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VALLEY: Bolts & Bulls ONLY > SECTION 1 Basic Sciences > Flashcards

SECTION 1 Basic Sciences Flashcards

1
Q

Describe the murmurs heard for Mitral stenosis ?

A

Opening snap that occurs early in diastole and a RUMBLING diastolic murmur

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2
Q

What is the stethoscope location for mitral stenosis murmur where they are best heard?

A

Best heard with the chest piece placed over the APEX

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3
Q

Describe the murmurs heard for Mitral Regurgitation?

A

The cardinal feature of mitral regurgitation is a blowing holosystolic murmur HEARD THROUGHOUT SYSTOLE

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4
Q

Where does mitral regurgitation murmur radiates to?

A

AXILLA

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5
Q

Murmur heard throughout systole

A

Mitral regurgitation murmur

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6
Q

2 murmur heard over the CARDIAC APEX

A

Mitral stenosis and mitra regurgitation

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7
Q

Describe the murmurs f the patient has aortic

Stenosis

A

Systolic murmur,

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8
Q

Best stethoscope location for AORTIC Stenosis

A

second right intercostal space (over the aortic arch)

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9
Q

Murmur that radiates to the neck?

A

AORTIC Stenosis

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10
Q

Murmur description for aortic regurgitation

A

Diastolic murmur

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11
Q

Best murmur heard over the Left sternal border?

A

Aortic Regurgitation

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12
Q

When the ventricle fills more during diastole, more blood is ejected during systole. Whose law is this?

A

Starling’s (or Frank-Starling’s) law of the heart.

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13
Q

Starling’s law of the heart relates ventricular filling during diastole to the

A

amount of blood ejected during systole.

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14
Q

Starling Law, the greater the ventricular filling during diastole , meaning the greater the _______, the

A

Preload; The greater the quantity of blood pumped into the aorta during systole.

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15
Q

What causes a change in blood pressure when changing the patient’s position?

A

Altered preload (altered venous return) is most responsible for a change in blood pressure when the patient is re-positioned.

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16
Q

What nerves carry the afferent and efferent signals of the Bainbridge reflex?

A

stretch receptors send Afferent signals to the medulla via the vagus nerve. The medulla then transmits Efferent signals via the sympathetic nerves to increase heart rate (by as much as 75%) and myocardial contractility.

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17
Q

What does the Bainbridge reflex help prevent?

A

The Bainbridge reflex helps prevent damming up of blood in veins, the atria, and the pulmonary circulation.

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18
Q

When does the Bainbridge reflex get activated?

A

When the great veins and right atrium are stretched by increased vascular volume

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19
Q

Describe the venous drainage of the lung. BAHIB

A

The venous drainage of the bronchi occurs through the bronchial, azygous, hemiazygos, and intercostal veins, which then drain into brachiocephalic veins of the neck and ultimately the superior vena cava.

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20
Q

The pulmonary circulation returns to the heart via

A

the pulmonary veins, which empty into the left atrium.

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21
Q

Describe the Valsalva maneuver.

A

Forced expiration with the glottis closed.

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22
Q

Valsava maneuver increase what kind of pressure?

A

All intrathoracic pressures including intrapleural and intrapulmonary pressures.

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23
Q

With valsava maneuver, intrapleural pressures changes from _______. What happens to CO and BP?

A

Negative to positive, so venous return to the RV decreases and CO and BP decrease

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24
Q

With valsava maneuver what causes an increase in HR?

A

The decrease in BP results in a reflex increase in HR.

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25
Q

The healthy adult lung receives each minute an alveolar ventilation (V) of about how many L?

A

4 L/min is the alveolar ventilation rate.

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26
Q

Normal pulmonary blood flow (Q) per min?

A

5L/min

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27
Q

What is the average resting ventilation:perfusion (V/Q) ratio?

A

0.8 (4/5 = 0.8)

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28
Q

A V/Q ration between zero and 1 indicates (0

A

Relative shunt

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29
Q

A V/Q ration greather than 1 indicates what?

A

Dead-spacing

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30
Q

Compared with the apex of the lung, the base exhibits GREATER or LESSER PERFUSION?

A

GREATER

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31
Q

Perfusion (blood flow) is best in which part of the lung?

A

Dependent

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32
Q

The base on the lung is dependent in what position?

A

In the upright (sitting or standing)

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33
Q

What is the total quantity of CO2 delivered to, and used by, the tissues each minute?

A

250 ml/min of 02 is normally delivered to, and used by, the tissues.

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34
Q

VO2 (oxygen consumption) is how much per min?

A

3-4 mlO2/kg/min

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35
Q

What are the three ways C02 is transported in the blood? What percent for each route of transport?

A

(l) physically dissolved in solution, 5% to 10%;
(2) as bicarbonate ion (HCO~ · ), 80% to 90%;
{3) protein bound (plasma proteins and hemoglobin)-these are called carbamino compounds, 5% to 10%.

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36
Q

The majority of CO2 is transported in blood in the form of

A

Bicarbonate 80-90%

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37
Q

A large number of diverse insults can trigger acute respiratory distress syndrome. List factors that can lead to
ARDS.

A 
SHAFT BRUDDS  CPM
Shock
Head injury
Aspiration
Fat or air embolus
Trauma
Burns
Radiation of thorax
UREMIA
Drug Ingestion
Drowning
Sepsis 
Cardiopulmonary bypass
Pancreatitis
Massive Blood transfusion
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38
Q

What are the pulmonary consequences of prolonged 100% oxygen administration?

A

Loss of surfactant (due to prolonged exposure to oxygen radicals), leading to ARDS (adult respiratory distress syndrome).

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39
Q

What is responsible for creating the resting membrane potential?

A

The resting membrane potential of nerve and muscle is due primarily to the diffusion of potassium ions (K+) out of cells through potassium leak channels.

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40
Q

Give two reasons for up-regulation of adrenergic receptors.

A

(1) Sympathetic denervation, and (2) treatment with a sympathetic competitive antagonist (e.g., beta blockade) causes adrenergic receptors to up regulate)

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41
Q

Identify two forms of the enzyme, monoamine oxidase (MAO).

A

The two known forms of monoamine oxidase (MAO) are type A (MAO-A) and type B (MAO-B).

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42
Q

What substances are metabolized by MAO-A (SEND)

A

Serotonin
Epinephrine
Norepinephrine
Dopamine

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43
Q

What substances are metabolized by MAO-AB

A

Tyramine (cheese, red wine beer)
Phenylethylmaine
Dopamine

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44
Q

What substance is metabolized by both MAO-A and MAO-B?

A

Dopamine

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45
Q

Where is monoamine oxidase type A (MAO-A) found?

A

Monoamine oxidase type A (MAO-A) is an enzyme present in the central nervous system, adrenergic nerve endings, liver and gastrointestinal tract.

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46
Q

MAO-A was involved in metabolic degradation of SEND (Serotonin, epi, nore, dopamine) by

A

Oxidative deamination

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47
Q

What two tracts transmit impulses from the motor cortex to the spinal cord?

A

Pyramidal and extrapyramidal tracts.

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48
Q

Impulses from the motor cortex are carried directly to the spinal cord via the

A

pyramidal tract (aka CORTICOSPINAL TRACT)

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49
Q

Impulses are also carried through the basal

ganglia, cerebellum and brainstem nuclei to the spinal cord by

A

Extrapyramidal system

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50
Q

What are components of the extrapyramidal system?

