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Section 2 study Flashcards

1
Q

DECREASE IN CELL SIZE DUE TO LOSS OF SUB-CELLULAR COMPONENTS, WHICH LEADS TO A DECREASE IN THE SIZE OF THE TISSUE OR ORGAN.

A

ATROPHY

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2
Q

INCREASE IN THE SIZE OF THE CELLS DUE TO THE SYNTHESIS OF MORE SUB-CELLULAR COMPONENTS, WHICH IN TURN LEADS TO AN INCREASE IN TISSUE AND ORGAN SIZE

A

HYPERTROPHY

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3
Q

AN INCREASE IN THE ACTUAL NUMBER OF CELLS IN AN ORGAN OR TISSUE, USUALLY RESULTING IN AN INCREASE IN THE SIZE OF AN ORGAN OR TISSUE.

A

HYPERPLASIA

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4
Q

AN ALTERATION IN THE SIZE, SHAPE, AND ORGANIZATION OF CELLS.

A

DYSPLASIA

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5
Q

THE REVERSIBLE CELLULAR ADAPTATION IN WHICH ONE ADULT CELL TYPE IS REPLACED BY ANOTHER ADULT CELL TYPE.

A

METAPLASIA

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6
Q

A TENDENCY TO CONTANCY OR STABILITY IN THE BODY’S INTERNAL ENVIRONMENT; PROCESSES THAT BALANCE THE SUPPLY AND DEMAND OF THE BODY’S NEED.

A

HOMEOSTASIS

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7
Q

LACTATED RINGER SOLUTION

A

USED IN THE FIELD FOR PATIENTS WHO HAVE SIGNIFICANT BLOOD LOSS. IT CONTAINS LACTATE, WHICH IS METABOLIZED IN THE LIVER TO FORM BICARBONATE - THE KEY BUFFER THAT COMBATS THE INTRACELLULAR ACIDOSIS ASSOCIATED WITH SEVERE BLOOD LOSS.

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8
Q

WHAT ARE THE EFFECTS OF SEVERE PROLONGED STRESS?

A

MAY CAUSE THE BODY TO LOSE ITS ABILITY TO FIGHT DISEASE.

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9
Q

DEFINE AND DESCRIBE DISTRIBUTIVE SHOCK.

A

OCCURS WHEN THERE IS WIDESPREAD DILATION OF THE RESISTANCE VESSELS, THE CAPACITANCE VESSELS, OR BOTH. CIRCULATING BLOOD VOLUME THEN POOLS IN THE EXPANDED VASCULAR BEDS, AND TISSUE PERFUSION DECREASES. THREE MOST COMMON TYPES: ANAPHYLACTIC, SEPTIC, AND NEUROGENIC SHOCK.

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10
Q

WHAT IS THE MOST PREVALENT CATION IN THE EXTRACELLULAR FLUID?

A

SODIUM

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11
Q

WHAT IS THE DIFFERENCE BETWEEN TYPE 1 AND TYPE 2 DIABETES?

A
  • TYPE 1 - INSULIN-DEPENDENT - NOT CURABLE
  • TYPE 2 - NON-INSULIN-DEPENDENT - MANAGED WITH WEIGHT LOSS, PHYSICAL ACTIVITY, AND MEDICATIONS.
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12
Q

HOW DO ASPIRIN AND NSAIDS REDUCE INFLAMMATION AND PAIN?

A

THEY INHIBIT PROSTAGLANDIN SYNTHESIS.

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13
Q

ASCITES

A

ACCUMULATION OF FLUID IN THE PERITONEAL CAVITY.

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14
Q

THE PURPOSE OF MAGNESIUM AND WHERE IS IT STORED?

A

COENZYME IN THE METABOLISM OF PROTEINS AND CARBOHYDRATES, CONTROLS NEUROMUSCULAR IRRITABILITY. STORAGE: 50% BONES, 49% CELLS, 1% EXTRACELLULAR FLUID.

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15
Q

ALZHEIMER EARLY STAGE NOTICEABLE CHANGES:

A

MEMORY LOSS, LACK OF SPONTANEITY, SUBTLE PERSONALITY CHANGES, AND DISORIENTATION TO PLACE AND TIME.

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16
Q

DIFFERENCE BETWEEN BASOPHILS AND MAST CELLS.

A

BASOPHILS IN THE BLOODSTREAM. MAST CELLS IN CONNECTIVE TISSUE.

