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2nd Year PCP > EMRG1305 TERM TEST 2 > Flashcards

EMRG1305 TERM TEST 2 Flashcards

1
Q

Pharmacodynamics

A

the study of the biochemical and physiological effects of drugs and their mechanisms of action (what the drug does to the body)

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2
Q

Pharmacokinetics

A

the study of how the body interacts with administered substances for the entire duration of exposure (what the body does to the drug)

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3
Q

Pharmacotherapeutics

A

the use of drugs for the prevention, treatment, diagnosis, and modification of normal functions. E.g., pregnancy prevention

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4
Q

Toxicology

A

the study of the adverse effects of chemicals or physical agents on living organisms

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5
Q

Additive effect

A

2+2=4
combining 2 meds = the sum of each
e.g., tylenol and advil

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6
Q

Antagonism

A

2+2=1
give 2 meds but it cancels each other out so it only half works

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7
Q

Potentiation

A

0+2=10
Increase strength or effect, first medication didnt do anything then the second one makes it work

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8
Q

Synergism

A

2+2=20
a+b=abcde
you get too many outcomes/side effects

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9
Q

Absorption

A

From its site of administration into the body to specific target organs and tissues. Can be through active and passive transport. Goal is to reach therapeutic concentration in blood.

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10
Q

Distribution

A

Process by which a medication moves throughout the body. Blood is primary distribution vehicle.

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11
Q

Biotransformation

A

Body metabolizes medications. Body systems create chemical alterations to create compounds that are more easily excreted from the body.

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12
Q

Excretion

A

Body eliminates the remnants of the drug. Occurs primarily through kidney.

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13
Q

Chronotropic effect

A

Changes HR

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14
Q

Inotropic effect

A

Changes the contractility of the heart.

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15
Q

Dromotropic effect

A

Affects conduction speed in the AV node, and rate of electrical impulses in the heart.

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16
Q

Beta blockers - Class 2

A

Reduces the amount of oxygen the heart needs.
B1- cardiac stimulation
B2- bronchial relaxation
Blocks the effect of epi and norepi, REDUCES HR!!!
Dilates blood vessels, REDUCES BP!!!!

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17
Q

Calcium Channel Blockers - Class 4

A

Main action is to relax smooth muscle, decreasing peripheral resistance. Typically used to treat HTN.
2 types:
- 1 localizes the smooth muscle
- 2 decreases cardiac workload, HR and cardiac contractions

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18
Q

Diuretics

A

Act on kidneys to increase diuresis. Excrete more water from the body.
Used to treat HTN, edema, renal diseases, and hepatic diseases.

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19
Q

Loop Diuretics

A

Prevents sodium, potassium, and chlorine. transports proteins in the loop of henle.
Causes reduction in the reabsorption of sodium which significantly increases diuresis.
Some pt’s may lose too much potassium so they may be on supplements.

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20
Q

Potassium Sparing Diuretic

A

Increases diuresis but without causing potassium to leave the body.

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21
Q

Thiazide Diuretics

A

Act by inhibiting NaCl reabsorption into the distal convoluted tubule of the kidney. Mainly used to treat HTN, heart failure, kidney stones and diabetes.

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22
Q

Antihyperlipidemic Agents (cholesterol meds)

A

Excessive buildup of fats can cause strokes and MI’s.
HDL (high-density lipoprotein) vs LDL (low-density lipoprotein) :
- HDL= good
- LDL= bad
Used to lower the amount of LDL in the system.

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23
Q

Antiplatelet Medication

A

Interfere with steps of clot formation. Normally platelets enter the site of injury, activated by thrombin and collagen to increase clotting. These patients bleed a lot. *ASA is not a blood thinner its an antiplatelet

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24
Q

Anti Coagulants

A

Used to make the blood less viscous (blood thinner)
Obtained by increasing the levels of antithrombin, which then prevents clotting factors.

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25
Q

Ace Inhibitors

A

Used to treat HTN.
Lowers SBP and DBP by blocking the action of Angiotensin-converting enzyme. Angiotensin II levels rise = vasoconstriction, release of epi and norepi –> HTN, increased HR, increased CO.
Ace inhibits prevent the release of angiotensin II and aldosterone. This reduces peripheral resistance and lowers BP.

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26
Q

Anti anginals

A

Used to increase blood and O2 supply to the heart while reducing the workload of the heart. Vasodilation/ reducing vasospasm.