A

basal ganglia, cerebellum and brainstem nuclei

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51
Q

Are the effects of sympathetic stimulation of a motor or sensory nature?

A

Motor (efferent)

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52
Q

Where do preganglionic PARAsympathetic nerves originate?

A

Preganglionic parasympathetic nerves arise from nuclei of cranial nerves Ill, VII, IX and X in the brainstem and also from sacral segments (S2-S4) of the spinal cord

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53
Q

Owing to these origins, the parasympathetic system

is also known as the

A

craniosacral division.

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54
Q

Which autonomic nerves are cholinergic in nature?

A

Those fibers that release acetylcholine are cholinergic.

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55
Q

The cholinergic autonomic nerves are the the

A
  1. sympathetic and parasympathetic preganglionic neurons
  2. parasympathetic postganglionic neurons and the 3. sympathetic postganglionic neurons that
    innervate sweat glands and piloerector muscles.
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56
Q

Sympathetic neurons release NE and EPI except two that release what?

A

Sympathetic postganglionic neurons that release SWEAT GLANDS and PILOERECTOR MUSCLES

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57
Q

Which three cranial nerves supply SENSORY innervation to the oropharynx? VGF

A

vagus (CN X), facial (CN VII), and glossopharyngeal (CN IX) nerves

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58
Q

Describe the anatomy and functions of the glossopharyngeal nerve (CN IX).

A

The glossopharyngeal nerve (GPN) supplies general and special (taste} sensory innervation to the posterior third of the tongue via the lingual branch (caution: not the lingual nerve, which is a terminal branch of the
mandibular division of CN V), the vallecula, the anterior surface of the
epiglottis, the posterior and lateral walls of the pharynx, and the tonsillar
pillars. Motor innervation from the glossopharyngeal nerve is to one of the
muscles of deglutition (swallowing).

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59
Q

Supply the posterior THIRD of the tongue

A

Glossopharyngeal nerve.

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60
Q

One of the muscles of deglutition (swallowing). [

A

Motor innervation from the glossopharyngeal nerve

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61
Q

The glossopharyngeal nerve (GPN) supplies general and special (taste} sensory innervation to the posterior third of the tongue via the

A

lingual branch

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62
Q

Innervates the vallecula

A

Glossopharyngeal nerve

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63
Q

Innervates the anterior surface of the epiglottis

A

Glossopharyngeal nerve

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64
Q

Innervates the posterior and lateral walls of the pharynx,

A

Glossopharyngeal nerve

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65
Q

Innervates the tonsillar pillars.

A

Glossopharyngeal nerve

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66
Q

What are the 3 division of Trigeminal nerve? OMaxMan

A

the ophthalmic, maxillary, and mandibula

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67
Q

Which nerve provides motor innervation to the muscles of mastication (chewing, “moves the mandible”)

A

masseter nerve

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68
Q

Which nerve give rise to the masseter nerve?

A

The anterior branch of the mandibular nerve (V3) gives rise to the masseter nerve

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69
Q

Provides sensory innervation to the lower teeth and gums (“feels the mouth inside and out”}.

A

The posterior branch of the mandibular nerve

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70
Q

The lingual nerve is a terminal branch of the

A

mandibular nerve:

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71
Q

General sensory innervation to the lingual mucous membranes,

A

The lingual nerve

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72
Q

Sensory innervation to the anterior two-thirds of the tongue

A

Lingual nerve (Mandibular nerve branch)

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73
Q

Sensory to the floor of the mouth

A

Lingual nerve (Mandibular nerve branch)

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74
Q

What is the chorda tympani nerve ?

A

A branch of the facial nerve, CN VII

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75
Q

What is the relationship between the chorda tympani nerve (branch ofCN VII) and the lingual nerve (Terminal branch of CN V3)

A

Chorda tympani joins lingual nerve, and courses with the lingual nerve to the anterior 2/3 of the tongue.

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76
Q

The chorda tympani supplies special sensory fibers to the

A

taste buds on the anterior two-thirds of the tongue.

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77
Q

What is the function of the Circle of Willis?

A

The Circle of Willis provides collateral blood flow to the brain if a major vessel carrying blood to the brain becomes obliterated.

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78
Q

What percent of the intracranial volume is occupied by brain?

A

80% brain matter and intracellular water

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79
Q

What percent of the intracranial volume is occupied by Blood?

A

12%

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80
Q

What percent of the intracranial volume is occupied by CSF?

A

8%

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81
Q

The composition of cerebrospinal fluid (CSF) differs from the composition of plasma LYTES?

A

7% more sodium
Higher magnesium
Higher Chloride
40% less Potassium

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82
Q

The composition of cerebrospinal fluid (CSF) differs from the composition of plasma GLUCOSE

A

30% less glucose

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83
Q

The composition of cerebrospinal fluid (CSF) differs from the composition of plasma HYDROGEN IONS

A

Higher H+ (lower pH);

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84
Q

How much cerebrospinal fluid is produced per day?

A

CSF production is about 500-750 mL/day

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85
Q

Cerebrospinal fluid production ranges from

A

15 mL/24 hours to 30 mL/24 hours,

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86
Q

What four factors determine how much of a substance will diffuse across the blood-brain barrier?

A

The movement of a given substance across the blood-brain barrier is governed simultaneously by its
size, charge, lipid solubility, and degree of protein binding in blood.

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87
Q

A substance generally must be_____and/or______ in order to cross the blood-brain barrier in substantial amounts.

A

very small or lipid soluble

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88
Q

What are the results of electrical stimulation to the reticular activating system (RAS)?

A

Stimulation of the reticular activating system (RAS) increases alertness..

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89
Q

Diffuse electrical stimulation of the RAS causes immediate and______cause a ________

A

marked activation of the cerebral cortex and will even cause a sleeping individual to awaken instantaneously

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90
Q

What is the typical time-frame for onset of autonomic hyperreflexia following spinal cord injury?

A

Autonomic hyperreflexia usually follows a period of spinal shock that typically lasts 1- 3 weeks. SO ONSET Is about after 3 weeks

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91
Q

How long does spinal shock last?

A

1-3 weeks

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92
Q

Onset of Hyperreflexia following SCI can be?

A

Few months to many years

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93
Q

What are four components for treatment for the syndrome of inappropriate antidiuretic hormone secretion?
RARA

A
  1. Remove the underlying cause(
    3) Antagonize the effects of ADH on the renal tubule by giving demecolcine
    (2) restrict water intake,
    (4) administer hyperosmotic saline with or without diuretics.
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94
Q

Identify the gland that is both endocrine and exocrine.

A

Pancreas

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95
Q

What hormone does the pancreatic islet delta cells produce?

A

Somatostatin

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96
Q

What is the role of the hormone somatostatin?

A

Inhibits GI motilitiy and secretion including the production of HCL

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97
Q

The main physiologic function of glucagon .

A

increase serum glucose concentration by causing hepatic gluconeogenesis and glycogenolysis (breakdown of glycogen).

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98
Q

Plays a key role in glucose homeostasis

A

Glucagon

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99
Q

How does glucagon maintain homeostasis, 2 processes

A

Hepatic gluconeogeneis

Glycogenolysis

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100
Q

Antagonize effects of insulin

A

Glucagon

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101
Q

Effects of glucagon on gastric motility?

A

Inhibit gastric motility

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102
Q

Glucagon: Effects of gastric acid secretion?

