MED surg1 Flashcards by Stephanie Martin

Acute pain responses

Increased HR, Increased BP, Increased RR, dilated pupils, sweating

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Assessing pain approach. (PQRSTU)

Precipitating or palliative, Quality or quantity, region or radiation, severity scale, timing, understudying

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Caused by damage to somatic or visceral tissue, activating peripheral —–; GENERALLY responsive to NSAIDs and opioids

Nociceptive Pain

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Type of pain; deep, aching, throbbing, well localized; arises from bone, joint, muscle, skin, or CT

Somatic Pain

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Type of pain; from stimuli such as tumor involvement or obstruction; arises from internal organs

Visceral Pain

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Type of pain; caused by damage to peripheral nerves or CNS, results in abnormal processing of stimuli; burning, numbing, shooting, stabbing, or itchy sensation

Neuropathic Pain

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What are the 3 drug groups?

Non-opioids, opioids, adjuvants

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Used for mild pain; acetaminophen, aspirin, NSAIDs; lack of ability to produce tolerance or dependence, available without prescription

Non-Opioids

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Common side effects of NSAIDs

Bleeding tendencies, GI ulcers and bleeding, renal and CNS dysfunction

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Strongest analgesics, inhibit transmission of nociceptive input from periphery to CNS; pure agonists; morphine (MS contin), oxycodone (Oxycontin), methadone, codeine. Used for mod-severe pain

Opioids

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Common side effects of Opioids

sedation, respiratory depression, constipation, nausea, vomiting, pruritus

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used for antidepressants, anticonvulsants, alpha-adrenergic agonists, corticosteriods (neuropathic pain)

Adjuvants

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Level 1 (1-3)

Use non-opioids

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Level 2 (4-6)

Use weak opioids alone or with adjuvant

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Level 3 (7-10)

Use strong opioids

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4,500-11,000/mm3

Leukocytes (WBCs)

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3 Granulocytes

Neutrophils, Eosinophils, Basophils

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3 Agranulocytes

Lymphocytes, Monocytes, Bands or stabs

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Positively charged CATIONS from ECF (3)

Sodium, calcium, magnesium

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Negatively charged ANIONS from ECF (2)

Chloride, Bicarbonate

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135-145 mEq/L

Sodium

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3.5-5.5 mEq/L

Potassium

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8.5-10.5 mg/dL

Calcium

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3-4.5mg/dL

Phosphorus

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1.6-2.6mg/dL

Magnesium

Helps regulate osmolarity, maintains concentration and volume of ECF, generation and transmission of nerve impulses, acid-base balance, regulates water balance (water follows this)

Sodium

Hyponatremia is less than? caused by? watch for?

Less than 135 Causes: Increased loss of sodium, too much water Watch: mental status changes and seizures (below 125); do not correct too quickly (brain damage)

Hypernatremia is more than? causes? give what?

Above 145 Causes: diabetes insipidus, low water intake or excessive loss of water Give: hypotonic fluids, oral care important (dry mouth)

Transmission and conduction of nerve impulses, normal cardiac rhythms, skeletal and smooth muscle contraction, metabolic functions, acid-base balance

Potassium

Hypokalemia is less than? results in? watch for? treatment? | RESPIRATORY ALKALOSIS via hyperventilation

less than 3.5 Results: severe vomiting, diarrhea, arrhthmias, tachy, thready pulse Watch: ECG changes Tx: IV (MUST DILUTE)

Hyperkalemia is more than? causes? tx?

Above 5.5 Causes: Kidney impairment, METABOLIC ACIDOSIS, muscle twitching, low BP, dysrhythmias, abdominal cramping, diarrhea Tx: Kayexalate (secreted in stool), IV insulin, dialysis if high

Transmission of nerve impulses, myocardial contractions, blood clotting, forming teeth and bone, muscle contractions- most found in skeletal system

Calcium

give patients their own blood through preoperative donation; typically coordinated in setting of a pre-arranged, elective surgery, when physician anticipates a need for post-operative blood transfusion

Autologous Blood

“donor directed”; blood source is from an individual designated by a patient or a patient’s family, who is interested in donating blood for the patient -Bank blood: donated by general public

Donor Specific Blood

Used in a hemorrhage situation to replanish both the volume and the oxygen-carrying capacity of the circulatory system; treats decreased hemoglobin and hematocrit levels with hypovolemia

Whole blood

Given when decreased hemoglobin and hematocrit levels accompany a normal blood volume.