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17
Q

INDICATIONS OF DECOMPENSATED SHOCK

A
  • ALTERED MENTAL STATUS
  • HYPOTENSION
  • LABORED OR IRREGULAR BREATHING
  • THREADY OR ABSENT PERIPHERAL PULSES
  • ASHEN, MOTTLED, OR CYANOTIC SKIN
  • DILATED PUPILS
  • DIMINISHED URINE OUTPUT (OLIGURIA)
  • IMPENDING CARDIAC ARREST
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18
Q

CARDIOGENIC SHOCK CAN OCCUR FROM NUMEROUS CAUSES, WHICH IS THE MOST COMMON?

A

MYOCARDIAL INFARCT, SINGLE EVENT OR CUMULATIVE.

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19
Q

INFLAMMATION IS NORMALLY CAUSED BY WHAT CONDITIONS?

A

PRESENCE OF CELLULAR INJURY, INCLUDING TRAUMA, INFECTION, AND HYPOXIA

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20
Q

DURING AN IMMUNE RESPONSE, WHAT IS THE CHIEF WHITE BLOOD CELL?

A

LYMPHOCYTES

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21
Q

SYNCOPE CAN BE A SYMPTOM OF A MORE SERIOUS PROBLEM. WHEN MIGHT SYNCOPE NOT INDICATE A SERIOUS PROBLEM?

A

ORTHOSTATIC HYPOTENSION, VAGAL VASAL.

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22
Q

WHERE IS NON-STRIATED MUSCLE LOCATED, AND WHAT IS ANOTHER NAME FOR IT?

A

VESSELS, GLANDS, AND GASTROINTESTINAL TRACT, SMOOTH MUSCLE

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23
Q

WHICH FLUIDS ARE CONSIDERED OR ARE CLASSIFIED AS INTERSTITIAL?

A

FLUID OUTSIDE THE BLOOD VESSELS AND IN THE SPACES BETWEEN THE BODY CELLS.

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24
Q

WHAT SIGNS AND SYMPTOMS WOULD INDICATE ANAPHYLACTIC SHOCK.

A

WHEEZING, HIVES, URTICARIA, DIFFICULTY BREATHING, TIGHTNESS IN CHEST, TROUBLE SWALLOWING, HYPOVOLEMIA, SWELLING, BRUISING.

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25
Q

WHAT HORMONES ARE CONSIDERED ENDOCRINE AND EXOCRINE?

A

ENDOCRINE EXCRETE WITHOUT DUCTS. EXOCRINE EXCRETES THROUGH DUCTS.

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26
Q

WHAT CONDITIONS WOULD CAUSE A RETENTION OF CO2?

A

COPD, SLEEP APNEA, HYPOVENTILATION.

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27
Q

WHAT CONDITIONS MAY CAUSE HYPERKALEMIA AND HOW MIGHT IT MANIFEST ON EKG?

A

RENAL FAILURE, MEDICATIONS THAT INHIBIT SECRETION OF POTASSIUM, BURNS, CRUSH INJURIES, METABOLIC ACIDOSIS, AND INSULIN DEFICIENCY. MAY SHOW FATAL DYSRHYTHMIA ON EKG.

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28
Q

WHERE ARE BARORECEPTORS LOCATED? WHAT CHANGES ARE THEY MOST SENSITIVE TO?

A

ARTERY WALLS, VEINS, AND HEART, MOST IMPORTANT ARE IN THE CAROTID SINUS AND HEART. DETECTS PRESSURE CHANGES IN RESISTANCE VESSELS AND HEART.

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29
Q

WHAT TYPE OF SHOCK WOULD OCCUR WITH A LOSS IN SYMPATHETIC NERVOUS SYSTEM TONE?

A

NEUROGENIC SHOCK

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30
Q

DEFINE AND CHARACTERIZE ACIDOSIS IN REGARDS TO HYDROGEN IONS AND PH.

A

IF THE INTRACELLULAR PH IS LOW, THEN THE EXCESSIVE NUMBER OF HYDROGEN IONS IN THE EXTRACELLULAR FLUID WILL SIGNAL THE CELL TO ACCEPT MORE HYDROGEN IONS GIVING IT AN OVERALL POSITIVE CHARGE. IN AN ATTEMPT TO RETURN ITS CHARGE TO NEUTRAL, THE CELL BEGINS TO SHIFT POTASSIUM AND OTHER CATIONS INTO THE INTERSTITIAL FLUID.