A

Inhibit gastric secretion

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103
Q

Glucagon on bile secretion

A

Enhanced

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104
Q

Glucagon effects on tissue

A

Increased blood flow to tissues, especially kidneys

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105
Q

Glucagon effects on insulin

A

Increases insulin secretion

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106
Q

Glucagon and cardiac effects

A

inotropic and chronotropic

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107
Q

Glucagon and biliary effects?

A

relaxation of smooth muscle (biliary sphincter)

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108
Q

Identify the biochemical triad that defines diabetic ketoacidosis.

A

ketonemia, hyperglycemia, and acidemia.

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109
Q

What are the diagnostic criteria for diabetic ketoacidosis?

A

ketonemia or significant ketonuria
blood glucose above 250 mg/dL or known diabetes mellitus; and
serum bicarbonate below 18 mmol/L or arterial pH< 7.3.

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110
Q

It is generally recommended to cancel nonurgent or elective surgery in the patient with diabetes mellitus if the serum glucose rises above what value?

A

Above 400 mg/dL

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111
Q

The clinical syndrome of diabetic ketoacidosis (DKA) includes

A

dehydration and hypovolemic shock from hyperglycemic osmotic diuresis
compensatory hyperventilation {Kussmaul pattern)
life· threatening electrolyte depletion (especially hypokalemia and hypophosphatemia)

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112
Q

AG gap with DKA

A

Greater than 10

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113
Q

Anion GAP formula is

A

Na+ - (Cl+HCO3)

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114
Q

The increase in hepatic arterial flow in response to a decrease in portal blood flow occurs for two reasons:

A

(l) to maintain hepatic oxygen supply, and (2) to maintain

total hepatic blood flow, which is essential for clearance of many compounds.

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115
Q

What is the “arterial buffer respons”?

A

Adjusting hepatic arterial flow in response to changes in portal blood flow

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116
Q

What are seven functions of the liver?

A

storage and filtration of blood,

(2) metabolic functions such as carbohydrate, fat, and protein metabolism
(3) secretion of bile
4) storage of vitamins
(5) blood coagulation
(6) storage of iron
(7) detoxification and excretion of drugs.

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117
Q

How does glomerular filtration rate (GFR) change if the efferent arteriole dilates relatively more than the afferent
arteriole?

A

Glomerular filtration rate will decrease if the efferent arteriole dilates more than the afferent.

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118
Q

How does GFR change If the efferent arteriole constricts relatively more than the afferent arteriole?

A

GFR will increase if the efferent arteriole constricts more

than the afferent.

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119
Q

How does GFR change if the afferent arteriole dilates relatively more than the efferent arteriole?

A

Glomerular filtration rate will increase if the afferent arteriole dilates more than the efferent

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120
Q

How does GFR change if the afferent arteriole Constricts relatively more than the efferent?

A

GFR will decrease if the afferent arteriole constricts more

than the efferent.

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121
Q

List and define three causes of perioperative

acute renal failure

A

Prerenal failure
Renal failure
Post renal failure

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122
Q

Cause of prerenal failure

A

Decreased renal blood flow

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123
Q

Cause of IntraRenal failure

A

Renal tubular damage secondary to decreased renal

blood flow, nephrotoxic drugs, or release of hemoglobin or myoglobin

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124
Q

Causes of Postrenal failure?

A

Obstruction of urine flow due to for example obstruction of the ureters or urethra

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125
Q

What is the best indicator of renal reserve?

A

The best indicator of renal reserve is the trend in serum creatinine values.

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126
Q

An important early step in hemostasis is

A

vasoconstriction of the damaged vessel.

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127
Q

An important early step in hemostasis is vasoconstriction? _______play a key role in this initial vasoconstriction by release of what substances?

A

Platelets; The vascular contraction is a result of autonomic nervous system reflexes and the release of thromboxane A2

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128
Q

The endothelium releases many procoagulant

factors following vascular injury: name two key procoagulants released by the endothelium.

A

Endothelial damage following vascular injury initiates release of many procoagulant factors including tissue factor (flII, TF) and factor VIII:vWF(von willebrand’s factor)

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129
Q

In addition to its role in early vasoconstriction, thromboxane A2 plays a key role in

A

activation and aggregation of platelets.

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130
Q

Once platelets adhere, they are activated by a complex series of steps including

A

release of ADP and thromboxane A2

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131
Q

Describe the actions ofTxA2 in activation and adhesion of platelets.

A 
Adenosine diphosphate (ADP) and TxA2 are ligands for G protein coupled receptors (P2Yu and • TPa, respectively} that trigger signal transduction pathways, ultimately
leading to expression ofGPIIb/IIIA receptors (fibrinogen receptors) on the platelet surface. TxA2 appears to amplify the signal and action of more potent platelet agonists, such as thrombin (Ila) and ADP
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132
Q

What may be given to treat the patient with a fibrinogen {factor I) deficiency?

A

Cryoprecipitate

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133
Q

Which two veins combine to form the hepatic portal vein?

A

The (hepatic) portal vein is formed by the union of the splenic vein and superior mesenteric vein posterior to the neck of the pancreas at the level of L2.

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134
Q

Usually drains into the splenic vein but occasionally

(10%) the Tip:

A

inferior mesenteric vein

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135
Q

inferior mesenteric vein joins the splenic and superior

mesenteric veins at their confluence at

A

portal vein.

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136
Q

Portal system: if a question asks for two vessels, the “best” answer, in our opinion, is

A

splenic and superior mesenteric veins.

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137
Q

If the immune system overreacts to an allergen, what occurs?

A

a hypersensitivity (allergic) reaction occurs.

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138
Q

Immune-mediated hypersensitivity reactions are classified

into

A

Four groups

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139
Q

Type I immune mediated reactions are

A

anaphylactic or immediate-type hypersensivity reactions.

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140
Q

Type II immune mediated reactions are

A

Cytotoxic reaction (antibody-dependent cell-mediated cytotoxicity)

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141
Q

Type III reactions are

A

immune complex reactions that produce tissue damage by deposition of the immune complexes.

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142
Q

Type IV reactions are

A

Delayed type hypersensitivity reactions from interactions of sensitized lymphocytes with specific antigens.

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143
Q

Describe type I allergic (hypersensitivity) reactions

A

In type I allergic reactions (immediate type, anaphylactic}, a specific antigen called an allergen interacts with specific IgE antibodies on tissue mast cells or circulating basophils to trigger mediator release

144
Q

The key mediator of type I reactions is

A

histamine.

145
Q

Examples of type I reactions are

A

allergic rhinitis, extrinsic asthma, and anaphylaxis

146
Q

Describe type II hypersensitivity (allergic)reactions: include participating
cells and antibody(ies} and list common
examples of type II reactions

A

Type II cytotoxic reactions are mediated by lgM and lgG antibodies directed against antigens on the surface of foreign cells or extracellular tissue components.

147
Q

The cell damage in type II reactions is produced by

A

(I) direct cell lysis after complete complement cascade
activation
(2) increased phagocytosis by macrophages
(3) killer T-cell lymphocytes producing antibody-dependent cell mediated cytotoxic effects.

148
Q

Examples of type II reactions

A 
ABO incompatible transfusion reactions
drug-induced immune hemolytic anemia
Hepain-induced thrombocytopenia
Myasthenia gravis
Goodpasture's syndrome.
149
Q

Describe Type III allergic hypersensitivity reactions

A

Result from circulating soluble antigens and antibodies that bind to form insoluble complexes which then DEPOSIT in the microvasculature.