Packed red blood cells

For patients previously sensitized to transfusions. Blood is rinsed with a special solution that removes white blood cells and plasma proteins, thus decreasing the chance of a transfusion reaction. Typically contains approximately 250 mL of volume.

Washed packed red blood cells

Similar to PRBCs combined with the removal of approximately 95- 99% of the leukocytes. The removal of leukocytes helps to prevent a febrile reaction from leukocyte antibodies. Typically contains approximately 200 mL of volume.

Leukocyte-poor red blood cells

Universal Donor

O negative

Universal recipient

AB positive

Classic triad of chills, flank pain, and blood stained urine

Acute Hemolytic Reaction

Mild fever, jaundice and decreased post transfusion hematocrit

Delayed Hemolytic Reaction

Fever, chills, flushing, nausea most common type

Febrile non-hemolytic reaction

lack of fever, urticaria, dyspnea, chest tightness and hypotension, decreased oxygen saturation

Anaphylactic reaction

Fever or hypothermia, chills or rigors, abdominal pain, nausea

Bacterial Infection

concentrates intravascular space- water moves from inside to outside of cell (cell shrinks)

Hypertonic

dilutes intravascular space- water moves from outside to inside of cell (cell swells) Isotonic: same osmotic pressure as plasma- no fluid shift

Hypotonic

Most physiologically adaptable fluid, no calories To replace fluids in those who need electrolyte replacements- burn, surgery, and trauma patients, GI tract fluid losses, fistula drainage, metabolic acidosis

Lactated Ringer's

volume expanders, longer duration than crystalloids (typically several days) Treat hypoproteinemia and malnourished states

Colloids

Expensive Contraindicated in severe anemia, heart failure, sensitivity Withhold ACE inhibitors for 24 hours before administering

Albumin

nutritional support with glucose, protein, vitamins, electrolytes, elements, and sometimes fat

TPN: Total parenteral nutrition

Common symptoms of respiratory

dyspnea, cough, wheeze, chest pain

most important symptoms of respiratory insufficiency

Dyspnea

Chest pain- if respiratory

DOES NOT radiate, tenderness on palpation

Earliest sign of hypoxia

Mental status changes

Respiratory assessment

IPPA

7.35-7.45

80-100

PaO2

35-45

PaCO2

22-26

HCO3

Low pH

Acidic

High pH

Basic

CO2 Below 35=? Above 45=?

Below 35=alkalotic | Above 45=acidic

HCO3 Below 22=? Above 26=?

Below 22=acidic | Above 26=alkalotic

Hyperventilating is blowing off CO2=

Alkalosis (less acid available)

respiratory alkalosis=?

hyperventilation

COPD (retain CO2)=

acidosis

respiratory acidosis=

hypoventilation

Respiratory system can change in -- to --; metabolic system takes -- to -- to compensate

15-30min | hours- days

common cold: spread by droplets or direct hand contact Irritation/ sneezing/ nasal secretions, obstruction/ elevated temp/ malaise/ headache More common in winter

Acute viral rhinitis

Management of what?: rest, fluids, antihistamine/decongestant, antipyretics, analgesics Avoid crowds, wash hands frequently, avoid hand to face contact, intranasal decongestant no more than 3 days

Acute viral rhinitis

inflammation or hypertrophy of mucosa, secretion build up Sinus pain/ headaches/ nasal drainage, obstruction/ congestion/ fever/ malaise Management: control allergies/asthma, increase fluids, nasal irrigation Antibiotics to treat infection if it persists longer than 7 days without treatment 1st choice- amoxicillin (10-14 days) 2nd choice- bactrim or erythromycin Oral or topical decongestants, nasal corticosteroids, antihistamines

Sinusitis

70% is viral Scratchy throat, pain while swallowing, red and edematous pharynx Management: increase fluid intake Strep- antibiotics; candida- mycostatin (swish and swallow

Acute Pharyngitis

complication of acute pharyngitis or acute tonsillitis Tonsils enlarged, high fever, leukocytosis, “hot potato voice,” chills Management: emergency tonsillectomy

Peritonsillar Abscess

inflammation of larynx Hoarseness, S&S of upper respiratory tract infection Antibiotics if bacterial infection, voice rest, increase intake of cool liquids, use humidifier

