Pharm2 -FINAL- EXAM OF MY LIFE Flashcards

Question

Cause of Pulmonary Edema r/t ARDS

Answer 1

injury + inflammatory response r/in leaky vessels which leaks into pulmonary interstitial space r/in pulmonary edema

Answer 2

Sepsis, pneumonia | Trauma, burns, chemical inhalation

Answer 3

Light Moderate (Conscious, Procedural) Deep General Anesthesia

Answer 4

Normal response to verbal commands | Cognition impaired but ventilation/CV fx unaffected

Answer 5

Depressed LoC, pt responds to verbal commands | Ventilation/CV tx not needed

Answer 6

Depressed LoC, not easy to awake (req. repeated/painful stimuli) Impaired spontaneous ventilation, requires airway management... but CV fx usually adequate

Answer 7

Unarousable even to painful stimuli | Impaired spontaneous ventilation and req. management (possible mechanical ventilation), CV function may be impaired

Answer 8

``` Ø breathing for > 10 seconds Hematocrit ↑ r/t ↓ O2 (kidneys release erythropoetin in low O2 environments which ↑ RBC count to ↑ O2 capacity) Variations in SpO2 ABGs... Hypoxemia (PaO2 less than 80 mmHg) Hypercarbia (PaCO2 more than 45 mmHg) Respiratory Acidosis ```

Answer 9

first 24 hours 3rd spacing occurs r/in ↑ HH ↓ Na due to third spacing ↑ K due to cell destruction

Answer 10

48 - 72 hours ↓ Na, ↑ K ↑ WBC's r/t inflammation, then ↓ r/t left shift ABGs show hypoxemia, metabolic acidosis (r/t hypovolemia and kidney perfusion)

Answer 11

Critical during first 24 hrs to avoid burn shock Establish 2 large bore IVs Initiated in adults when >20% TBSA (Total Body Surface Area) Elderly when >5-15& Children >10-15% (more, 5.8 mL/kg/% TBSA)

Answer 12

``` 4 mL Ringer's Lactate x TBSA % x kg = total fluid to be infused in 24 hrs 1/2 is infused in first 8 hrs second 1/2 infused over next 16 hrs Ø Dextrose b/c osmotic diuretic effect RINGER'S LACTATE!!! NOT DEXTROSE!!! ```

Answer 13

``` Exposure to heat, thermal burn Extreme cold Caustic Chemicals, Chemical Burns Radiation Electric Current, Electric Burns ```

Answer 14

Exposure to flame/hot object Microvascular inflammatory response Burn edema, burn shock

Answer 15

Severe cold temperatures (frostbite) dependet on insulation, nutritional status, exertion, heat generation, alcohol, drug use. Tissue damage takes weeks to determine extent Vasoconstriction of peripheral vasculature to preserve core temperature r/in tissue freezing and death.

Answer 16

Exposure to acid, alkali, or organic substances Acid - Eschar Alkali - ↑ Tissue Damage Organic Substance - systemically absorbed r/in renal/hepatic toxicity Inhaled - lung parenchymal injury Chemicals - systemic pulmonary, CV, renal, and hepatic issues Various Results, such as hydrofluoric acid which reacts with Ca and Mg r/in arrhythmias

Answer 17

Radiant Energy being transferred to body Bad for skin, blood vessels, intestinal lining, and bone marrow Production of cellular toxins

Answer 18

Conversion of electrical activity to heat dependent on pathway/resistance Nerves/blood cells act as electrical conductors Internal damage, difficult to determine. Exit site most often foot.

Answer 19

``` Superficial Superficial Partial Deep Partial Full-Thickness Subdermal ```

Answer 20

epidermis only can be caused by sun/brief exposure to liquids erythema, pain, minimal edema Ø blisters, dry skin heals in 3 -5 days via sloughing, no scars

Answer 21

epidermis + papillary layer of dermis (superficial layer) hot liquids, brief contact with objects/flash flame erythema, brisk cap refill, blisters, moist moderate edema, VERY painful heals in 10 - 14 days via re-epitheliaization Ø scarring, but potential for hypo/hyperpigmentation

Answer 22

epidermis + reticular layer (deep) caused by flame, hot liquids/objects, radiation, tar erythematous or pale, sluggish cap refill moist or dry, Ø blisters significant edema and altered sensation heals in 2 - 3 weeks potential scarring for hypo/hyperpigmentation MAY require skin grafting for optimal fx and appearance

Answer 23

epidermis, dermis, and SQ layer nerve damage MAY, may or may not have pain flame, electricity, or chemicals dry, leathery, white Øcap refill requires skin grafting heals via contraction and granulation of tissue definite scarring and hypo/hyperpigmentation

Answer 24

epidermis, dermis, SQ, muscle, tendon/bone electricity or prolonged contact charred, dry REQUIRES skin grafting, flap, or amputation

Answer 25

Pathway/Progression - ↓ CO2, tissue perfusion, and O2 deliver to cells r/in anaerobic metabolism and lactic acidosis Compensatory - neuroendocrine responses activated to restore CO and O2 Progressive - Compensatory mechanism can't restore homeostasis (1. Major d/fx of many organisms, 2. Continues low blood flow with poor perfusion which builds metabolic wastes MODS Refractory - cell destruction so severe that death is inevitable and pt is resistant to conventional therapy