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31
Q

APOPTOSIS

A

NORMAL CELL DEATH. IT IS GENETICALLY PROGRAMMED INTO THE CALL AS PART OF NORMAL DEVELOPMENT, ORGANOGENESIS, IMMUNE FUNCTION, AND TISSUE GROWTH. IT HAS A NORMAL ROLE IN AGING, EARLY DEVELOPMENT, MENSES, LACTATING BREAST TISSUE, THYMUS INVOLUTION, AND RED BLOOD CELL TURNOVER.

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32
Q

HOW DO ASPIRIN AND NSAIDS REDUCE INFLAMMATION AND PAIN?

A

THEY INHIBIT PROSTOGLANDIN SYTHESIS, REDUCING INFLAMMATION AND PAIN

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33
Q

DEFINE AND DESCRIBE DISTRIBUTIVE SHOCK

A

OCCURS WHEN THERE IS A WIDESPREAD DILATION OF THE RESISTANCE VESSELS, THE CAPACITANCE VESSELS, OR BOTH. THE CIRCULATING BLOOD VOLUME POOLS IN THE VASCULAR BEDS, AND TISSUE PERFUSION DECREASES.

34
Q

WHAT ARE THE EFFECTS OF SEVERE PROLONGED STRESS?

A

IT MAY CAUSE THE BODY TO LOSE ITS ABILITY TO FIGHT DISEASE IN AN EFFORT TO MANAGE THE STRESS.

35
Q

WHAT IS THE CARDINAL SIGN OF OVER-HYDRATION?

A

EDEMA

36
Q

WHAT IS THE MOST PREVALENT CATION OF THE EXTRACELLULAR FLUID?

A

SODIUM

37
Q

HOW DO BACTERIA AND VIRUSES DIFFER?

A

BACTERIA ARE LIVING ORGANISMS THAT CAN SURVIVE AND MULTIPLY ON THIER OWN, VIRUSES ARE NOT LIVING AND REQUIRE A HOST CELL.

38
Q

WHERE IS EPITHELIAL TISSUE LOCATED?

A

EVERYWHERE IN THE BODY BUT FOR OUR CHAPTER, THE LOWER RESPIRATORY TRACT.

39
Q

WHAT DESTROYS FOREIGN MATERIAL SUCH AS BACTERIA AND OTHER ORGANISMS?

A

NEUTROPHILS

40
Q

WHAT IS THE DIFFERENCE BETWEEN TYPE 1 AND TYPE 2 DIABETES?

A

TYPE 1 IS CONSIDERED INSULIN DEPENDENT AND NOT CURABLE, TYPE 2 IS NOT CONSIDERED INSULIN DEPENDENT, AND CAN BE MANAGED BY LIFETSTYLE CHANGES AND MEDICATIONS.

41
Q

CONDITIONS THAT CAN CAUSE HYPERVENTILATION.

A

DRUG OVERDOSE (ESPECIALLY ASPIRIN), FEVER, OVER-BVM VENTILATION.

42
Q

SIDE EFFECTS OF DIGESTING ASPIRIN.

A

ALKALOSIS

43
Q

RESULT OF OXYGEN NOT REACHING THE CELL.

A

CELLS THAT ARE HYPOXIC FOR MORE THAN A FEW SECONDS PRODUCE MEDIATORS THAT MAY DAMAGE AREAS NEAR OR FAR FROM THE INITIAL AREA OF DAMAGE IN THE BODY. THE RESULT ID A POSITIVE FEEDBACK CYCLE IN WHICH MEDIATORS LEAD TO MORE CELL DAMAGE, WHICH LEADS TO MORE HYPOXIA, THEN MORE MEDIATORS ETC ETC.

44
Q

BIGGEST CAUSE OF CARDIAC FUNCTION DECLINE WITH AGE.

A

ATHERSCLEROSIS

45
Q

BASICS OF WHEN BABIES START INTERACTING / TALKING.

A
  • ONE TO TWO WORDS = 1 YEAR
  • BASIC LANGUAGE MASTERY = 36 MONTHS
  • YEARS 2 TO 5 = NUMBER OF WORDS EQUAL # OF YEARS.
  • BY AGE 3-4 SPEAK FULL SENTENCES AND BEGIN INTERACTION WITH OTHER CHILDREN.
46
Q

BODY RESPONSE TO HYPOPERFUSION.

A

WHEN THE BODY SENSES TISSUE HYOPERFUSION IT SETS COMENSATORY MECHANISMS INTO MOTION. IN SOME CASES THIS ACTION IS SUFFICIENT TO STABILIZE THE PATIENTS CONDITION. AT THIS POINT, THE SHOCK IS CALLED COMPENSATED SHOCK.