Laryngitis

nosebleed Sneeze with mouth open, monitor respiratory status Avoid vigorous nose blowing, lifting, strenuous activity, aspirin, and NSAIDs Posterior nasal bleeding= emergency

Epistaxis

on vocal cords from vocal abuse or irritation Hoarseness Voice rest and adequate hydration

Laryngeal polyps

Acute or chronic infection of one or both lungs | High risk: very young, very old, immunocompromised

Pneumonia

How to assess for pneumonia

Assessment: fever, chills, sweats, cough (with or without sputum), pleuritic chest pain, dyspnea, RR>20, temp>37.8 (100.0), tachycardia, crackles

Prevention of pneumonia

Prevention: handwashing, balanced diet, rest, exercise, avoid smoking, good oral care, vaccines + incentive spirometry, coughing and deep breathing, ambulate, oral hygiene, adequate hydration, elevate head of bed 30-45 degrees with enteral feedings

Risk factor in 80-90% of cases= smoking 90% originate from epithelium of bronchus Takes 8-10 years for tumor to reach 1cm (smallest lesion detectable on x-ray) Non-small cell lung cancer- 20%; small cell lung caner- 80% Goals: effective breathing pattern, adequate airway clearance, adequate oxygenation of tissues, minimal to no pain, realistic attitude toward treatment and prognosis

Lung Cancer

most common injury from blunt trauma (ribs 5-10 most common) Pain during inspiration and coughing- does not take deep breaths so risk for atelectasis and pneumonia Treatment: NSAIDs, opioids, nerve block agents

Fractured Ribs

fracture of 2 or more ribs in 2 or more locations Chest wall doesn’t provide structural support- crepitus near rib fractures Prevents adequate ventilation of lung and increases work of breathing Treatment: airway management, adequate ventilation, oxygen, pain control, reexpand lung

Flail Chest

accumulation of fluid in alveoli and interstitial spaces of lungs Complication of heart and lung diseases; left sided heart failure= most common cause Emergency

Pulmonary edema

chronic dilation of bronchioles (acquired or congenital) | Increased mucus formation, dyspnea, crackles at bases of lungs, hypoxemia, hemoptysis

Bronchiolectasis

cavity in lung parenchyma containing purulent material; formed by necrosis of lung tissue Oral care important

Lung abscess

inhalation of fungal spores; not transmitted person to person S&S similar to pneumonia Treatment: oral antifungals, amphotericin B, IV fluconazole

Pulmonary fungal infections

Chronic inflammatory disorder of airways; not a progressive disease Wheezing, expiration may be prolonged, difficulty breathing, chest tightness, cough, tachycardia, cyanosis, hyperexpansion of thorax

Asthma

Medications for asthma

start with SABA as needed for symptoms SABA: short acting beta2-agonists- quick relief, not long term control LABA: long acting beta2-agonists- not for acute symptoms or exacerbations ICS: inhaled corticosteroid- long term therapy, daily, rinse mouth and spit after use Oral systemic corticosteroid- acute exacerbations, not long term control

Autosomal recessive Chronic, progressive disease- moves from small to larger airways and leads to lung destruction Affects exocrine mucus-producing glands (median survival age= 31) Purulent secretions (bronchial plugging), inflammation (bronchial wall thickening), mucus dehydrated (air trapping and hyperinflation of lungs), productive cough, wheezing, dyspnea, recurrent infections, bronchiectasis (dilation and destruction), infiltrates, scarring on chest x-ray Promote clearance of secretions, control lung infections, and provide adequate nutrition Treatment: mucomyst; lung transplant only for advanced disease

Cystic Fibrosis

Droplet contact and inhalation of aerosolized particles Pneumonia is common complication Increase fluid intake, good nutrition/ hand hygiene/ analgesic and antipyretics/ bedrest

Influenza

amount myocardial fibers are stretched before contraction- determined by amount of volume at end of diastole

Preload

amount of pressure ventricle must generate to push its contents into circulation Ejection fraction: % of blood emptied from ventricle (60-70% normal)

