Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
59 Cards in this Set
- Front
- Back
|
Carbon monoxide poisoning |
Fire -increased CO2 inhaled displaces O2 on Hg -hypoxia (carboxyhemoglobinemia) *cherry red skin |
|
|
Mucosal Burns of oropharynx
|
From smoke or steam inhaled above glottis = thermal below glottis = chemical |
|
|
Burn process |
-inflammation -vasodilation -edema -decreased BP and perfusion -decreased intravascular volume -increased Hct (fluid in tissues increased [Hct] in blood *can cause burn shock |
|
|
Electrical burns can cause |
-injury - fall -dysrythmias - electrical current disrupts hearts electrical current -acidosis - inflammation caused cells to rupture releasing K into ECF -renal failure - muscle damaged released myoglobin |
|
|
Full thickness Burn |
-dry -waxy, white or black -decreased sensation |
|
|
Partial Thickness Burn |
-serous exudate -pink-cherry red -painful with exposure to air |
|
|
Risks of burns |
-infection -decreased resp function or blockage -compartment syndrome |
|
|
Burns increased damands |
-cardo system and renal system because of fluid and electrolyte shift -resp system because of obstruction or increased O2 for healing |
|
|
Phases of Burn Management |
Emergent Phase (24-48hr)
-mobilization of ECF -reestablish perfusion Acute Phase (weeks-months) -burn covered by skin graft heals Rehab Phase |
|
|
Burn immunological changes |
-inflammation impairs WBCs -decreased skin barrier = easier for pathogen to enter *infection risk |
|
|
Topical Dressing burns |
antimicrobial dressing- |
|
|
escharotomy |
-incision through necrotic tissue to resotre circulation -decreases circumfrontial pressure and increased circulation to area |
|
|
Tx for burns |
-fluid resusitation -O2 -analgesics -eteral feedings (increase calorie and protein) -reposition limbs to prevent contracture -monitor labs |
|
|
Managing airway with occlusive edema |
-intubate within 1-2 hours -extubate once edema subsides (3-6 days) |
|
|
>30% TBSA burned |
-central venous line -artery line (continuous BP and blood specs) |
|
|
Burn wound care |
-debride and then skin graft |
|
|
Why shouldn't a burn patient bathe? |
-water is hypotonic so it draws electrolytes out of fluid -cross contamination -hypothermia after bath |
|
|
IM and PO meds for burns |
IM - med pools in edema and then pt overdoses once fluid mobilizes PO - not absorbed fast enough or enough due to decreased GI perfusion |
|
|
Burns - hypermetabolic state |
Large burn -increased resting metabolic expendature -increased catecholamine -increased glucongeagenesis = increased BG - maybe needs insulin -increased protein breakdown = increased lactic acid = acidosis |
|
|
Why are burn patients at risk for contractures? |
-pain = decreased movement and flexion -scar tissue shortens tissue at joints *splints and reposition |
|
|
5 types of shock |
-cardiogenic - low blood flow
-neurogenic - maldistribution of blood -hypovolemic - low blood flow -anaphalaxis- maldistribution of blood -septis- maldistribution of blood |
|
|
Low blood flow shock main cause |
-heart failing |
|
|
Maldistribution of blood flow main cause |
-vasodilation causes fluid shift into tissues and is in the wrong place |
|
|
Cardiogenic shock |
-pump impaired -SV and CO decreased = decreased tissue perfusion -congestion of pulm vessels = pulm edema -decreased O2 in blood = decreased perfusion *heart can't pump blood out of heart so hydrostatic pressure increases |
|
|
Cardiogenic shock S/S |
-changes in LOC -confusion -cyanosis -cool and clammy skin -pallor -increased cap refill -increased GFR -decreased UO -increased RR, HR -decreased SBP -decreased Bowel sounds -N&V |
|
|
Hypovolemic shock |
-decreased venous return to heart -decreased preload -decreased SV =decreased CO = decreaed perfusion *impairs cellular metabolism |
|
|
DIC |
Disseminated Intravascular Coagulation |
|
|
DIC process |
Shock -coaggulation mechanisms enhanced -microemboli form - use up clotting factors -decreased blood flow = risk of organ failure -bleeding risk *hard to treat |
|
|
Vasodilators(drugs)
|
-excessive constriction -decreases perfusion -increased workload of heart -decreases CO and BP = decreased perfusion |
|
|
Goals for hypovolemic shock |
-fluid replacement -Tx cause |
|
|
Glucose during early and late sepsis |
early - BG is high late - BG is low |
|
|
Goals for shock |
-halt shock process -restore circulation - increase BP with fluids -correct pH imbalance |