47
Q

HYPONATREMIA, CAUSE AND TREATMENT.

A

SODIUM SERUM LEVEL LESS THAN OR EQUAL TO 135 mEq/L. LIMIT FLUID INTAKE, SALINE REPLACEMENT, DIURETICS.

48
Q

ANAPHYLACTIC SHOCK. TYPE OF SHOCK, CAUSE, TREATMENT.

A

ANAPHYLACTIC SHOCK IS A FORM OF DISTRIBUTIVE SHOCK. CAUSED BY HISTAMINE AND OTHER VASODILATOR PROTIENS ARE RELEASED ON EXPOSURE TO AN ANTIGEN. * REMOVE FROM OFFENDING AGENT. * MONITOR AIRWAY, INTERVENTION MAY BE REQUIRED. * ADMINISTER ANTIHISTAMINE (EPI) * HIGH FLOW O2 * LACTATED RINGERS OR NORMAL SALINE.

49
Q

RESPIRATORY ALKALOSIS - WHAT CAUSES CARPO-PEDAL SPASMS?

A

HYPOCALCEMIA. ALKALOSIS INCREASED RESP RATE DECREASED Co2 DECREASED H2Co3

50
Q

VENTRICULAR HYPERTROPY AS IT RELATES TO HYPERTENSION.

A

LEFT VENTRICLE HYPERTROPPHY IN RESPONSE TO HIGH RESISTANCE PRESSURE FROM HYPERTENSION.

51
Q

DEFECTIVE X GENE, WHERE DOES IT COME FROM?

A

MOTHER OR FATHER. FEMALE RECEIVES X FROM EACH. MALE RECEIVES X FROM MOTHER.

52
Q

HYPOKALEMIA EFFECTS

A

MILD TO MODERATE CASES:

  • MUSCLE WEAKNESS
  • FATIGUE
  • MUSCLE CRAMPS

SEVERE CASES:

  • FLACCID PARALYSIS
  • HYPOREFLEXIA
  • TETANY
53
Q

HYPERKALEMIA EFFECTS

A
  • MUSCLE WEAKNESS
  • FLACCID PARALYSIS (RARE)
  • DYSRHYTHMIA
54
Q

HEALTH RISKS ASSOCIATED WITH OBESITY.

A
  • HYPERTENSION
  • HYPERLIPIDEMIA
  • CARDIOVASCULAR DISEASE
  • GLUCOSE INTOLERANCE INSULIN RESISTANCE
  • DIABETES
  • GALLBLADDER DISEASE
  • INFERTILITY
  • CANCER OF THE ENDOMETRIUM, BREAST, PROSTATE, AND COLON.
55
Q

KNOW EVERYTHING ABOUT “B” LYMPHOCYTES

A
  • BORN AND MATURE IN MARROW (FROM STEM CELL)
  • CLONAL SELECTION THEORY MAKES ANTIBODIES WITH ONLY ONE TYPE OF ANTIGEN-BINDING REGION. SPECIFIC FOR A SPECIFIC ANTIGEN (KNOWN AS COGNATE ANTIGEN)
  • ANTIBODIES ARE ON THE SURFACE OF “B” CELLS, WHERE THEY ARE ABLE TO RECOGNIZE THE PRESENCE OF THEIR COGNATE ANTIGEN. UPON RECOGNITION OF THE COGNATE ANTIGEN, THE B CELL PROLIFERATES TO MAKE MORE IDENTICAL B CELLS IN AN EXPONENTIAL MANNER. EACH OF THESE CAN MAKE ANTIBODIES THAT RECOGNIZE THE SAME ANTIGEN.
  • FOR B CELLS TO PRODUCE ANTIBODIES, B CELLS MUST FIRST BE ACTIVATED MOST COMMONLY BY HELPER T CELLS SECRETING LYMPHOKINES.
  • PARENT CELL CREATES A GROUP OF IDENTICAL CELLS. THE CLONE COMPROMISES TWO TYPES OF IDENTICAL CELLS THAT HAVE DIFFERENT FUNCTIONS: PLASMA CELLS WHICH MAKE ANTIBODIES, AND MEMORY CELLS THAT REMEMBER THE INITIAL ENCOUNTER WITH THE ANTIBODY.
56
Q

WHAT TYPES OF DISEASES CAN CAUSE DELAYS IN WOUND HEALING?