150
Q

2 things that can lead to type III reactions?

A

Protracted infections

Autoimmune processes

151
Q

3 diseases associated with type III reactions

A

SLE
RA
Glomerulonephrities
CLASSIC SERUM SICKNESS>

152
Q

Describe type IV allergic (hypersensitivity) reactions: include participating
cells and antibody(ies) and list common
examples of type IV reactions.

A

Type IV delayed hypersensitivity reactions result from the interactions of sensitized lymphocytes with specific antigens.

153
Q

Delayed hypersensitivity reactions are mainly

mononuclear, manifest in

A

18 to 24 hours, peak at 40 to 80 hours, and disappear in 72 to 96 hours.

154
Q

In Type IV hypersensitivity reaction what occurs?

A

Cytotoxic T cells are produced specifically to kill target cells that bear antigens identical with those that triggered the reaction.

155
Q

Type IV examples of reations

A 
tissue rejection
Graft vs host reactions
Contact dermatitis
Tuberculin immunity 
Steven Johnsons syndrome
156
Q

Another form of type IV hypersensitivity is

A

granulomatous hypersensitivity, in which chronic infection leads to the formation of granulomas in tissues.

157
Q

Granulomatous diseases include

A

tuberculosis, sarcoidosis, and Crohn’s disease

158
Q

What is anaphylaxis?

A

Anaphylaxis is a severe, generalized, life threatening immediate hypersensitivity reaction marked by interstitial edema-particularly laryngeal edema bronchospasm, and cardiovascular collapse

159
Q

The most common type of immune-mediated anaphylaxis results when

A

-previous exposure to antigens in drugs or foods evokes production of antigen-specific lgE antibodies.
Subsequent exposure to the same or a chemically similar antigen results in antigen-antibody interactions that initiate marked degranulation of mast cells and basophil

160
Q

Most common with anaphylaxis?

A

Urticaria and pruritus are common.

161
Q

How does non-immune-mediated anaphylaxis (also known as anaphylactoid reaction) compare with anaphylaxis?

A

Non-immune-mediated anaphylaxis (also known as anaphylactoid reaction) is nearly identical to anaphylaxis; however, the triggering antigen directly stimulates mast cell and basophils- there is no IgE-mediated trigger.

162
Q

Symptoms anaphylactoid vs anaphylaxis?

A

Symptoms of non-immune-mediated anaphylaxis are generally less severe than IgE-mediated anaphylaxis

163
Q

What are the normal ranges for pH, PCO2 and bicarbonate in arterial blood?

A

pH - 7.35- 7.45; pC02 = 35 45 mm-Hg; bicarbonate - 22-27 mEq/L.

164
Q

What is the normal HC0.1 /H1C0.1 ratio? What is the significance of this?

A

The normal HC03 /H2C03 ratio is 20: 1. When the HC03 :H2C03 ratio is 20:1, pH= 7.40. The pH increases when the ratio increases, and pH falls when the ratio decreases.

165
Q

The pH increases when the HCO3:H2CO3 ratio

A

Increases

166
Q

pH relationship to HCO3:H2CO3 ratio is

A

directly proportional

167
Q

What is the anion gap?

A

The anion gap= major measured cations - major measured anions

168
Q

What is the utility of measuring the anion gap?

A

The anion gap is used in the differential diagnosis of metabolic acidosis. Some metabolic acidoses are associated with a high anion gap (anion gap > 25
mEq/liter). Other metabolic acidoses are associated with a normal, or near normal, anion gap

169
Q

Normal AG is

A

9-15

170
Q

At what sodium level will the patient begin to exhibit signs and symptoms of hyponatremia?

A

A serum sodium concentration of 120 mEq appears to be borderline for development of severe reactions.

171
Q

How is hyponatremia treated?

A

Treatment of hyponatremia is diuretics or infusion of hypertonic saline

172
Q

Treatment of hyperkalemia can be divided into three categories, based upon mechanism of action: list these 3
categories.

A

l) physiologic antagonists and membrane stabilizers (calcium)
(2} agents that shift or drive potassium into cells (insulin, beta adrenergic agonists, sodium bicarbonate and hyperventilation
(3} agents or process that remove potassium from the body

173
Q

Agents that shift or drive potassium into cells are

A

insulin, beta adrenergic agonists, sodium bicarbonate and hyperventilation

174
Q

Treatments of hyperkalemia, state the onset {minutes) and duration of action (minutes or hours): calcium salts,
insulin-glucose infusion, sodium poly-
styrene sulfate (Kayexalate), and loop
diuretics.

A

l) calcium salts: onset in 1-3 minutes duration of action 30- 60 minutes;

175
Q

Treatments of hyperkalemia, state the onset {minutes) and duration of action (minutes or hours):sodium bicarbonate,

A

onset of action : 5-10 minutes; a duration of action 1-2 hours;

176
Q

Treatments of hyperkalemia, state the onset {minutes) and duration of action (minutes or hours): LOOP Diuretics

A

loop diuretics:Onset 15-30 minutes duration of action of 2-3 hours;

177
Q

Treatments of hyperkalemia, state the onset {minutes) and duration of action (minutes or hours): Insulin glucose infusion

A

insulin-glucose infusion, onset of action is 30 minutes, followed by a duration of action of 4-6 hours; and

178
Q

Treatments of hyperkalemia, state the onset {minutes) and duration of action (minutes or hours):Kayexalate

A

sodium polystyrene sulfate (Kayexalate), onset in 1 2 hours, duration of action 4-6 hours.

179
Q

How does serum K• change with acute acidosis? Acute alkalosis? Explain.

A

Serum K+ increases in acidosis and decreases in alkalosis

180
Q

Serum K changes with acute acidosis explain?

A

With acidosis, H+ diffuses into cells because of the increased extracellular H+ . As H+ enters cells, K+ leaves. This H+ - K+ exchange increases extracellular K+ concentration.

181
Q

Serum K changes with acute alkalosis explain?

A

With alkalosis, W diffuses out of cells. As W leaves cells, K• enters. This H+-K+ exchange decreases extracellular K’ concentration.

182
Q

List functions of magnesium.

A

Magnesium is an intracellular cation that functions as a cofactor in many enzyme pathways

183
Q

Magnesium is important for the regulation of the

A

sodium-potassium pump, the regulation of the enzyme adenyl cyclase, and the regulation of slow calcium channels.

184
Q

Magnesium antagonizes

A

calcium.

185
Q

Magnesium controls the

A

threshold potential and serves as a membrane stabilizer

186
Q

An important function of magnesium is the

A

regulation of the release of acetylcholine from nerve

terminals.

187
Q

What are the manifestations of hypomagnesemia
when serum [Mg2] < 1.2- 1.6 mg/dL ( < 1.0-1.5 mEq/L,
0.5-0.75 mmol/L)?

A

When serum [Mg2•]

188
Q

Tetany, seizures, and arrhythmias occur when serum magnesium falls below what level?

A

Tetany, seizures, and arrhythmias occur when serum magnesium concentrations are <1.2 mg/dL {

189
Q

Where is the J-point in the ECG waveform?

A

The J-point is the point on the ECG when the QRS complex ends and the ST segment begins

190
Q

How is the J-point used in ECG interpretation?

A

ST elevation or depression is measured by comparing
lead voltage at 60 or 80 milliseconds after the J-point to the isoelectric value, usually measured during the PR interval.

