Pharm2 -FINAL- EXAM OF MY LIFE Flashcards
Phenytoin (6 - TCIA sfx I) Trade Name Class Indications Action S/Fx Implementation
Dilantin Anti-arrythmic/convulsive Seizures r/t Digoxin toxicity ↓ seizures by infl. ion transport ↓ CNS, ↓BP, bleeding gums Seizure precautions, HypoTN
Naloxone (6 TCIAsfxI)
Narcan Opiod Agonist Opiod OD Competitively blocks opiod receptors Ventricular arrhythmias, N/V Pain management r/t opioid antagonism
Morphine (6 TCIAsfxI) + COUNTER
none Opiod Pain Opiate receptor agonist and ↓ CNS Respiratory depression, constipation, ↓LoC, HypoTN Monitor LoC, RR, GI, BP
COUNTER with Naloxone
Flumazenil (6 TCIAsfxI)
Romazicon Benzo antagonist Benzo antagonist Reverses fx of benzodiazepines Seizures, N/V Seizure precautions, amnesia
Haloperidol (6 TCIAsfxI)
Haldol
Anti-psychotic
Schizo, manic, psychoses, agitation
Block dopa. receptors in brain… also anticholi and anti-hista.
EPS (Extra Pyrimidal S/S such as dystonia, akathsia, tardiv dyskinesia), blurred vision, constipation, dry mouth
Monitor EPS, oral care, Ø EtoH
Phenylephrine (6 TCIAsfxI)
Neo-Synepherine Adrenergic-Agonist, vasopressor HypoHTN r/t shock or anesthesia Constricts blood vessels, stimulating alpha adrenergic receptors r/in vaso-constriction Altered CNS, arrhythmias, dyspnea Monitor BP and EKG for arrhythmias
Nitroprusside (6 TCIAsfxI)
Nipride Vasodilator HTN crisis, cardiogenic shock Peripheral vasodilation Diziness, H/A, Abd. pain, N/V Monitor for HypoTN, cyanide and thiocyanate toxicity
Midazolam (6 TCIAsfxI) + COUNTER
Versed Benzodiazepine Sedation and amnesia for procedures, seizures General CNS Depression ↓ LoC, Respiratory Depression N/V Educate on amnesia fx
COUNTER with Flumazenil
Methylprednisol (6 TCIAsfxI)
Solumedrol
Steroid
Allergic/Inflammatory Dz
Supresses inflammatory and normal immune response
Altered mental status, HTN, acne, muscle wasting, osteoporosis, Cushings dz s/s
Monitor glucose, GI bleeds, immunosuppression
Propofol (6 TCIAsfxI)
Diprivan
Anesthetic
Procedures, intubation, sedation and anesthesia
Hypnotic + some amnesia
Bradicardia, HypoHTN, burning @ site
Propofol infusion syndrome (↑K, ↑TriGlys, ↑ liver size)
Assess CNS fx and level via Richmond Agitation Sedation Scale (RASS)
Mannitol (6 TCIAsfxI)
Osmitrol
Osmotic Diuretic
Acute renal failure, edema, ICP, IOP
↓ re-absorption @ kidneys
Confusion, chest pain, dehydration, electro imbas
Monitor extravasation, urine output 30 - 50 mL/hr
Vasopressin (6 TCIAsfxI)
Hormone (ADH) Deficient ADH, vasodilatory shock, GI hemorrhage ↑ re-absorption @ kidneys GI distress, angina, dizziness Water intoxication
Gabapentin (6 TCIAsfxI)
Neurontin
Analgesic adjunct/Anti-convulsant
Neuralgia, bipolar, anxiety, neuropathy
↓ pain, migraines r/t nerve generated pain
↓ LoC, depression, ataxia
Withdrawal crisis, wean off, monitor for SI (Self-Injury)
Manifestations of Severe Acute Respiratory Syndrome (SARS) (8) + Diagnose with…?