A

DIABETES AIDS HEMATOLOGIC ABNORMALITIES

57
Q

AS THE BODY CHANGES WITH AGE, HOW DOES THIS AFFECT THE VASCULAR SYSTEM (IE BLOOD PRESSURE)

A

THE VASCULAR SYSTEM BECOMES STIFF, CAUSING A HIGHER DIASTOLIC BLOOD PRESSURE.

58
Q

NORMAL PH RANGE (ACID / BASE)

A

ACIDOSIS < 7.35 < NORMAL PH < 7.45 < ALKALOSIS

59
Q

WHICH CELLS DESTROY ORGANISMS THAT ARE INVADING?

A

PHAGOCYTES

60
Q

ASCITES

A

ACCUMULATION OF EXCESS FLUID IN THE PERITONEUM, CAUSING EDEMA. A COMMON CAUSE IS CIRRHOSIS OF THE LIVER.

61
Q

RENAL (KIDNEY) RESPONSE TO HIGH AMOUNTS OF ACID (ACIDOSIS).

A

KIDNEYS REABSORB HYDROGEN AND EXCRETE POTASSIUM.

62
Q

ACUTE INFLAMMATORY RESPONSE

A

ARTERIOLES CONSTRICT TO LIMIT BLOOD LOSS, THEN DILATE, ALLOWING AN INFLUX OF BLOOD UNDER INCREASED PRESSURE. THIS CAUSES BLOOD VESSELS TO EXPAND MAKING THE VESSEL WALLS THINNER. HIGHER PRESSURE AND INCREASED VESSEL WALL PERMEABILITY CAUSE FLUID TO LEAK INTO THE INTERSTITIAL SPACES (EDEMA). WHEN ENOUGH FLUID HAS ESCAPED, INTRAVASCULAR PRESSURE IS RELEASED, VESSEL WALLS CONTRACT AND FLOW SLOWS, LEADING TO THE POOLING OF BLOOD IN THE CAPILLARIES.

63
Q

BASOPHIL

A

A WBC THAT RELEASES HISTAMINE DURING INFLAMMATION.

64
Q

EOSINOPHIL

A

A WBC THAT PHAGOCYTIZES THE ANTIGEN-ANTIBODY COMPLEX; ATTACKS PARASITES

65
Q

NEUTROPHILS

A

A WBC THAT PHAGOCYTIZES BACTERIA. MOST ABUNDANT WBC.

66
Q

MONOCYTES

A

A WBC THAT PHAGOCYTIZES BACTERIA, DEAD CELLS, AND CELLULAR DEBRIS.

67
Q

LYMPHOCYTE

A

A WBC INVOLVED IN IMMUNE PROTECTION; ATTACKS CELLS DIRECTLY OR PRODUCES ANTIBODIES.

68
Q

MACROPHAGE

A

A WBC WITHIN TISSUES; PRODUCED BY DIFFERENTIATION OF MONOCYTES. FUNCTIONS INCLUDE PHAGOCYTOSIS AND STIMULATING LYMPHOCYTES AND OTHER IMMUNE CELLS TO RESPOND TO PATHOGENS; ONE OF THE FIRST-LINE DEFENSES IN THE INFLAMMATORY RESPONSE.

69
Q

MAST CELLS

A

A WBC THAT IS FOUND IN THE CONNECTIVE TISSUES, BELOW THE SKIN, IN THE GASTROINTESTINAL MUCOSA, AND IN THE MUCOSA MEMBRANES OF THE RESPIRATORY SYSTEM. FUNCTIONS RELATE TO ALLERGIC REACTIONS, IMMUNITY, AND WOUND HEALING.

70
Q

PLASMA CELLS

A

WBC THAT DEVELOP FROM B CELLS AND PRODUCE LARGE VOLUMES OF SPECIFIC ANTIBODIES.

71
Q

B CELLS (B LYMPHOCYTES)

A

CELLS THAT MATURE IN THE BONE MARROW WHERE THEY DIFFERENTIATE INTO MEMORY CELLS OR IMMUNOGLOBULIN-SECRETING (ANTIBODY) CELLS. FUNCTIONS INCLUDE ELIMINATING BACTERIA, NEUTRALIZING BACTERIAL TOXINS, PREVENTING VIRAL INFECTION, AND PRODUCING IMMEDIATE INFLAMMATORY RESPONSES. REQUIRE T CELLS TO ACTIVATE.

72
Q

HELPER B CELLS

A

A TYPE OF REGULATOR CELL THAT ACTIVATES B CELLS TO PRODUCE ANTIBODIES

73
Q

MEMORY B CELLS

A

A TYPE OF B CELL THAT AIDS IN THE QUICK RESPONSE TO SUBSEQUENT EXPOSURES TO AN ANTIGEN BECAUSE MEMORY CELLS RECALL THE ANTIGEN IS FOREIGN. THESE CELLS RAPIDLY PRODUCE ANTIBODIES.

