenosis treatment
valve replacement
62
infective endocarditis clinical manifestations
```
Acute: Non specific: symptoms are flu like
Fever in >90%
New/changing systolic murmur
Sub-acute: more generalized symptoms
Ha, back pains, body ache
```
63
Treatment for IE
Treat the causative agent may need valve replacement
64
pericarditis
inflammation of the sac
65
hall mark finding of pericarditis
Pericardial friction rub
also Severe angina, sharp & pleuritic in nature
Worse w/ deep breathing
66
complications of pericarditis
Pericardial effusion: accumulation of excess fluid in the pericardium. Can be rapid or slow.
Cardiac tamponade: effusion increases in volume, compresses the heart.
67
leads with pericarditis
ST elevation present in all leads
68
HFrEF
Heart Failure with reduced ejection fraction
Systolic Failure…“Failure of systole”
Inability of the heart to pump effectively
69
hallmark sign of HFrEF
Hallmark sign is decreased EF, usually less than 45%
70
HFpEF
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
71
signs of left sided HF
pulmonary congestion and edema - back up of blood into the pulmonary veins
72
Compensatory Mechanisms in HF
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
73
Counter-regulatory Mechanisms
```
ANP, BNP (renal, CV, and hormonal effects)
Nitric Oxide (NO)…vasodilation
```
74
what happens during Acute Decompensated Heart Failure
Engorgement of the pulmonary vascular system, as this increases, alveolar lining cells disrupted – RBCs leak w/ fluid
75
s/s of Acute Decompensated Heart Failure
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
76
meds for Acute decompensated HF
Diuretics, Vasodilators, morphine, positive inotropes
77
positive inotropes
```
Increases myocardial contractility and CO
Includes dobutamine (preferred), milrinone, and digoxin
```
78
meds for chronic HF
diuretics, ACE, ARB, vasodilator, Beta blocker, positive inotropes, antiarrythmic, anticoagulant
79
beta blockers
Metoprolol, carvedilol (preferred)- assists with blocking ventricular remodeling during HF
Can help with rate control
80
managing acute decompensation
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
81
complications of HF
pleural effusions, dysrhythmias, thrombus, hepatomegaly, renal failure
82
women and MI
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
83
cause of ACS
```
Occlusion of coronary artery…#1 cause
Endothelial damage occurs
Atherosclerotic plaque disruption “rupture”
Platelet aggregation
Thrombus formation
```
84
N-STEMI
Non-ST-segment-elevation myocardial infarction
| will have positive trops
85
STEMI
ST-segment-elevation myocardial infarction
Manifests w/ signs and symptoms of dyspnea, diaphoresis & change in ECG
will have positive trops
86
troponins
show cardiac ischemia!
87
chest pain work up
trop, 12 lead EKG, H&P, cardiac monitor, O2, pain relief, ASA, fibrolytics
88
STEMI management
Get the artery open ASAP, immediate cath lab
| Fibrolytics (NO cath lab available)
89
NSTEMI management
ASA, heparin, monitor and Cath lab later
90
door to needle
less than 30 minutes
91
door to balloon
less than 90 minutes
92
H&P with chest pain
Assess pain – PQRST or OLDCARTS
| Assess age, race, co-morbidities, risk factors, family history, recent drug use
93
does a normal ECG rule out ACS/AMI
no
94
primary identifier of STEMI
ST segment elevation in 2 or more consecutive leads
95
what differentiates old MIs from acute process
T-wave inversions and pathologic Q-waves develop after an MI
96
ST elevation
infarction
97
ST depression
Ischemia
98
Lateral leads
CIR - I, AVL, V5, V6
99
anterior leads
LAD (left anterior descending artery) - V1, V2, V3
100
Inferior leads
RCA - II, III, AVF
101
which STEMI carries the worst prognosis
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
Inferior MI
Right Coronary Artery RCA
| ST elevation in leads II, III and aVF
103
pharm management with ACS/AMI
MONA (aspirin is key), atorvastatin
104
Criteria for stress test:
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
what can decrease the effectiveness of Cardiac Nuclear Stress Tests
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
What would make us want to immediately stop a stress test?