|
|
Why might GFR decrease during shock? |
-vasodilation = decreased perfusion to kidneys -liver failure - decreased albumin = edema -microemboli(DIC) block vessels and decrease blood flow to kidneys |
|
|
SIRS |
systemic inflammatory response syndrome -inflammation = vasodilation |
|
|
Fluid resuscitation for shock
|
-hypovolemic -sepsis(corticosteroids) -anaphalaxis (epi and corticosteroids) -maybe neurogenic -may overwork the heart if HR is decreased and increase in fluids -vasocontricotrs and bolus may cause fluid overload |
|
|
Neurogenic Shock |
SCI at T5 or above (T1-T5 supply heart and blood vessels with nerves) -SNS stimulation decreased *decreased BP and HR (only form of shock where BP and HR are decreased right away) |
|
|
Anaphylactic shock |
Exposure to antigen -vasodilation -fluid moves to tissues -laryngeal edema and pulm edema (crackles) -bronchospasms (wheezes) |
|
|
Septic Shock |
-infected blood -vasodilation |
|
|
Stages of Shock |
1. Compensatory Stage -reversible stage -compensatory mechanisms effection -HR increased 2. Progressive Stage -compensatory mechanisms need more O2 - become ineffective -vital organ perfusion decreased -increased capillary permeability 3.Refractory Stage -vasoconstriction = decreased perfusion = anearobic metabolism |
|
|
vasopressors for shock |
-peripheral vasoconstriction -shunt blood to core from extremities |
|
|
Vasodilators for shock |
-decrease workload of heart = increase output |
|
|
nitrates for shock |
dilate coronary arteries and systemicly |
|
|
diuretics for shock |
-decreased preload |
|
|
Beta blockers for shock |
-inhibit SNS -decrease HR and improve contractility |
|
|
Definition of hepatitis |
inflammation of the liver |
|
|
some causes of hepatitis |
- virus - bacteria - drugs - alcohol - chemicals |
|
|
Etiology (set of causes) for types of Hepatitis
|
Hep A: from orally consuming contaminated foods, water/other drinks, blood, stool & direct contact; overcrowding/poor hygiene & risk of contamination with fecal matter (acute: 2 month incubation period) - Hep B: Blood/bodily fluids; increased risk of liver cancer or being chronic - Hep C: Blood exposure; long-term liver damage without cancer, chronic |
|
|
Signs & Symptoms of acute hepatitis |
- increased PT/INR
- Increased liver enzymes - anorexia - N/V - RUQ discomfort - fatigue - decreased albumin |
|
|
unconjugated bilirubin |
- lysed RBCs produces this - cannot be renally excreted |
|
|
conjugated bilirubin |
- by liver - may be renally excreted |
|
|
What is an optimal diet for someone with acute hepatitis? |
- increased calories - increased carbs - decreased fat (d/t lack of bile) - decreased protein - decreased alcohol (ETOH) **Also encourage +++rest for patient with acute hepatitis** |
|
|
How long until you will see detectable serum levels of hepatitis antigens & antibodies appear for diagnosis? |
2 month window period |
|
|
How does the medication lamivudine help chronic hep B patients if its chronic? |
- with someone presenting with a decrease in liver enzymes (GGT; AST; ALI), this lamivudine decreased the viral load and also helps with decreasing liver damage |
|
|
What meds are administered for chronic Hep C? |
A combination therapy of Ribavarin & Interferon |
|
|
How does alcohol abuse lead to cirrhosis and a decrease in optimal liver functioning? |
-it leads to fat deposits in the lever cells (this is reversable if pt stops using alcohol; if continued used of alcohol, cell necrosis occurs causing scar formation). -this condition leads to disorganized regeneration and decreased blood flow (which may cause hypoxia). -all this leads to a decrease in liver function |
|
|
Toxic hepatitis |
heads straight for cell necrosis, leading to disorganized regeneration and decreased blood flow, ending at a decrease in liver function |
|
|
Chronic Hep B & C |
there is chronic inflammation which leads to necrosis & fibrosis, all equaling a decrease in liver function |
|
|
Manifestations of Cirrhosis |
- due to a decreased metabolism of carbs, fats, and proteins, this leads to weight loss, decreased energy, increased serum levels of albumin and GI symtpoms (N/V, diarrhea, etc.) - the blood flow through the liver is backing up, causing a host of things to happen (portal HTN, liver & spleen enlargement - leading to RUQ pain & heavy feeling) |
|
|
Splenomegaly |
- abnormal enlargement of spleen - usually associated with portal hypertension |