191
Q

ST elevation or depression may also be measured at the

A

J-point.

192
Q

Left bundle branch block (LBBB) is uniquely characterized by:

A

Broad Notched R wave in leads I, aVl, V5, V6
Deep S in the Right precoardial leads
Absent septal Q waves

193
Q

LBBB and RBBB both characterized by a

A 
HR <100
Regular rhytm
Normal PRI
QRS > 120ms
ST segment and T waves in the opposite direction of the R wave.
194
Q

Left bundle branch block (LBBB) is uniquely characterized by:

A

Prominent notched R waves with M patter (rabbite ears)
rsr’, rsR’, or rSR’ on the righst side leads, (aVR, V1)
Wide S on left side leads.

195
Q

Which is more prevalent, RBBB or LBBB? Which is more ominous?

A

RBBB occurs in about 1 % of hospitalized patients and is much more common than left bundle branch
block (LBBB). LBBB, however, is more ominous LBBB does not occur in healthy individuals.

196
Q

Right bundle branch block (RBBB) is common in

A

the general healthy population without clinical evidence of structural heart disease and has • no prognostic significance in this group

197
Q

LBBB is often associated with

A

ischemic heart disease, hypertension, and valvular heart disease. LBBB obscures or simulates other ECG patterns.

198
Q

In the presence of LBBB, the diagnosis of

A

LVH, acute ischemia, or myocardial infarction may be difficult or impossible

199
Q

What is one concern with pulmonary artery catheter placement in a patient with left bundle branch block?

A

Insertion of a pulmonary artery catheter (PAC) may precipitate right bundle branch block, thus insertion of a PAC in a patient with left bundle branch block may precipitate complete heart block (third-degree block).

200
Q

What is a dose-response curve?

A

A dose-response curve depicts the relationship between the dose of a drug administered (x- axis) and the resulting pharmacologic effect (y- axis).

201
Q

Define volume of distribution (Vd)

A

Vd=’Q/C , where Vd is the volume of distribution, Q is the quantity of drug injected and CP is the plasma concentration of the drug that would be achieved if the drug distributed instantaneously within its volume of
distribution after its injection

202
Q

Drugs that are absorbed from the gastrointestinal

tract must first pass through which organ before reaching the general circulation?

A

The drugs are delivered to the liver via the portal circulation. Drugs that are absorbed from the GI tract may be metabolized to some extent in the liver-this is the.first-pass effect

203
Q

What are the vapor pressures of halothane?

A

244 mmHg

204
Q

What is the vapor pressure of isoflurane?

A

240 mmHg

205
Q

What is the vapor pressure of enflurane?

A

172 mmHg

206
Q

What is the vapor pressure of desflurane?

A

669 mmHg

207
Q

What is the vapor pressure of sevoflurane?

A

170 mmHg

208
Q

List volatile agents according to their vapor pressure (lowest to highest vapor pressure). SEIHD

A

Sevo< enflurane

209
Q

Which volatile agents most depress the baroreceptor reflex?

A

Halothane and sevoflurane most depress the baroreceptor reflex

210
Q

Which volatile agentst least depress the baroreceptor ?

A

isojlurane and desflurane least depress the baroreceptor reflex (

211
Q

NO Baroreceptor reflex means that there are

A

There are no increases in heart rate despite decreases in blood pressure with these agents

212
Q

Baroreceptor reflex is working when

A

heart rate tends to increase reflexly with the decreases

in blood pressure produced by these agents

213
Q

What are the minimum alveolar concentration (MAC) requirements for a full-term infant, compared to the adult?

A

The minimum alveolar concentration (MAC) value for a full-term infant is the same as for the adult.

214
Q

At what age (months) is the minimum alveolar concentration (MAC) highest? Which agent is the exception to this rule?

A 
By 6 months of age, the minimum alveolar concentration (MAC) is 50% greater compared to adult MAC. For example, the MAC of desflurane for a 6-month old is 9.9% compared to 5.8% for the adult. The exception to this rule is sevoflurane: the MAC of sevoflurane is greatest in
the neonate (3.3%), compared to 2% for the adult.
215
Q

Where and how are volatile anesthetics metabolized?

A

The modern inhaled anesthetics are primarily excreted via the lungs. The minimal amount of biotransformation 0.02% to 5%) of modern volatile anesthetics takes place in the liver by the cytochrome P450 enzyme system.

216
Q

The cytochrome P450 enzymes are also known as

A

mixed-function oxidases.

217
Q

The modern inhaled anesthetics are primarily excreted

A

via the lungs.

218
Q

Amount of biotransformation of VA in the liver is

A

0.02% to 5%

219
Q

What opioid receptor promotes respiratory depression?

A

Mu-2

220
Q

Which opioid can block voltage-dependent sodium channels, in other words, which opioid has local anesthetic properties?

A

Meperidine

221
Q

Which opioid has local anesthetic properties?

A

Meperidine

222
Q

Meperidine is an agonists to

A

M and K receptors

223
Q

Meperidine has well-known local anesthetic properties, particularly after

A

epidural administration.

224
Q

What affect do opioids have on the blood C02 dissociation curve?

A

If respiratory depression occurs, Pa02 decreases, and the C02 curve shifts.

225
Q

Except for remifentanil, how are opioids eliminated?

A

Except for remifentanil, opioids are eliminated by hepatic metabolism.

226
Q

What are the implications for a patient with liver disease receiving an opioid?

A

In a patient with liver disease, the clearance of all opioids except remifentanil will be delayed (slowed) and significant accumulation can occur

227
Q

Naltrexone is administered to treat what problems

A

Naltrexone is a long-acting opioid antagonists administered to treat alcohol addiction

228
Q

Which intravenous agents will decrease intracranial pressure? BEBOP

A 
Barbiturates
Etomidate
Benzodiazepines, 
Opioids
Propofol.
229
Q

Venous thrombosis and phlebitis are most likely after intravenous administration of what nonopioid anesthetics?
Why?

A

Diazepam, lorazepam and etomidate, because they are dissolved in the organic solvent, propylene glycol.

230
Q

Name two nonopioid induction drugs that are associated with the excitatory phenomena during induction

A

Methohexital and etomidate

231
Q

Which intravenous sedative-hypnotic inhibits platelet aggregation?

A

Propofol inhibits platelet aggregation that is induced by TxA2 and platelet-activating factor, although propofol does NOT alter tests of coagulation or platelet function

232
Q

List the local anesthetics that are amides

A

Local anesthetics with an amide linkage are lidocaine, prilocaine, mepivacaine, bupivacaine, levobupivacaine, and ropivacaine

233
Q

What antimicrobial preservatives are added to commercial preparations of local anesthetic solutions in multi-dose
vials?

A

Paraben derivatives such as methyl paraben, ethyl paraben, and propyl paraben.

234
Q

Should preservative-containing solutions of local anesthetic be used for spinal, epidural, or intravenous regional anesthesia

A

No, because parabens are potentially cytotoxic (neurotoxic).

235
Q

How do local anesthetics work?

A

Local anesthetics work by preventing voltage-gated fast Na• channels in nerve axons from opening. Local anesthetics bind to sodium channels inside
the neuron when they are in the Inactivated state.

236
Q

Does conduction block by local anesthetics require the ionized form, unionized form, or both ionized and
unionized forms?

A

Both forms. The un-ionized form crosses the lipid bilayer to enter the neuron, and the ionized form binds to the gated sodium channel while in the inactivated state

237
Q

Identify the part of the nerve cell that is affected by local anesthetics.