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27
Q

Nitrates

A

Oldest class of drugs to treat angina. Dilates blood vessels and increase O2 supply to the heart. Reduces fluid backup in the ventricles, thereby reducing cardiac workload. Vasodilation.

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28
Q

Long Acting Beta Agonist and Corticosteroids

A

Taken to prevent asthma symptoms- called controllers- work by relaxing the muscles lining the airways.
Long acting beta agonists need to be used with corticosteroids
Reserved for those patients whose symptoms cannot be controlled by short acting bronchodilators. Steroids decrease inflammation.

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29
Q

Short Acting Beta Agonist

A

Prove short term rapid relief of asthma symptoms. Reverse bronchospasm and open airways. Acts on B2 cells of smooth muscle in the airways. Relaxes bronchial smooth muscle.

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30
Q

Proton Pump Inhibitors

A

Effective in treating GERD.
Decrease gastric acid levels.
Recommended to take on an empty stomach since that is when stomach acid is the lowest.

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31
Q

Histamine 2 Inhibitors

A

Most commonly used in treating GERD.
Action- histamine stimulates acid secretion in the gastric cells- by production of pepsin. (Pepsin is a digestive enzyme found in the gut.

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32
Q

Anti Nausea

A

Primary goal is to block the nausea sensation in the brain, or reduce the cause of nausea.

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33
Q

Laxatives

A

Administered to relieve constipation

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34
Q

Opioids

A

Bind to the opioid receptors found at the base of the spinal cord, brainstem, thalamus, hypothalamus, and limbic system. Have a large impact of chemoreceptors, which maintain our intrinsic drive to breathe.

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35
Q

NSAIDs

A

Have anti-inflammatory, analgesic, and antipyretic properties. Reduce production of prostaglandins- chemicals that promote inflammation, pain and fever.

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36
Q

Benzodiazepines

A

Often used to treat anxiety, slow brain activity. Depresses the limbic system- reduces emotions, anxiety, fear, panic, etc.
Works on GABA receptors in the brain, reduces neuronal excitability.

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37
Q

Antidepressants

A

TCA- tricyclic antidepressants, mostly affect norepinepherine levels.
SSRIs- selective serotonin reputake inhibitors, mostly affect serotonin levels.

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38
Q

Antipsychotics

A

Blocks levels of dopamine being secreted and absorbed by the body. At the medulla, brainstem and hypothalamus point. Cross the blood brain barrier easily.

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39
Q

Oral Diabetic Medication

A

Work by stimulating insulin release from pancreatic beta cells. Also decrease glycogenosis- process of converting glycogen to glucose.

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40
Q

Hyperthyroid meds

A

Work by depleting excess thyroid hormones.

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41
Q

Hypothyroid meds

A

Stimulates the release of TSH (thyroid stimuilating hormone)
Mimic the natural actions of the thyroid hormones produced by the body.

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42
Q

Sympathetic Nervous System

A

Responsible for the “fight or flight” response. The SNS prepares the body for physical activity and it can be stimulated by immune response.

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43
Q

Parasympathetic Nervous System

A

Responible for “rest and digest”

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44
Q

What happens to the body when the sympathetic nervous system is activated?

A

Increases cardiac output, increases RR, releases glucose, and dilates pupils. Prevents digestion and urination during emergencies.

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45
Q

What does the autonomic nervous system consist of?

A

Sympathetic and Parasympathetic Nervous systems.

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46
Q

What happens when the parasympathetic nervous system is activated?

A

Decreases HR, Decreases RR, Removes waste and stores energy, stimulates digestion.

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47
Q

Neurotransmitters

A

The body’s chemical messengers. They are molecules used by the nervous system to transmit messages between neurons, or from neurons to muscles.

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48
Q

Alpha 1 receptors

A

Vasoconstriction, increased peripheral resistance, blood pressure, and mydriasis.

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49
Q

Alpha 2 receptors

A

prevents norepherine release, prevents acetylcholine release, prevents insulin release.

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50
Q

Beta 1 receptors

A

increases HR, lipolysis, myocardial contractility, increased renin

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51
Q

Beta 2 receptors

A

Vasodilation, decreased peripheral resistance, bronchodilation, increased glycogenolysis, increased glucagon release, relaxes smooth muscle

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52
Q

Cholingergic/Anticholinesterase

A

Cholingeric toxicity is caused by medications, drugs, and substances that stimulate, enhance or momic the neurotransmitter acetylcholine, which is the primary neurotransmitter of the parasympathetic nervous system.

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53
Q

Anticholinergics

A

Block the action of acetylcholine by blocking the nicotinic and muscarinic receptors.