Similar to respiratory infx Fever > 100.4F, or > 38C HA General Body Ache Cold symptoms Within 2 - 7 days dry cough/difficulty breathing Hypoxia, low O2sat, breathlessness X-rays show pattern similar to PNA Manifestations + Rapid SARS test that detects SARS-CoV RNA in blood after 2 days S/S begin
Treatment of Sepsis (2)
Fluid resuscitation for hypovolemic + distributive shock
(begin immediately to pts with serum lactate levels > 2)
Early initiation of Broad Spectrum Antibiotics/Antifungals
Antibiotic/Fungal Types and Respective Therapy (4)
Chemotherapy/GI flora organisms (Gram negative) tx with aminoglycosides and cephalosporins cefazolin (Ancef) and ceftizoxime (Cefozox)
Indwelling Catheter-Staph tx with vancyomycin
Oral infx (strept/candida) tx with nystatin
Aspiration PNA - tx with clindamycin
Stages of Acute Respiratory Distress Syndrome (ARDS) (3 and length)
Exudative Phase ( 1 - 3 days )
Fibroproliferative ( 3 - 7 days )
Repair and Recovery ( up to 6 months )
ARDS is characterized by (4) Criteria for Diagnosis
–Characterized by bilateral pulmonary infiltrates in X-ray
–Acute Onset
–PAWP/PCWP 18 mm Hg less with NO CHF
PAWP - pulmonary artery wedge pressure
PCWP - pulmonary capillary wedge pressure
–PaO2/FiO2 ratio less than 200 mm Hg
ARDS Pathophysiological Results (3)
Inflammatory Injury
Pulmonary/Alveolar Epithelium disrupted, r/in fluid in pulmonary interstitial space, r/in pulmonary edema
Inflammatory response in pulmonary vasculature r/t injury
ARDS S/S (7)
Initial injury r/in inflammation/infx (PNA -> sepsis) Cough w/ sputum HypoHTN Dyspnea Hypoxemia (shock!) Similar to CHF, use CXR to differentiate Respiratory Alkalosis
ARDS Exudative Phase (length + 3)
1 - 3 days
Diffuse microvascular injury and alveolar damage
Invasion of imflammatory cells into interstitium
Development of Hyaline membranes in alveolar spaces (Ø surfactant r/in difficulty breathing)
ARDS Fibroproliferative phase (length + 2)
3 - 7 days
Lung repair period
Recovery dependent on severity and influence of other factors
ARDS Repair and Recovery Phase (length + 3)
up to 6 months
Return to normal compliance/gas exchange
Permanent dmg to lung architecture
Reduced quality of life throughout recovery
ARDS treatment (5) + THE CAUSE OF IT ALL?!
Tx underlying cause (sepsis, PNA, burns, trauma, etc)
Vent with PEEP (Positive End Expiratory Pressure) to keep alveoli inflated
Fluid management (diuretics or restriction)
Anti-inflammatories to ↓ response in vasculature
Nitric Oxide ↑ blood flow to vasculature
NEUTROPHILS!
Cause of Pulmonary Edema r/t ARDS
injury + inflammatory response r/in leaky vessels which leaks into pulmonary interstitial space r/in pulmonary edema
5 Predisposing Factors of ARDS
Sepsis, pneumonia
Trauma, burns, chemical inhalation
Types of Sedation (4)
Light
Moderate (Conscious, Procedural)
Deep
General Anesthesia
Light Sedation (2)
Normal response to verbal commands
Cognition impaired but ventilation/CV fx unaffected
Moderate (Conscious, Procedural) Sedation (3)
Depressed LoC, pt responds to verbal commands
Ventilation/CV tx not needed
Deep Sedation (2)
Depressed LoC, not easy to awake (req. repeated/painful stimuli)
Impaired spontaneous ventilation, requires airway management… but CV fx usually adequate
General Anesthesia (2)
Unarousable even to painful stimuli
Impaired spontaneous ventilation and req. management (possible mechanical ventilation), CV function may be impaired
Lab Values r/t Obstructive Sleep Disorders (4) Breathing HH SpO2? ABGs (3)
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
Burn Initial Shift (time + 3)
first 24 hours
3rd spacing occurs r/in ↑ HH
↓ Na due to third spacing
↑ K due to cell destruction
Burn Fluid Remobilization (time + 4)
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)
Burn Fluid Resuscitation Notes (6)
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)
Parkland Formula (5)
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!!!