74
Q

T CELLS (T LYMPHOCYTES)

A

A WBC THAT IS PRODUCED IN THE BONE MARROW, BUT MATURE IN THE THYMUS. TWO MAJOR TYPES WORK TO DESTROY ANTIGENS, REGULATOR CELLS (HELPER T CELLS) AND EFFECTOR CELLS (KILLER T CELLS.

75
Q

KILLER T CELLS

A

A TYPE OF T CELL THAT DESTROYS CELLS INFECTED WITH VIRUSES BY RELEASING LYMPHOKINES THAT DESTROY CELL WALLS; ALSO CALLED CYTOTOXIC OR EFFECTOR CELLS.

76
Q

SHOCK

A

ABNORMAL STATE ASSOCIATED WITH INADEQUATE OXYGEN AND NUTRIENT DELIVERY TO THE METABOLIC APPARATUS OF THE CELL, RESULTING IN THE IMPAIRMENT OF CELLULAR METABOLISM AND, ULTIMATELY, INADEQUATE PERFUSION OF VITAL ORGANS. TYPES ARE:

  1. CENTRAL SHOCK
    1. CARDIOGENIC SHOCK
    2. OBSTRUCTIVE SHOCK
  2. PERIPHERAL SHOCK
    1. HYPOVOLEMIC SHOCK
    2. DISTRIBUTIVE SHOCK
      1. ANAPHYLACTIC SHOCK
      2. SEPTIC SHOCK
      3. NEUROGENIC SHOCK
77
Q

COMPENSATED SHOCK

A

WHEN THE BODY’S COMPENSATORY MECHANISMS TO SYSTEMIC HYPOVOLEMIA SUFFICIENTLY STABILIZE THE PATIENTS CONDITION. SYMPTOMS MAY INCLUDE:

  • AGITATION, ANXIETY, RESTLESSNESS
  • SENSE OF IMPENDING DOOM
  • WEAK, RAPID (THREADY PULSES)
  • CLAMMY (COOL, MOIST) SKIN
  • PALLOR WITH CYANOTIC SKIN
  • SHORTNESS OF BREATH
  • NAUSEA, VOMITING
  • DELAYED CAPILLARY REFILL (INFANTS AND CHILDREN)
  • THIRST
  • NORMAL BP
78
Q

DECOMPENSATED SHOCK

A

HYPOPERFUSION OVERWHELMS THE NORMAL COMPENSATORY MECHANISMS AND THE PATIENT’S CONDITION PROGRESSIVELY DETERIORATES. SYMPTOMS MAY INCLUDE:

  • ALTERED MENTAL STATUS
  • HYPOTENSION
  • LABORED OR IRREGULAR BREATHING
  • THREADY OR ABSENT PERIPHERAL PULSES
  • ASHEN, MOTTLED, OR CYANOTIC SKIN
  • DILATED PUPILS
  • DIMINISHED URINE OUTPUT (OLIGURIA)
  • IMPENDING CARDIAC ARREST
79
Q

DESCRIBE AIRWAY CHANGES WITH AGE

A

THE SIZE OF THE AIRWAY INCREASES AND THE SURFACE AREA OF THE ALVEOLI DECREASES. THE NATURAL ELASTICITY OF THE LUNGS DECREASES, FORCING PEOPLE TO RELY ON THEIR INTERCOSTAL MUSCLES TO BREATHE. CALCIFICATION OF THE RIBS TO THE STERNUM CAUSES CHEST RIGIDITY, DIAPHRAGM AND INTERCOSTALS BECOME WEAKER.

80
Q

EDEMA OF THE UPPER EXTREMITIES PARTICULARLY POST-MASTECTOMY.

A

REMOVAL OF LYMPH NODES IN A MASTECTOMY CAN CAUSE EDEMA.

81
Q

ALLERGY

A

HYPERSENSITIVITY REACTION TO THE PRESENCE OF AN ANTIGEN (ALLERGEN).

82
Q

AUTOIMMUNITY

A

PRODUCTION OF ANTIBODIES OR T CELLS THAT WORK AGAINST THE TISSUES OF ONE’S OWN BODY, PRODUCING HYPERSENSITIVITY REACTIONS OR AUTOIMMUNE DISEASE.

EMS (7 decks)

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