Substernal chest pain, ST elevation on ECG or lethal rhythm
107
4 stages of shock
initial, compensatory, progressive and refractory
108
Initial stage of shock
Begins at cellular level, not clinically apparent
Oxygen to cells impacted by decreased perfusion
decrease cardiac output
Metabolism changing from aerobic to anaerobic
109
Anaerobic Metabolism =
lactic acid buildup
110
Compensatory Stage of Shock
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
Compensatory stage Clinical manifestations
```
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
Progressive Stage
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
Progressive Stage Clinical Manifestations
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
Systemic Inflammatory Response Syndrome (SIRS)
Generalized inflammation in organs remote from the initial insult
115
DIC
Bleeding and Clotting disorder
ALWAYS a complication of another disorder
Massive trauma (hemorrhagic shock)
Sepsis
116
what happens in DIC
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
LABS that will be decrease for DIC
```
Decreased:
Hgb/Hct - bleeding
Platelets (key…rapid decline)
Fibrinogen
aPTT (early DIC)
```
118
LABS that will be increased for DIC
PT/INR
aPTT (late DIC)
D-dimer
Fibrin degradation products
119
Refractory Stage of shock
↓ 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
Cardiogenic Shock
Impaired ability of ventricle to pump blood forward
121
Cardiogenic Shock manifestations
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
meds for cardiogenic shock
inotropes, vasopressor, diuretics, vasodilators, antidysrhythmic agents
123
Hypovolemic Shock
Loss of intravascular fluid volume
124
Hypovolemic Shock manifestations
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
Obstructive Shock
Physical obstruction impeding the filling/outflow of blood flow occurs resulting in ↓ CO
126
types of distributive shock
sepsis and anaphylactic
127
medications for Anaphylactic Shock
Epinephrine, Benadryl, Bronchodilators, fluids, Corticosteroids, H2 Blockers
128
Leading cause of inpatient death in non-coronary adult ICUs in the US
septic shock
129
septic shock
Persisting BP requiring vasopressors to maintain MAP ≥65 and LA >2 despite adequate volume resuscitation. (Surviving Sepsis Campaign)
130
3 major pathophysiologic effects of septic shock
Vasodilation
Maldistribution of blood flow
Myocardial depression
131
sepsis 1 hour bundle
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
levophed (norepinephrine)
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
phenylephrine (neosynephrine)
peripheral pusher - alpha 1- increase SVR and BP but can cause reflex bradycardia
134
vasopressin (ADH)
commonly used as an adjunct to norepinephrine - vasoconstriction and increases volume by increasing H20 reabsorption
135
signs of sepsis
increase temp, tachypnea, warm and flushed skin, respiratory alkalosis
136
septic shock signs
cool and mottles (cold shock is dead shock), respiratory failure, GI bleed or paralytic ileus, myocardial dysfunction
137
The Gold Standard of Treatment for someone having a MI
Percutaneous Cardiac Intervention (PCI )
138
what do you need to do before Cardiac Catheterization
```
Medication Hx & Allergies
assess pulses!
Check Labs (Which Ones & Why?)
Pt/Ptt/INR – need to know clotting
kidney function labs
IV assess
pt understands procedure and consent
```
139
Takotsubo
broken heart syndrome - Chest pain, ST elevation, mildly elevate troponins - caused by stress
140
post Cardiac Catheterization
MONITOR PULSES. position leg straight, monitor for reclusion- s/s ischemia, thrombosis, bleeding and Trops will go up first then down
141
CORONARY ARTERY BYPASS GRAFT (CABG)
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
who is a CABG for
Failed Medical Mgt
| Have Left Main or 3 diseased vessels with significant blockage.
143
who is not a candidate for CABG
Failed PCI
Newly added criteria
Diabetes Mellitus
Expected longer term benefits/outcomes
144
dopamine
(hulk)- squeeze! - vasoconstriction
145
Addison's Disease
Incurable disease controlled w/ hormone replacement
| 90% of adrenal cortex destroyed
146
Adrenal glands produce
cortisol and aldosterone
147
what does cortisol do
helps the body respond to stress, maintains BP, balance the effects of insulin…has hundreds of functions
148
Patient Presentation in Addison’s Disease
Low BP, dizziness, orthostatic HoTN, hypoglycemia, fatigue, weight loss, hair loss, salt craving
149
acute adrenal failure results in
Circulatory collapse and electrolyte imbalance
150
causes acute adrenal failure
stress, Adrenal surgery/hemorrhage
151
A patient’s circulatory collapse in an addisonian crisis is often refractory to fluids and vasopressors…. WHY???
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
diagnostics in acute adrenal failure
ACTH stimulation test, Insulin-induced hypoglycemia test, CT, MRI
153
during acute adrenal failure there is Ongoing cortisol monitoring to monitor efficacy of steroid dosage. when do you take them?
Highest early in “morning” (0600 – 0800)
| lower in the evening (1600 – 1800)
154
Assist patients to avoid what during acute adrenal failure
stress - Physical, Mental, Emotional, Spiritual
155
what do we need to administer during acute adrenal failure
Corticosteroid administration
156
education during acute adrenal failure
Importance to take cortisol replacement daily
↑ dose at times of stress (fever, flu, surgery, etc)
Double/triple doses!!!!!