Types of Burns (5)
Exposure to heat, thermal burn Extreme cold Caustic Chemicals, Chemical Burns Radiation Electric Current, Electric Burns
Exposure to Heat, Thermal Burn (Cause, Reaction, Result)
Exposure to flame/hot object
Microvascular inflammatory response
Burn edema, burn shock
Extreme Cold Burn (Cause, Reaction, Result)
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.
Caustic Chemicals, Chemical Burns (Cause, Reaction, Result)
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
Radiation Burns (Cause, Reaction, Result)
Radiant Energy being transferred to body
Bad for skin, blood vessels, intestinal lining, and bone marrow
Production of cellular toxins
Electric Current, Electrical Burns (Cause, Reaction, Result)
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.
Burn Depths (5)
Superficial Superficial Partial Deep Partial Full-Thickness Subdermal
Superficial Burn (5)
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
Superficial Partial Burn (6)
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
Deep Partial Burn (8)
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
Full Thickness Burn (8)
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
Subdermal Burn (4)
epidermis, dermis, SQ, muscle, tendon/bone
electricity or prolonged contact
charred, dry
REQUIRES skin grafting, flap, or amputation
Progression of Shock (4 Stages + Description)
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
Commonality between shocks Hypovolemic (1) ♥ Related (2) Distributive (3) Transport Shock (1)
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)
Burn shock types (3), Tx (3), and End point
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)
Fluid shift during Burns (2 routes)
instravascular to interstitial spaces and evaporation can result in a Hypervolemic state.
Burn shock is proportinal to…?
Extent and depth of injury
40% TBSA?
Great risk of death
Chemical and Vasoactive Mediators Cause and 2 Fx
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
Positioning of a pt with a brain injury (5)
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
2 Types of Posturing and indications of…
Decorticate (Flexor) - Arms like C’s, cervical spinal tract or cerebral hemisphere
Decerebrate (Extensor) - Arms like E’s, midbrain or Pons
What is Cerebral Perfusion Pressure (CPP)
Formula to determine
Normal Range (+3 notes)
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
Lower Motor Neuron SCI’s (Spinal Cord Injuries) (2)
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
Complete SCI’s meaning and 2 Types
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
Incomplete SCI’s meaning and 3 Types
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.
Secondary SCI’s meaning and 3 Types
24 hr period following injury that contributes to neural fx loss
Ischemia
Elevated Intracellular Calcium
Inflammatory Process
2ndary SCI Ischemia 4 Fx
↓ blood flow to spinal cord
↓ blow flow in thrombi
edema r/in ↓ perfusion
vasoconstrictive substances ↓ circulation
2ndary SCI Elevated Intracellular Calcium 4 Fx
Calcium accumulates at site of injury, breaks down protein & phospholipids
Ions ↑ inflammatory response
cell membrane is damaged, neuronal death occurs
2ndary SCI Inflammatory Process 3 Fx
leukocytes infiltrate injured area
Edema forms and ↓ blood supply, this also prevents assessment of extent of injury until it is resolved
3 Ways to Prevent 2ndary SCI’s
Administration of methylprednisolone
Surgical interventions: decompression/stabilization
Manual immobilization
3 Types of Shock r/t SCI’s
Spinal Cord
Neurogenic
Hemorrhagic
Spinal Cord Shock (5)
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
Neurogenic Shock (3)
HypoHTN, bradycardia, and peripheral vasodilation
8 ways to Tx a SCI patient
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
Tx a SCI patient (5 Medications)
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)
S/S of autonomic dysreflexia “hyperreflexia” (8)
Over distended bowel/bladder Stimulation of Skin Pain HTN Bradycardia Sudden onset throbbing headache Nasal Congestion Nausea