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54
Q

TCA’s

A

TCA’s cause a loss of vascular tone by blockage of alpha receptors, muscarinic receptors causing hot, dry skin, tachycardia and loss of bowel sounds as well as sodium channels, within the cardiac cycles. Blockage of sodium channels slows action potential within the cardiac muscle, and this cause the characteristic prolonged QT in TCA overdose. Prolonged QT occurs normally very wide QRS, and causes lethal rhythms if left untreated.

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55
Q

Sympathomimetics

A

Drugs that mimic or enhance the actions of endogenous. Catecholamines of the sympathetic nervous system. These agents are able to directly activate adrenergic receptors or to indirectly activate them by increasing norepinepherine and epinepherine.

56
Q

Epidermis

A

The outer layer of the skin, provides a waterproof barrier and contributes to skin tone.

57
Q

Dermis

A

Nerve endings, cutaneous blood vessels, sweat glands, hair follicles, sebaceous glands

58
Q

Subcutaneous layer of the skin

A

adipose tissue

59
Q

Severe burns cause?

A

Increase in capillary permeability, causing intravascular proteins and fluid to move into interstitial space, which increases edema.

60
Q

What does loss of volume cause in severe burns?

A

Decreased cardiac output, causing hypotension and end-organ failure.

61
Q

Zone of coagulation

A

Source of most damage, little to no blood flow

62
Q

Zone of stasis

A

Decreased blood flow and inflammation, necrosis can develop up to 48 hours later

63
Q

Zone of hyperemia

A

Least affected area, cells typically recover in 7-10 days.

64
Q

1st degree burns

A

Epidermis ONLY.
Skin is red
Painful
Example: sunburn

65
Q

What layers of the skin are involved in a second degree burn?

A

Epidermis and dermis

66
Q

Superficial partial-thickness burn

A

Skin is red; usually involved blisters or moisture present; painful; will heal spontaneously but may scar

67
Q

Deep partial thickness burn

A

Extends into dermis; damages hair follicle and sweat and sebaceous glands

68
Q

3rd degree burns

A

All layers of the skin are destroyed, skin white and pale, brown and leathery, or charred, no pain sensation.

69
Q

4th degree burns

A

destroys skin, plus bone tissue and tendons

70
Q

Eye burns

A

Tear ducts and eyelids lubricate the surface of the eyes

71
Q

Thermal burns

A

Caused by fire or other causes of heat injury.

72
Q

Flame burns

A

often partial or full-thickness burns; associated with trauma or inhalation injury. E.g., house fire

73
Q

Scald burns

A

Almost 2/3 of burns in children are from scalds from hot drinks/bath water. Most tend to be superficial/partial thickness.

74
Q

Contact burns

A

From prolonged contact or extremely hot object. These are common in industrial accidents or where a LOC occurred causing prolonged contact.

75
Q

Flash burns

A

Occur from explosions with no sustained fire. There is normally a single wave of heat, but in larger explosions blast injuries, fracture and internal trauma can occur.

76
Q

What types of shock can happen in patients with burns?

A

hypovolemic and distributive

77
Q

Clinical features of burn shock

A

hypovolemia, increased blood viscosity due to increased ratio of RBC to plasma, reduced cardiac output (low BP), increased HR

78
Q

Thermal inhalation burns

A

Can cause serious airway compromise, heat burns the airway tissue, infraglottic and lower airway damage, swelling due to burns in upper airway can be fatal, swelling of vocal cords can obstruct the airway completely.

79
Q

Carbon monoxide posioning

A

Should be considered when a group of people in the same place complain of nausea/headache, CO displaces oxygen from the alveolar air and the blood hemoglobin, CO binds to receptor sites on hemoglobin at least 250 times more easily than oxygen.

80
Q

What can smoke inhalation cause?

A

Thermal burns to airway, hypoxia from lack of oxygen, tissue damage and toxic effects caused by chemicals in the smoke.

81
Q

Where are chemical burns located?

A

Tend to be in deep tissue because they dont stop causing damage until they are removed completely

82
Q

Electrical burns

A

Tissue damage caused by heat from electricity following from the source of entry wound to exit wound. Cardiac arrhythmias are common.