Follow up with MD immediately
157
DKA and insulin
Insulin Deficiency
158
DKA what happens
```
Break down of FAT & PROTEIN→Ketones
Rapid onset
Liver continues to produce glucose
Hyperglycemia (> 250)
Osmotic Diuresis
Severe Dehydration
```
159
HHS and insulin
```
Insulin Present (Only Type II)
Liver continues to produce glucose
```
160
HHS what happens
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
DKA diagnostic criteria
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
HHS diagnostic criteria
```
Blood glucose ˃ 600 mg/dL
NO KETONES!!!!!
Serum bicarbonate can be ˃ 18 mEq/L
Serum osmolality can ˃ 320 mOsm/kg
pH ˃ 7.30
```
163
blood sugars in DKA
above 250
164
blood sugars HHS
above 600
165
what occurs during ketoacidosis?
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
DKA: Clinical manifestations
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
vital signs in DKA
Kussmaul respirations: fruity/acetone breath – compensation for metabolic acidosis
Tachycardia/HoTN/Orthostatic HoTN
Fever – why? – possible infection and increase stress response
168
Initial Interventions DKA and HHS
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
when do you know that you should switch to D5 in DKA/HHS treatment?
u/o ˃ 0.5ml /kg/hr and B/P normal
170
DI
Deficiency of antidiuretic hormone (ADH, vasopressin) results in inability to conserve water
171
SIADH
Excessive amounts of ADH secreted from posterior pituitary and other ectopic sources. – body not producing urine
172
commonality between DI and SIADH
ADH – key component that we see between the two
173
SIADH causes
80% r/t small cell carcinoma
174
risk factors for DI
head injury, neurosurgery, tumor
175
what happens in DI
Permeability of water is diminished, resulting in excretion of large volumes of hypotonic fluid.
176
what happens in SIADH
Water Retention
Hyponatremia (dilutional)
Hypo-osmolality - A continual release of ADH causes water retention from renal tubules and collecting ducts.
177
DI physical exam
```
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
SIADH physical exam
```
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
diagnostics of DI
```
Urinary OutPut- A few liters to 18L/d
Serum Osmo ↑ >290
Serum Na+ ↑ >150
Sp. Gravity < 1.005
Water deprivation study
```
180
diagnostics of SIADH
Serum Na+ ↓ < 130
Urine Na+ ↑
BUN ↓
urinary output low – urine will be concentrated
181
management of DI
Surgical:
Hypophysectomy
Medical:
IV Fluids – quarter saline – remember they are holding onto sodium
182
management of SIADH
```
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
initiating phase AKI
This begins at the time of the insult and continues until the signs and symptoms become apparent.
Lasting hours to days.
184
Oliguric Phase AKI
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
diuretic phase AKI
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
recovery phase AKI
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
hallmark of rhabdo
increase in serum Creatine kinase
188
normal CK
45-260 units/L
189
treatment for rhabdo
```
Removal of Tight Clothing
Fasciotomy or Escharatomy
NS @ to 1000-1500ml/hr to maintain UOP @ 300ml/hr
diuretic
dialysis
```
190
Continuous Renal Replacement Therapy (CRRT)
Used for hemodynamically unstable pts.
| Artificial kidney support.
191
Heparin Induced Thrombocytopenia (HIT)
immune reaction to heparin. lowers platelet count, and causes thromboses
192
acute pyelonephritis manifestations
flank pain, fatigue, chills, fever, dysuria
193
nephrotic syndrome marked by:
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
what is nephrotic syndrome
immune response that leads to damage of the glomeruli and third spacing of fluids (fluid accumulates into the tissues rather than circulating)
195
Anasarca
weeping of the skin- protein leaking from skin
196
Diagnosing Nephrotic Syndrome
blood and urine samples (Protein)