Answer 26

Commonality - ↓ oxygenation Hypovolemic - not enough blood due to bleeding, trauma, or dehydration ♥ related - 1. Cardiogenic (♥ can't pump enough to properly circulate (HF, MI, Valvular Dz)) 2. Obstructive Shock - External cause impeding pumping (tamponade, PE, pneumothorax) Distributive - 1. Septic - inflammatory response/infx dilates vessels and r/in leaking 2. Neurogenic - Ø sympathetic signalling through spinal cord r/in loss of vessel integrity/tone (High spinal cord injury) 3. Anaphylactic - immune response r/t histamine release r/in vasodilation Transport - impaired perfusion of O2 to tissues (anemia, CO poisoning)

Answer 27

Cardiogenic - ↓ CO Hypovolemic - ↓ intravascular volume Elevated Systemic Vascular Resistance Tx w/ fluid resuscitation and other shock tx (vasopressors, inotropes) Adequate urine output (signifies adequate perfusion to kidneys)

Answer 28

instravascular to interstitial spaces and evaporation can result in a Hypervolemic state.

Answer 29

Extent and depth of injury

Answer 30

Great risk of death

Answer 31

Cause arterial construction. Followed by vasodilation and ↑ capillary permeability r/in loss of capillary seal and massive fluid/electrolyte shift from intravascular space into interstitium

Answer 32

Head of bed 30 degrees (↓ ICP ↑ venous drainage from cerebral veins) Avoid head flexion, extension, rotation ( ↓ dmg from cerebral veins) Avoid hip flexion ( b/c it ↑ ICP via CSF shift) Ø Trendelenburg Consider cervical spine injury ruled out, use neck collar to keep spine straight and head midline

Answer 33

Decorticate (Flexor) - Arms like C's, cervical spinal tract or cerebral hemisphere Decerebrate (Extensor) - Arms like E's, midbrain or Pons

Answer 34

Pressure gradient necessary to supply blood to brain CPP = MAP - ICP 80 - 100 mmHg ischemia occurs at 40 - 70 mmHg MUST be > 70 mmHg for adequate oxygenation, with high ICP, goal for CPP is 80 mmHg if ICP rises to MAP level, brain perfusion stops and death occurs

Answer 35

Below L1, involving lumbar, sacral, and coccygeal nerves = "cauda equina" These are NOT considered SCI's Injuries adjaent to end of spinal cord (T11 - L1) often are a combination of upper and lower motor neuron injuries

Answer 36

Complete - loss of ALL voluntary/sensory fx below area of injury Paraplegia - in thoracolumbar (T2-L1) region, loss of motor fx in lower extremities Quadraplegia - in cervical/thoracic regions (C1-T1), impaired fx of arms, trunk, legs, and pelvic organs may occur

Answer 37

Incomplete - preservation of some sensory/motor fx below level of injury due to partial transection of spinal cord Anterior Cord Fx lot - motor, pain, temp, touch Fx present - proprioception, vibration Brown - Segard Fx lost - voluntary motor movement on side of injury, pain, temp, sensation ON OPPOSITE SIDE Fx present - side of body with best motor control has little to no sensation Central Cord Fx Lost - motor, sensory in upper extremities Fx present - motor, sensory in lower extremities, some blader and bowel fx.

Answer 38

24 hr period following injury that contributes to neural fx loss Ischemia Elevated Intracellular Calcium Inflammatory Process

Answer 39

↓ blood flow to spinal cord ↓ blow flow in thrombi edema r/in ↓ perfusion vasoconstrictive substances ↓ circulation

Answer 40

Calcium accumulates at site of injury, breaks down protein & phospholipids Ions ↑ inflammatory response cell membrane is damaged, neuronal death occurs

Answer 41

leukocytes infiltrate injured area | Edema forms and ↓ blood supply, this also prevents assessment of extent of injury until it is resolved

Answer 42

Administration of methylprednisolone Surgical interventions: decompression/stabilization Manual immobilization

Answer 43

Spinal Cord Neurogenic Hemorrhagic

Answer 44

r/in loss of ALL neurologic fx (including reflexes and rectal tone). Takes hours, days, or weeks to return Reflexes return from feet upward Bulba Caverosa Reflex - central reflex, first to return and is a sign that shock is resolving After resolved, SCI extent determined by which reflexes are intact

Answer 45

HypoHTN, bradycardia, and peripheral vasodilation

Answer 46

Immobilization used skeletal traction (Crtuchfield tongs, Halo traction) Medications Monitor Respiratory and Cardiac Status Bowel/Bladder Management Assess for skin breakdown Maintain normothermic environment Assess for S/S of autonomic dysreflexia "hyperreflexia" which are spinal lesions above T6 Surgical Inteventions: anterior cervical laminectomy with fusion or posterior laminectomy

Answer 47

Atropine for bradycardia r/t neurogenic shock Vasopressors (Dopamine) to ↑ Spinal Cord perfusion Methylprednisone Blood Transfusion - fluid resuscitation for hemorrhagic shock Darvon - H2 Agonists (Zantac, Pepcid)

Answer 48

``` Over distended bowel/bladder Stimulation of Skin Pain HTN Bradycardia Sudden onset throbbing headache Nasal Congestion Nausea ```