83
Q

Rule of 9’s

A

Stomach/chest- 18%
Head- 9%
Arms- 9% each
Legs- 18% each
Back- 18%

84
Q

Parkland burn formula

A

Amount of fluid needed in first 24 hours
- 4 ml solution x body weight (kg) x percentage of body surface burned
- Half of this in the first 8 hours, second half given over next 16 hours

85
Q

Superficial Burn Management

A
  • Rarely pose a threat to life
  • Cool superficial burns well:
  • Stop burning and relieve pain
  • Do not cool whole body
86
Q

Partial Thickness Burn Management

A
  • Cool as with superficial burns
  • Elevate burned extremities if possible to reduce edema
  • Do NOT rupture blisters
  • Establish IV and administer fluids
  • Pain management
    BLS:
  • Cover with moist sterile dressing. Followed by dry sheet
  • <15% moist dressing, cover with sheet, cooling should be
    <30 min
  • > 15% dry sterile dressing
87
Q

Full- Thickness Burn Management

A
  • Pain assessment and pain management
    BLS
  • Dry dressings
88
Q

Chemical Burn Management

A
  • Immediately flush exposed areas with copious quantities of water
  • Remove patients clothing
89
Q

Electrical Burn Management

A
  • Majority of damage will be internal
  • Start CPR, open airway, attach monitor
90
Q

Lightning-Related Injury Management

A
  • Patients with cardiac arrest caused by a lightning strike require aggressive, continuing CPR
91
Q

Radiation Burn Management

A
  • Consider whether the patient is contaminated with radioactive material
  • Irrigate open wounds gently to avoid further damage
92
Q

Submersion

A

The act of being completely covered by a liquid

93
Q

Immersion

A

Being partly covered by a liquid

94
Q

How long do victims take to lose consciousness when drowning?

A

within 2 minutes

95
Q

What happens prior to LOC in drowning?

A

Gasping, coughing can occur causing swallowing of large amounts of water.

96
Q

What happens when the water enters the pharynx and/or trachea?

A

The victim will suffer a laryngospasm, and this can be permanent or temporary

97
Q

What happens when you have a permanent laryngospasm?

A

There will be no aspiration, can occur in 10-15% of cases.

98
Q

What happens when the laryngospasm is temporary?

A

Fluid begins to enter the lungs further compounding hypercapnia and hyoxia causing causing cardiac arrest

99
Q

How long does it take for brain damage to occur after LOC?

A

4-6 minutes

100
Q

What is the progression of heart rhythms when someone is drowning?

A

tachy, brady, PEA, asystole

101
Q

What can aspiration of fluid lead to?

A
  • Decrease compliance
  • Patients can present with non-cardiogenic pulmonary edema (due to fluid overload)
  • With acute respiratory distress syndrome (ARDS) in later states due to sufactant washout
102
Q

What happens in cold water drowning?

A

Triggers the mammalian diving reflex causing bradycardia, peripheral vasoconstriction, and reduced O2 demand

103
Q

Small amounts of aspirated water can be…

A
  • Reabsorbed in vascular or
  • Can cause decrease in lung compliance
  • Loss of surfactant
  • Atelectasis
  • Hypoxia
104
Q

Acute Respiratory Distress Syndrome

A
  • A cascade of processes impacting avelio/capillaries causing increase capillary permeability, leading to non-cardiogenic pulmonary edema (from loss of protein) decreased sufactant
  • This transition to atelectasis, decreased lung capacity, ventilation/perfusion mismatch (if only one lung is impacted it will not be ventilated but still perfused) and hypoxia
105
Q

Boyles Law

A

At constant temperature, volume of gas is inversely proportional to its pressure. The pressure of a gas increases as its volume decreases, assuming constant mass and temperature.

106
Q

Daltons Law

A

The total pressure of a mixture of gases is the sum of the partial pressure of each gas

107
Q

Henrys Law

A

At constant temperature, the amount of gas dissolved in a liquid is proportional to the partial pressure of gas above the liquid

108
Q

Barotrauma

A

Can occur in any gas filled space but often occurs in middle ear, sinuses, GI system, or lungs. E.g., If a diver isnt able to pop ears b/c of a blockage. Most conditions are self limiting and include tinnitus, vertigo, nausea/vomiting.

109
Q

Pulmonary Over-pressurization Syndrome

A

When a diver makes his ascent there can be air trapped within the lungs from breath holding, bronchospasm, mucus plugs.
Can cause alveolar rupture. Clinically patient can present with dyspnea, pleuritic pain, sub-q emphysema, pneumothorax.

110
Q

Decompression Sickness

A

When nitrogen that is compressed in tissues/blood from increase pressure when diving turns back into gas bubbles when surfacing because it cannot be exhaled fast enough.
Causes joint pain and can affect spinal cord.
Can be minor or cause embolism or CVA type symptoms.