Afterload

Less than 200 mg/dL

Cholesterol (total)

less than 100 mg/dL

LDL

greater than 60 mg/dL

HDL

less than 150 mg/dL

Triglycerides

Male: 40-54%; Female: 38-47%

Hematocrit

Male: 14-18 g/dL; Female: 12-16 g/dL

Hemoglobin

150,000-300,000/ mcg

Platelets

5,000-10,000 mcg

WBCs

10-13.4 sec

60-70 sec

PTT

30-40 sec

aPTT

less than 2 (if not on warfarin)

INR

fatty streaks of arterial wall progress to hard fatty plaques that narrow lumen

Atherosclerosis

CAD risk factors

hyperlipidemia, hypertension, smoking, DM, obesity, sedentary lifestyle, male

: ischemia due to coronary artery spasms

Prinzmetal's variant

Medications to prevent angina

nitrates, beta-blockers, calium channel blockers

medications to precent MI and death

antiplatelets, ACE inhibitors, lipid lowering agents, aspirin helps relieve pain and thrombus formation

performed during heart cath, stent used to keep vessel open and prevent re-stenosis, usually on long-term aspirin

Percutaneous transluminal coronary angioplasty (PTCA)

Ranges from unstable angina to acute MI | Disruption of atherosclerotic plaque and formation of thrombus→ severe or complete obstruction of artery

acute coronary syndrome

NSTEMI, unstable angina

Partially occluded

STEMI

fully occluded

Greatest danger period for sudden cardiac death?

24 hours after MI

Treatment for MI: MONA

Morphine, oxygen, nitrate, aspirin

Infection of inner layer of heart Subacute: preexisting valve disease, caused by enterococci Acute: healthy valves, rapid onset Fever occurs in 90% of patients Splinter hemorrhages in nail beds, petechiae, Osler’s nodes (fingers and toes), Janeway’s lesions (palms or soles), Roth’s spots, murmur, dyspnea on exertion, dysrhythmias, tachycardia, diaphoresis, positive blood cultures, increased ESR and cardiac enzymes Antibiotics; accurate identification of infecting organism is key to successful treatment

Infective endocarditis

inflammation of pericardial sac; cause usually unknown Progressive severe chest pain (pleuritic in nature), pericardial friction rub ECG abnormalities in 90% of patients

Acute Pericarditis

accumulation of excess fluid in pericardium

Pericardial effusion

develops as pericardial effusion increases in volume, increasing pressure on heart- chest pain, anxious, confusion, restless, decreased cardiac output, muffled heart sounds, narrowed pulse pressure, JVD, pulsus paradoxus Antibiotics for bacterial pericarditis; NSAIDs for pain and inflammation; corticosteroids

Cardiac Tamponade

results from scarring with loss of elasticity of pericardial sac Begins with acute pericarditis, characterized by fibrin deposition with undetected pericardial effusion Dyspnea on exertion, peripheral edema, ascites, weight loss, JVD, pericardial knock on auscultation Treatment of choice: pericardiectomy

Chronic constrictive pericarditis

inflammation of myocardium; frequently associated with pericarditis Infection of myocytes causes cellular damage and necrosis; results in cardiac dysfunction Treatment: digoxin- improves myocardial contractility and reduces ventricular rate; ACE inhibitors and beta-blockers- if heart is enlarged or for HF; diuretics- reduce fluid volume and preload; anticoagulation therapy; immunosuppressive therapy; oxygen

Myocarditis

acute, inflammatory disease of heart potentially involving all layers Occurs 2-3 weeks after group A strep pharyngitis- affects heart, skin, joints, CNS

Rheumatic Fever

chronic condition and complication resulting from rheumatic fever→ scarring and deformity of heart valves Antibiotics- only get rid of any existing group A strep bacteria left; anti-inflammatory agents- NSAIDs, corticosteroids, salicylates Early detection and treatment of group A strep→ penicillin

Rheumatic heart disease

valve orifice restricted, forward blood flow impeded, pressure gradient created across open valve; type of valvular heart disease

Stenosis

incomplete closure of valve leaflets, results in backward flow of blood Occur in children and adolescents from congenital conditions and in adults from CV disease

Type of valvular heart disease; Regurgitation

majority of adult cases from rheumatic heart disease | Scarring of valve leaflets and chordae tendineae

Mitral valve stenosis

majority of cases attributed to MI (MI with left ventricular failure increases risk for rupture of chordae tendineae and acute MR) Thready peripheral pulses, cool and clammy extremities, weakness, fatigue, palpitations, dyspnea, orthopnea, peripheral edema Audible S3