A

The nerve axon is the site of action of the local anesthetics. Only the axon has fast, voltage-gated sodium channels

238
Q

What are the three states of the fast, voltage-gated sodium channel?

A

(1) Closed, (2) open, and (3) inactivated.

239
Q

What is the primary determinant of local anesthetic potency?

A

Lipid Solubility (thnk SLP)

240
Q

In general, what structural characteristic of local anesthetic determines lipid solubility and, hence, potency

A

The total number of carbon atoms. “In general, lipid solubility (potency) is increased by increasing the total number of carbon atoms in the molecule

241
Q

State three specific ways, in addition to adding carbon atoms, of increasing potency of a local anesthetic

A

Lipid solubility and potency are increased by adding:
a halide (chloride ion, bromide ion, etc) to the aromatic (benzene) ring;
(b) an ester linkage;
(c) a large alkyl group on the tertiary amide nitrogen.

242
Q

What term defines the lowest concentration of local anesthetic that blocks impulse conduction along a given nerve fiber?

A

The Minimum Blocking Concentration (Cm) is the lowest concentration of a local anesthetic that blocks conduction

243
Q

Which local anesthetic agent is the standard for comparison of potencies of local anesthetics?

A

Lidocaine.

244
Q

The rapidity and extent of diffusion of a local anesthetic to its site of action depends primarily on what three factors?

A

(1) The pKa of the drug, (which determines the degree to which the drug is un-ionized), (2) the concentration injected, and (3) its lipid solubility.

245
Q

How does succinykholine produce bradycardia?

A

Succinylcholine stimulates muscarinic receptors at the sino-atrial node.

246
Q

Do patients with myasthenia gravis have increased or decreased sensitivity to nondepolarizing neuromuscular
blockers?

A

Patients with myasthenia gravis have greatly increased sensitivity to nondepolarizing agents

247
Q

Do patients with myasthenia gravis have increased or decreased sensitivity To depolarizing neuromuscular
blockers?

A

These patients may be either very sensitive or resistant

to succinylcholine.

248
Q

If possible, should muscle relaxants be avoided in the patient with myasthenia gravis?

A

If possible, muscle relaxants should be avoided in the

patient with myasthenia gravis

249
Q

What type of muscle relaxant is preferred (short, intermediate or long-acting) if skeletal muscle paralysis in a patient being treated for myasthenia gravis is necessary?

A

Short or intermediate-acting (cisatracurium or mivacurium) muscle relaxants are preferred

250
Q

Succinykholine is routinely administered before a paralyzing dose of a nondepolarizing agent. Does the succinylcholine antagonize or potentiate the nondepolarizing drug?

A

When administered after succinykholine, the potency of nondepolarizing muscle relaxants is enhanced. This is unexpected and may be related to unrecognized phase II blockade.

251
Q

State the signs and symptoms of Beta receptor antagonist overdose. Which specific Beta receptor properties correlate with these signs and symptoms?

A

The manifestations of Beta receptor antagonist overdose depend on the characteristic of the drug, particularly its Beta-1 selectivity, intrinsic sympathomimetic activity, and membrane-stabilizing properties.

252
Q

Are common signs of beta blocker toxicity.

A

Hypotension, bradycardia, prolonged AV conduction times and widened QRS complexes. Seizures and depression may occur, as well as hypoglycemia and bronchospasm.

253
Q

Describe the treatment of Beta-adrenergic antagonist (beta blocker) overdose.

A

Overdose of Beta-blocking drugs may be treated with atropine, but isoproterenol, dobutamine, or GLUCAGON infusion (or some combination) may be required along with cardiac pacing to ensure an adequate rate of contraction.

254
Q

The alpha-2 adrenergic receptor agonist, clonidine, acts where centrally to produce what therapeutic effect?

A

Stimulation of alpha-2A receptors of inhibitory neurons in the vasomotor center of the medulla in the brain stem inhibits sympathetic nervous system outflow. This action decreases blood pressure.

255
Q

Alpha-2 adrenergic receptor agonists antagonize the sympathetic nervous system peripherally. How?

A

Alpha-2 receptors are found peripherally in the surface membrane of the norepinephrine-containing presynaptic nerve terminals of sympathetic postganglionic neurons. Stimulation of these receptors decreases the release of norepinephrine from the presynaptic nerve terminal. This decreased release of norepinephrine contributes modestly to the clonidine·induced decrease in blood pressure.

256
Q

By what receptor and second messenger system does glucagon exert its positive inotropic and chronotropic effects?

A

Glucagon acts through its own G-protein coupled receptor (GPCR) and generation of cyclic adenosine monophosphate (cAMP). In other words, glucagon binds to glucagon receptors to promote the formation of cAMP.

257
Q

The hemodynamic benefits of glucagon might be useful in what 5 situations?

A

The hemodynamic benefits of glucagon-positive inotropy and positive chronotropy may be beneficial in:
(I) low cardiac output syndrome following cardiopulmonary bypass;
(2) low cardiac output syndrome with myocardial infarction; (3) chronic congestive heart failure;
(4) anaphylactic shock with refractory hypotension; and,
(5) excessive Beta-adrenergic blockade

258
Q

Define autacoid.

A

Autacoids (or autocoids) are biological factors that act like local hormones, that is they have a paracrine (neighboring) effect.

259
Q

List examples of autacoids.

A

Notable human autacoids include eicosanoids, angiotensin, nitric oxide (NO), kinins, histamine, serotonin, and endothelins

260
Q

Unlike hormones, autacoids are produced in

A

minute quantities and have local, evanescent (brief)

effects.

261
Q

What are eicosanoids?

A

Eicosanoids (from the Greek eicosa “twenty”) are signaling molecules derived from omega-3 and omega-6 fatty acids including arachidonic acid.

262
Q

Eicosanoids include

A

prostaglandins, thromboxanes, leukotrienes, and lipoxins.

263
Q

Eicosanoids are not

A

stored but rather are produced on demand.

264
Q

How are prostanoids related to eicosanoids?

A

Prostanoids are metabolic derivatives of arachidonic acid, therefore prostanoids are a category of eicosanoids.

265
Q

Cyclooxygenase (COX) acts on_____To produce

A

arachidonic acid to produce PGH2.

266
Q

Three types of prostanoids are then derived from

PGH2

A

prostaglandins, prostacyclins, and thromboxanes.

267
Q

Arachidonic acid, an omega-6 fatty acid, is liberated from membrane phospholipids by the action of what enzyme?

A

Phospholipase A1 (PLA2). a calcium-dependent enzyme, acts upon membrane phospholipids to release arachidonic acid.

268
Q

What is the rate-limiting step in eicosanoid synthesis?

A

The release of arachidonic acid from membrane phospholipids

269
Q

Which prostanoid is implicated in the rebound prothrombotic state often seen following discontinuation of antiplatelet therapy?

A

An increased thromboxane A1 (TxA2) activity is seen during the rebound period following discontinuation of antiplatelet therapy

270
Q

Name two prostanoids that are potent inhibitors of platelet aggregation and thus promote and maintain an antithrombotic state in vessels?

A

The vascular endothelium releases prostacyclin (PGI2) and PGD2, along with nitric oxide (NO) and other factors to maintain an anticoagulant state

271
Q

Which prostanoid produces vascular smooth muscle contraction and is thus a potent vasoconstrictor?