| may order a 24-hour collection of urine
197
risk factors of renal cancer
2 X more often in men than women, cigarette smoking most common risk factor.
198
Carcinomas
Cancers that begin in the skin or in the tissue that line or cover internal organs
199
Sarcomas
Start in the connective tissue including bones, cartilage, tendons, and fibrous tissue
200
Leukemia
Bone marrow makes too many white blood cells, and they do not form correctly, but continue to build up in the blood
201
Lymphomas and Myelomas
cancer in the lymphatic system – system that filters bodily fluid and fights infection
202
Melanoma
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
Pancreatic Cancer common causes
Diabetics
Chronic pancreatitis
Smokers
204
Clinical manifestations of pancreatic cancer:
Clinical manifestations
Dark urine & clay stools
Fatigue & weakness
Jaundice
205
TNM staging system
T - tumor
N - nodes
M - metastasis
Once staging is complete is does NOT change
206
flare reaction
distinguishable from extravasation by lack of pain or swelling, presence of good blood return
207
nadir
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
life span of a neutrophil
7-12 hours
209
life span of platelets
7-8 days
210
life span of erythrocytes
90-120 days
211
mild neutropenic absolute neutrophil count
1000-1500
212
moderate neutropenic absolute neutrophil count
500-1000
213
severe neutropenic absolute neutrophil count
0-500
214
how to calculate Absolute Neutrophil Count (ANC)
ANC = Total WBC × (% Segmented Neutrophils + % Bands)
215
what meds can we give a chemo patient for infection prevention
colony-stimulating factors - Neupogen and Neulasta
216
both UC and Crohn's are characterized by
chronic inflammation of the intestine w/ periods of remission & exacerbation
217
UC
inflammation beginning in the rectum and spreading up the COLON (only) in a continuous pattern
218
crohns
Can affect any part of the GI tract from the lips to the anus
Most often seen in the terminal ileum and colon
219
Hallmark sign of crohns
skip lesions: Segments of normal bowel occurring between diseased portions causing classic cobblestone appearance
220
fistulas are seen more in
crohns - leaks out all the way to skin
221
nutrition with UC/Crohns
```
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
drugs for UC/Crohns
Aminosalicylates, Antimicrobials, Corticosteroids, Immunosuppressants, Biologic therapy, Antidepressants
223
Solid organs
liver, spleen, kidneys and pancreas; bleed profusely
224
Hollow organs
stomach, intestines, bladder, gallbladder; peritonitis/sepsis leakage after injury
225
most common cause of blunt abdominal trauma
MVCs
226
hollow organs can collapse
and absorb force
227
Cullen’s Sign
bruising around the umbilicus - Intra-peritoneal hemorrhage
228
Grey Turner’s sign
flanks- Retro-peritoneal hemorrhage
229
what is used with ABD trauma in rural areas when CT is not available
Diagnostic Peritoneal Lavage DPL - old technique
230
Intra-abdominal pressure (IAP) in a normal adult
0-5
| elevation in IAP ≥ 12 mmHg = hypertension (IAH)
231
What does abdominal compartment syndrome (ACS) mean for your patient?
```
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
Gold standard for intra-abdominal indirect intermittent pressures
Urinary bladder pressure monitoring
| Utilizes a foley catheter for monitoring
233
Most common prognostic systems Acute Pancreatitis
Ranson’s Criteria - Estimating the severity of acute pancreatitis
234
Acute pancreatitis causes
Most Common (80% of cases):
Gallbladder Disease
Excessive ETOH
235
labs for Acute pancreatitis
```
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
Collaborative Management for Acute Pancreatitis
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
Classic triad of chronic pancreatitis
calcification, steatorrhea, and diabetes
| history of heavy ETOH use
238
gold standard for dx for chronic pancreatitis
Surgical biopsy of pancreas
239
Anticipate medications for GI bleed
```
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
acute liver failure causes
```
Drugs are #1 cause
#1: Tylenol (acetaminophen), NSAIDs (all types), INH, mushrooms
#2: Hepatitis B & C
```
241
outcomes for acute liver failure
75 - 90% DIE!; 10-25% “SURVIVE”…W/ INTENSIVE CARE!
| NEED A LIVER
242
Collaborative CareAcute Liver Failure
Lower the AMMONIA LEVEL!
Neomycin, metronidazole, rifaximin or LACTULOSE (gold standard)
Correction of coagulopathies: best through PREVENTION!
243
TIPS
Trans jugular intrahepatic porto systemic shunt
| Manage complications of portal HTN
244
Bariatric Surgery
```
to qualify: BMI>40 or >35 with comorbidities
5+ years
Understand risks/benefits
Tried and failed at weight loss
No serious endocrine disorders
```
245
Restrictive bariatric Surgeries
gastric banding - ↓ stomach to 30 mL, feeling fuller faster
246
malabsorption bariatric surgeries
Various lengths of the small intestine bypassed ↓ absorption of nutrients
Less food is absorbed – DOES alter digestion
247
Roux-en-Y Gastric bypass
```
Stomach size is ↓ w/ gastric pouch
Most common bariatric procedure in US
Considered gold standard
Low complication rates
Excellent patient tolerance
```
248
Preoperative Concerns with bariatric surgeries
Liquid Diet for up to 6 wks preop
| Detailed health hx, address comorbidities
249
post op complications in bariatric surgeries
Dehiscence or leaking
- First sign is tachycardia
Anemia: malabsorption of Iron and Vit B
Increased risk of Infection
250
Nutritional Goals: after bariatric surgery
```
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
```