Mitral valve regurgitation

most common form of valvular heart disease in the U.S. Unknown cause, most patients asymptomatic for life Late or holosystolic murmur, dysrhythmias, palpitations, dizziness, light-headedness B-adrenergic blockers to control palpitations and chest pain Stay hydrated, exercise regularly, avoid caffeine

Mitral valve prolapse

usually discovered in childhood, adolescence, or young adulthood; could result from rheumatic fever later in life Left ventricular hypertrophy, decreased cardiac output, pulmonary hypertension Angina, syncope, exertional dyspnea→ left ventricular failure Nitroglycerin contraindicated because it reduces preload Diminished or absent second heart sound

Aortic valve stenosis

retrograde blood flow from ascending aorta to left ventricle → volume overload Pulmonary hypertension, right ventricular failure, myocardial contractility declines, “water-hammer” pulse Soft or absent S1, presence of S3 and S4, diastolic murmur

Aortic valve regurgitation

associated with rheumatic mitral stenosis, IV drug abusers, dopamine agonists Right atrial enlargement

Tricuspid valve stenosis

backward flow of blood from right ventricle; congenital | Right ventricle hypertension and hypertrophy

Pulmonic valve stenosis

Drug therapy to treat/control HF?

digitalis, vasodilators, diuretics, beta-blockers, anticoagulants, antidysrhythmics, low sodium diet

3rd most common cause of death in U.S. and Canada

Stroke

Transient ischemic attack: transient episode of neurologic dysfunction without acute infarction of the brain, symptoms last

Ischemic

bleeding within brain caused by rupture of vessel, hypertension is most important cause, during periods of activity

Intracerebral hemorrhage

more likely to result in memory problems related to language

Left-brain stroke

more likely to cause problems in spatial-perceptual orientation

Right-brain stroke

Difficulty in judging position, distance, and movement Impulsive, impatient, and denying problems related to stroke Respond best to directions given verbally Which side stroke?

Pts with stroke on right side of brain

Slower in organization and performance of tasks Impaired spatial discrimination Have fearful, anxious response to stroke Respond well to nonverbal cues Which side stroke?

Pts with stroke on left side of brain

when a group of cells has the ability to generate electrical impulse spontaneously

Automaticity

capacity of the cardiac cell to depolarize in response to electrical impulse

Excitability

ability of cardiac cells to transmit an impulse

Conductivity

ability of cardiac muscle in response to a stimulus to shorten to produce systole

Contractility

primary pacemaker of the heart, 60-100 bpm

SA node

to slow electrical impulse between atria and ventricles to give time for atria to contract and empty contents into ventricles, 40-60 bpm

AV node

continuation of AV node that allows impulses to enter into ventricles, divides into left and right bundle branches (LBB divides into 2 fascicles, RBB contains 1)

Bundle of His

P wave is what?

atrial depolarization

estimate of the amount of time it takes the impulse to travel from the SA node through the AV nodes, the bundle of His, and the main part of the left bundle branch

PR interval

ventricular depolarization Amount of time it takes for the impulse to travel from the left bundle branch and traverse the rest of the ventricle through the remainder of the conduction system

QRS complex

amount of time it takes for ventricular depolarization and repolarization

QT interval

Progressing narrowing and degeneration of arteries of neck, abdomen, and extremities Atherosclerosis= leading cause Typically appears at ages 60s to 80s, largely undiagnosed

PAD

Classic symptom of PAD

intermittent claudication

numbness or tingling in toes or feet

Paresthesia

Most serious complication of PAD

nonhealing arterial ulcers and gangrene

1st tx goal with PAD

modify CVD risk factors regardless of severity of symptomsAntiplatelet agents: aspirin (81-325 mg/day), clopidrogel (plavix) ACE inhibitors: increase peripheral blood flow, ABI, walking distance; decrease CV morbidity and mortality

chronic ischemic rest pain lasting longer than 2 weeks, arterial leg ulcers, and/or gangrene of leg

Critical limb ischemia

episodic vasospastic disorder of small cutaneous arteries (fingers and toes) Mainly in young women, response to SNS stimulation Prevention is key- keep warm, stress free Calcium channel blockers

Raynaud's Phenonmenon

often asymptomatic | Most common manifestation: deep diffuse chest pain, pain may extend to interscapular area

Thoracic aortic aneurysms