A

Thromboxane A2 (TxA2) produces contraction of vascular smooth muscle and is a potent vasoconstrictor.

272
Q

TxA2 has local effects at the

A

systemic vasculature, coronary vasculature, and renal vasculature (decreased RBF and decreased GFR).

273
Q

List two prostanoids that cause bronchodilation. List three prostanoids that cause bronchoconstriction.

A

PGEi and PGh are bronchodilators, whereas PGF2a • PGD2, and TxA2 cause bronchoconstriction

274
Q

How are leukotrienes related to eicosanoids?

A

Leukotrienes are metabolic derivatives of arachidonic acid, therefore leukot rienes (LT) are a category of eicosanoids.

275
Q

Lipoxygenase (LOX) acts on _____To produce what?

A

arachidonic acid to produce the Leukotriene family.

276
Q

Leukotrienes that increase smooth muscle contraction,

microvascular permeability, and airway mucus secretion.[

A

LTC4 , LTD4, LTE4 and LTB 4

277
Q

What action do leukotrienes (LT) have on the lungs?

A

Leukotrienes evoke inflammatory responses in the lungs including intense bronchoconstriction and increased pulmonary vascular permeability.

278
Q

Leukotrienes also promote

A

eosinophil degranulation and attract neutrophils, both key players in the inflammatory response.

279
Q

What is another name for the mixture of leukotrienes C4, D4 and E4?

A

The mixture ofleukotrienes C4, D4, and E4 is the classic slow-reacting substance of anaphylaxis (SRS-A).

280
Q

Which herbal supplement is a potent inhibitor of thromboxane synthetase and thus has synergistic effects with other antiplatelet agents?

A

Ginger is a potent inhibitor of thromboxane synthetase and thus increasesbleeding time and morbidity

281
Q

Which herbal supplement is a potent inhibitor of thromboxane synthetase and thus has synergistic effects with other antiplatelet agents?

A

Ginger is a potent inhibitor of thromboxane synthetase and thus increases bleeding time and morbidity

282
Q

Which dopamine antagonists is the only FDA-approved agent for treatment of Diabetic GASTROPARESIS

A

Metoclopramide is the only drug approved by the FDA for diabetic gastroparesis

283
Q

How does metoclopramide work?

A

Via cholinergic stimulation , acts as a gastrointestinal prokinetic drugs that increases LES tone and stimulated motility of the upper GI tract.

284
Q

List 7 common adverse effects of metoclopramide?

TRES-GIA

A
  1. Treatable hypotension and tachycardia
  2. Restlessness
  3. EPS
  4. Sedation
  5. Galatorrhea
  6. Inhibition of plasma cholinesterase
  7. Abdominal cramping
285
Q

4 contraindications to administration of metoclopramide (PRIM)

A

Parkinson’s disease
Restless leg syndrome
Intestinal obstruction ,(Because metoclopramide prokinetic effect)
Movement disorders related to dopamine inhibition or depletion

286
Q

For what conditions are alpha-glucosidase inhibitors administered?

A

The medical treatment of insulin resistance and hyperglycemia in metabolic syndrome, type 2 diabetes, and obesity is usually achieved with oral hypoglycemic drugs including a-glucosidase inhibitors,
sulfonylureas, meglitinides, D-phenylalanine derivatives, diguanides, and thiazolidinediones

287
Q

How do alpha-glucosidase inhibitors work?

A

a-Glucosidase inhibitors (acarbose, miglitol) decrease postprandial carbohydrate digestion and absorption at the intestinal brush border. By reducing absorption of starch, dextrose, and disaccharides, a-glucosidase inhibitors blunt the rise of postprandial glucose.

288
Q

Medications that blunt the rise of postprandial glucose?

A

Alpha glucosidase inhibitors

289
Q

What medications are classified as alpha glucosidase inhibitors?

A

Acarbose

Miglitol

290
Q

List the most common side effects of alpha-glucosidase inhibitors (FAD)

A

Flatulence
Abdominal cramping,
Diarrhea are side effects that frequently
result from undigested carbohydrates that reach bacteria in the lower colon.

291
Q

Medications for diabetes, Safe and nontoxix With the exception of occasional increases in liver transaminases,

A

alpha-glucosidase inhibitors

292
Q

What type of metabolic disturbance may furosemide (Lasix) promote?

A

Furosemide (Lasix) causes increased delivery of Na+ to the distal tubules and collecting ducts which increases K+ and H+ secretion, leading to HYPOKALEMIA and METABOLIC ALKALOSIS

293
Q

What type of metabolic disturbance may Acetazolamide (Diamox) promote?

A

Acetazolamide {Diamox) may promotes excretion of an alkaline urine and a resulting HYPERCHLOREMIC METABOLIC ACIDOSIS

294
Q

What diuretics is an inhibitor of carbonic anhydrase?

A

Acetazolamide

295
Q

Where does carbonic anhydrase act?

A

Proximal tubule

296
Q

Where does acetazolamide act?

A

Proximal tubule

297
Q

Osmotic diuretics medications are (3)

A

{mannitol, glycerin, isosorbide)

298
Q

Where do osmotic diuretic medication work

A

Loop of Henle (If you see proximal tubule may be right as well)

299
Q

What are loop diuretics (34) BET Fu

A

Bumetanide
Ethacrynic acid
Furosemide
Torsemide

300
Q

Loops diuretics act by

A

Inhibition of Na+-K-2Cl- symport acting at the thick ascending limb (TAL) of the Loop of Henle.

301
Q

Loop diuretics work where

A

TAL of LOOP of HENLE

302
Q

What are the thiazide and thiazide like diuretics name a few?

A

HCTZ, chlorothiazide, Methylclothizide, -zide, -azone, -one)

303
Q

How do the thiazide diuretics work?

A

Inhibition of Na+-Cl- symport at the distal tubules

304
Q

What are 2 of the potassium-sparing diuretics?

A

Triamterene

Amiloride

305
Q

How does potassium sparing diuretics work?

A

Inhibit renal sodium channels in the LATE DISTAL TUBULE and COLLECTING TUBULE

306
Q

Where does potassium sparing diuretics work

A

LATE DISTAL TUBULE

COLLECTING TUBULE

307
Q

What are the medications classified as ANTAGONISTS of mineralcorticoid receptors?

A

Spironolactone

Eplerenone

308
Q

Where do Antagonists of mineralcorticoid receptors work?

A

Late Distal tubule

collecting ducts

309
Q

A human recombinant BNP is what medications?

A

Nesiritide

310
Q

Where does nesiritide, a human recombinant BNP work?

A

at the inner medullary collecting duct

311
Q 
Mnemonic to remember where medications class work 
COL TKA
A 
Carbonic anhydrase inhibitors
Osmotic diuresis
Loop diuretics
Thiazides
K+ Sparing
Aldosterone Antagonists.
312
Q

Bleomycin is toxic to what body organ?

A

Bleomycin, an antibiotic/chemotherapeutic, is toxic to the pulmonary system.

313
Q

Why does bleomycin accumulate in the pulmonary system?

A

Bleomycin is concentrated preferentially in the lung because the enzyme that inactivates bleomycin {hydrolase) is relatively deficient in lung tissue

314
Q

In what two ways does bleomycin damage the lung?

A

l) Bleomycin initially produces pulmonary capillary endothelial damage, progressing to alveolar epithelial injury with necrosis of type I and proliferation of type II alveolar cells. Interstitial fibrosis develops and may progress to involve the entire lung. (2) Pulmonary injury also occurs because of the production of reactive oxygen metabolites.