111
Q

Nitrogen Narcosis

A

With deep diving, nitrogen becomes dissolved in blood and passes the blood brain barrier. It acts similar to alcohol, which causes the diver to make poor decisions. Can cause death if impairment is enough to remove respirator.

112
Q

Thermoregulation

A

Thermoregulatory center is located in the anterior hypothalamus and recieves information from both peripheral and central temperature receptors.

113
Q

Peripheral receptors

A

Skin, muscles and mucus membranes; there is more cold than warm receptors peripherally

114
Q

Central receptors

A

Great veins, spinal cord, hypothalamus and viscera; there are more warm the cold in the center

115
Q

Thermogenesis

A

Production of heat for the body via the sympathetic nervous system. The body SHUNTS blood from peripheries to core via vasoconstriction, and this causes piloerection (goosebumps)

116
Q

Thermolysis

A

Release of stored heat from the body, via the parasympathetic nervous system via peripheral vasodilation.

117
Q

4 main conditions of heat related injuries

A
  • Heat syncope
  • Cramps
  • Exhaustion
  • Stroke
118
Q

Hyperthermia can occur from?

A
  • Environmental causes
  • +- physical excertion
  • Failure of the hypothalamus
119
Q

Heat Syncope

A

Result of hypovolemia from volume depletion and vasodilation. Often occurs to people who are unacclimated to heat, or elderly who have less vasomotor tone.
Can cause orthostatic hypotension causing decreased brain perfusion causing a LOC.

120
Q

Heat Exhaustion

A

Hyperthermic <39 degrees. May have evidence of poor perfusion evidence of volume loss with orthostatic BP assessment, can also have mild confusion/irritability.
Pt’s may complain of dizziness, headache, nausea, etc.

121
Q

Heat Stroke

A

Most dangerous, temperature 40 degrees or even higher. Can occur from environment, intracranial hemorrhage, overdose. It is divided into 2 types: classic and exertional.

122
Q

Classic Heat Stroke

A

Due to prolonged heat exposure and can be compounded by comorbities and their medications. Can occur also from overdose or increased ICP.

123
Q

Exertional Heat Stroke

A

Athletes/military who operate in hot/humid environments, and cannot disperse heat fast enough to maintain normal temperatures

124
Q

Heat Stroke Presentation

A
  • Fever greater than 40 degrees
  • Decreased LOA
  • Coma
  • Seizure
125
Q

Treatment for Heat Stroke

A

Remove clothing, withhold oral fluids, cover with wet sheets, apply cold packs to axillae, groin, neck and head. Manage seizure, hypotension, airway compromise as per BLS/ALS.

126
Q

Cold-Related Injuries

A

Freezing of tissues from ice crystals forming in tissue; most often unprotected body parts.
- Fluid shifts to extravascular space, blood vessels damaged, edema causing ischemia.
- When warmed, blood flow is normally restricted due to numerous microvascular emboli, this causes hypoxia and tissue death.

127
Q

Frostnip

A

Mild blanching, mild pain

128
Q

Superficial Frostbite

A

Waxy, white skin, cold numb area becomes painful during rewarming. Area becomes edematous and blisters. Eschar tissue forms, and then peels away leaving red shiny skin.

129
Q

Deep Frostbite

A

Cold, hard skin. Affects subdermal layers, and perfusion is not restored. Non-viable skin mummify and most often require amputation.

130
Q

Management for Frostbite

A
  • Wrap the patients body/affected parts in a blanket or foil rescue blanket
  • Cover and protect the part
  • Do not rub or massage the skin, leave blisters intact
  • If dressing digits, dress separately
131
Q

Hypothermia

A
  • Most often due to exposure to cold with body temperature <35 degrees
  • Body attempts to compensate with thermogensis, but shivering stops at 32 degrees at which point hypothermia progresses quickly.
131
Q

Mild Hypothermia

A

Oriented, but may be slightly fatigued. Temp <35 but >34.

132
Q

Moderate Hypothermia

A

Confused, difficult making coordinated muscle movements.
<34 degrees. May or may not lose ability to shiver

133
Q

Severe Hypothermia

A

Unconscious <30 degrees. May have stiff limbs, bradycardia as a protective measure.

134
Q

What changes in the ECG in hypothermic patients?

A

In addition to bradycardia, you might see a J wave (osborn wave) which can occur in hypothermia especially in <30 degrees.

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2nd Year PCP (10 decks)

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