315
Q

In lungs, Bleomycin generates

A

superoxide anions which damage tissue and also attract and activate neutrophils and macrophages. Neutrophils and macrophages cause tissue damage when activated.

316
Q

Pulmonary toxicity occurs in what percentage of the patient’s treated with bleomycin?
4. Cisplatin is

A

Pulmonary toxicity occurs in 10-25% of patients on bleomycin. The toxicity ranges from a decrease in pulmonary function to severe pulmonary fibrosis.

317
Q

WIth BLEOMYCIN, Do pulmonary function tests demonstrate normal function, restrictive disease, or obstructive disease?

A

Pulmonary function tests demonstrate restrictive pulmonary disease

318
Q

What happens to pulmonary diffusing capacity with BLEOMYCIN?

A

decreased pulmonary diffusing capacity

319
Q

Cisplatin is toxic to what organ?

A

Kidney

320
Q

How does kidney function change during cisplatin therapy?

A

Cisplatin causes a progressive fall in glomerular filtration rate (GFR) and development of acute tubular necrosis beginning 3 to 5 days after administration.

321
Q

There is_______ and ________ with cisplatin therapy

A

Increase BUN and Creatinine

322
Q

2 issues with cisplastin aside from INcrease BUN and cr

A

Proteinuria
Hyperuricemia
There is a magnesium-wasting defect in up to 50% of patients. Renal impairment may progress to acute renal
failure requiring hemodialysis.

323
Q

Antiemetic agents typically block one (or more) of six receptors-list these six receptors. HiMuDoGSeN

A

(2) histamine receptors
(3) muscarinic Ach Receptors
((l) dopamine receptors (D2)
(5) GABA A receptors;
(4) serotonin receptors (S-HT3); and,
(6) NKl (neurokinin-l) receptors.

324
Q

Antiemetics and receptors: Dopamine receptors

A

metodopramide, droperidol, haloperidol, alizapride, perphenazine, and prochlorperazine

325
Q

Which dopamine receptor do antiemetic mostly work on

A

D2

326
Q

Antiemetic Medication that work on Histamine receptors (H1) receptors

A

dimenhydrinate, diphenhydramine, cyclizine, and promethazine. Muscarinic ACh receptors: hyoscine.

327
Q

Antiemetic Medications that work on Serotonin receptors (5-HT3) :” -setron”

A

ondansetron, dolasetron, granisetron, tropisetron,

ramosetron, and palonosetron.

328
Q

Antiemetic medication work on Neurokinin-1 receptors NK

A

Aprepitant

329
Q

The antiemetic mechanism of action of dexamethasone is

A

unknown

330
Q

List 8 treatments for hypercalcemia.

A

(l) volume expansion with normal saline (4-6 Lin first 24 hours)
(2} loop diuretics (enhances renal excretion of calcium)
(3) bisphosphonates (zoledronic acid, pamidronate, etidronate) to inhibit bone resorption of calcium
(4} mithramycin
(5) calcitonin
(6)Glucocorticoids
(7) phosphates, and
(8) rarely, plicamycin

331
Q

What is the Bronsted-Lowry theory?

A

The Bronsted-Lowry theory is a theory pertaining to acids and bases wherein the acid is a proton (hydrogen ion) donor and the base is a proton (hydrogen ion) acceptor

332
Q

What is the pH of a liter of water?

A

pH= 7, at 24 degrees C.

333
Q

What is an acid? Why is a substance called a weak acid?

A

An acid is a hydrogen ion, or proton, donor. A weak acid is one that does not ionize 100% in solution. Strong acids, such as hydrochloric acid, are 100% ionized in solution

334
Q

Why is carbonic acid considered a weak acid?

A

Carbonic acid ionizes only 0.2% in physiologic solution. An acid that does not dissociate 100% to its ionized form is a weak acid.

335
Q

What agents used in anesthesia are weak acids?

A

Barbiturates and propofol

336
Q

What agents used in anesthesia are weak bases?

A

Weak bases include: all local anesthetics; all opioids (fentanyl, alfentanil, morphine, etc); benzodiazepines (diazepam, midazolam, etc); etomidate;nand ketamine.

337
Q

What are optical isomers? Give two examples.

A

Optical isomers are mirror images. L-glucose and d-glucose are examples of optical isomers. L-ketamine and d-ketamine are also optical isomers.

338
Q

What is the name for two optical isomers mixed together in a solution?

A

A solution with two optical isomers is a racemic solution

339
Q

Le Chatelier’s principle, derived from the law of mass action is when

A

When the concentration of a reactant increases, the reaction is driven toward the production of products. Conversely, when the concentration of reactant decreases,
the reaction is driven toward the production of more reactants and less products.

340
Q

Le Chatelier’s principle, derived from what law?

A

law of mass action

341
Q

What effect does hypothermia have on gas solubility?

A

As a liquid is cooled, more gas dissolves in the liquid, therefore hypothermia will cause an increase in gas solubility.

342
Q

Define the inverse square law.

A

Isaac Newton demonstrated that the strength of emanating energy is inversely proportional to the square of its distance from the source, the inverse square law.

343
Q

Newton’s original description was for the force of gravity and we now know the inverse square law applies to

A

pressure energy (sound), light, electricity, and radiation

344
Q

Occupational exposure to radiation comes primarily from X-rays scattered by the patient and the surrounding
equipment, rather than directly from the X-ray generator itself. State 4 methods to minimize exposure to scattered
radiation.

A

1) Limit the Duration of exposure.
(2) Increase the Distance from source (the inverse square law)
(3) Use protective shielding such as lead-lined garments or protective shields-Deflect the radiation.
(4) Use a Dosimeter to monitor exposure

345
Q

Since X-rays obey the inverse square law, the best protection from scattered radiation is physical separation. What is the minimum safe distance from the
X-ray source?

A

Since X-rays obey the inverse square law, the minimum recommended distance from an X-ray source is 6 feet.

346
Q

X-rays obey what law?

A

inverse square law,

347
Q

The greatest intensity of an X-ray is

A

directly in front of the beam generator.

348
Q

Standing at least 6 feet away and behind or to the side of the beam direction

A

lessens exposure

349
Q

What is the annual dose limit for occupational exposure to radiation?

A

In the United States, the National Council on Radiation Protection and Measurements (NCRP) recommends a limit for occupational exposure to radiation of 50 mSv (5 rem) in any 1 year.

350
Q

The lifetime dose limit for radiation exposure is

A

The lifetime limit for occupation exposure to radiation is 10 mSv (1 rem) multiplied by the individual’s age

351
Q

What is Dalton’s law?

A

Dalton’s law of partial pressures states that the total pressure (TP) of a group of gases is equal to the sum of their individual partial pressures. • Mathematically, Ptotal = P1 + P2 + P3.

352
Q

The formation of metanephrine is the result of:

A

catechol-O-methyltransferase metabolism of epinephrine

353
Q

Catechol-O-methyltransferase (COMT) metabolizes epinephrine to and norepinephrine to normetanephrine

A

metanephrine

354
Q

Subsequently, monamine oxidase (MAO) further metabolizes metanephrine and normetanephrine to

A

vanillymandelic acid (VMA).

355
Q

Catechol-O-methyltransferase (COMT) metabolizes norepinephine to

A

normetanephrine

VALLEY: Bolts & Bulls ONLY (4 decks)

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