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Intro to Disease > Exam 2: Ch. 11-15 > Flashcards

Exam 2: Ch. 11-15 Flashcards

1
Q

hemostasis

A

cease of bleeding caused by activation of blood coagulation mechanism

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2
Q

factors affecting hemostasis

A
  • integrity of small blood vessels
  • number of platelets
  • normal amt. of coagulation factors/inhibitors
  • amt. of calcium ions
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3
Q

integrity of small blood vessels

A

constrict upon injury to facilitate closure by clot

-first line of defense

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4
Q

platelets

A

fragments of cytoplasm from large precursor cells called megakaryocytes

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5
Q

survival period of platelets

A

avg. 10 days

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6
Q

3 platelet functions

A
  1. plug defects in vessel walls
  2. free vasoconstrictors, causing platelets to aggregate
  3. release substances that initiate coagulation
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7
Q

blood coagulation factors

A

complex chain reaction with 3 phases

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8
Q

phase 1 of blood coagulation

A

formation of thromboplastin by interaction of intrinsic or extrinsic factors

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9
Q

intrinsic factors

A

in blood, platelets and plasma factors

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10
Q

extrinsic factors

A

components outside circulatory system

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11
Q

phase 2 of blood coagulation

A

conversion of prothrombin into thrombin

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12
Q

phase 3 of blood coagulation

A

conversion of fibrinogen into fibrin by thrombin

  • thrombin splits and forms fibrin monomers
  • monomers join into long fibrin strands
  • strands bond to form a clot
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13
Q

blood clot

A

end stage of clotting process

-made of meshwork of fibrin threads with plasma, red and white cells, and platelets

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14
Q

coagulation inhibitors

A

“counterbalance” factors-they restrict clotting to a limited area

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15
Q

fibrinolysin

A

plasmin that is formed by plasminogen after fibrin is dissolved upon formation

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16
Q

what mineral will blood not clot without?

A

calcium

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17
Q

4 categories of classification of coagulation disturbances

A
  1. abnormalities of small blood vessels
  2. abnormality of platelet formation
  3. deficiency of 1+ plasma coagulation factors
  4. liberation of thromboplastin material
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18
Q

abnormality of small blood vessels

A

abnormal bleeding resulting from failure of small blood vessels to contract after injury
-due to thrombocytopenia

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19
Q

thrombocytopenia

A

deficiency of platelets in blood

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20
Q

petechiae

A

pinpoint sized hemorrhages of small capillaries in skin or mucous membranes
-indicative of defective/inadequate platelets

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21
Q

hemophilia

A

x-linked hereditary disease affecting males

-episodes of hemorrhage in joints and internal organs after minor injury

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22
Q

hemophilia A

A

-classic hemophilia

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23
Q

hemophilia B

A

christmas disease

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24
Q

von Willebrand disease

A

von Willebrand factor (vWf)

-vWf adheres to damaged vessel wall and helps form a clot and a complex

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25
Q

anticoagulant drugs inhibit what?

A

synthesis of vitamin K dependent factors

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26
Q

severe liver disease does what?

A

impairs synthesis of adequate amounts of coagulation factors

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27
Q

3 causes of thrombocytopenia

A
  1. injury or disease of bone marrow-damages megakaryocytes
  2. leukemic or cancer cells infiltrate bone marrow
  3. anti platelet antibody destroys platelets
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28
Q

disseminated intravascular coagulation syndrome

A

abnormal bleeding state

  • activation of coagulation mechanism
  • products of necrosis liberated into circulation
  • results in hemorrhaging b/c fibrinolysin is activated to dissolve all clots
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29
Q

3 factors that activate coagulation mechanism

A
  1. diseases associated with shock
  2. overwhelming bacterial infection
  3. estensive tissue necrosis
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30
Q

platelet count

A

examination of blood smear for platelet numbers-evaluates efficiency of coagulation process

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31
Q

bleeding time

A

time it takes for a small skin lesion to stop bleeding; used to evaluate the function of capillaries in the hemostatic process

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32
Q

clotting time

A

time it takes for blood to clot in a test tube

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33
Q

partial thromboplastin time (PTT)

A

time it takes for blood plasma to clot after lipid substance added to plasma sample; measures time of first phase coagulation

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34
Q

prothrombin time (PT)

A

measures time of combined second and third phases of coagulation
-as this increases, risk for venous thrombosis increases

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35
Q

thrombin time

A

bypasses first two phases of coagulation, primarily measures level of fibrinogen

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36
Q

pathogenesis (development) of intravascular clotting

A

stasis of blood flow
vessel wall damage
increased coagulability of blood

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37
Q

thrombus

A

intravascular clot; can occur in any vessel or in heart

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38
Q

embolus

A

detached clot carried into pulmonary or systemic circulation; plugs small vessel blocking blood flow and causing necrosis

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39
Q

infarct

A

tissue necrosis from interruption in blood flow

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40
Q

venous thrombosis

A

clot formation in leg veins

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41
Q

predisposing factors to venous thrombosis

A
  • prolonged bed rest
  • cramped position for extended period
  • varicose veins, any condition preventing normal emptying
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42
Q

outcome of venous thrombosis

A

leg swelling from partial blockage of venous return

pulmonary embolism can occur

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43
Q

pulmonary embolism

A

embolus from venous thrombosis carried and lodged in pulmonary artery

  • can completely block main artery or major branches, obstructing blood flow to lungs
  • causes cyanosis and shortness of breath (inadequate oxygenation of blood)
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44
Q

what happens if the pulmonary embolus is large?

A

right side of the heart fills, pulmonary artery fills with blood, increasing pulmonary pressure, the left ventricle is unable to pump adequate blood to brain and vital organs, and blood pressure falls and shock can occur

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45
Q

what happens if the pulmonary embolus is small?

A

it may pass through the main pulmonary arteries and lodge in a peripheral artery, causing raise in pulmonary pressure and affected lung segment to undergo necrosis

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46
Q

if an infarct develops as a result of pulmonary embolism, what symptoms develop?

A

dyspnea, pleuritic chest pain, cough, and spitting up bloody sputum

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47
Q

chest x ray

A

can detect infarcts but not an embolus

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48
Q

radioisotope lung scans

A

detect abnormal pulmonary blood flow caused by embolus

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49
Q

pulmonary angiogram

A

gold standard

detects the blocked pulmonary artery

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50
Q

computed tomography (CT) scan

A

detects pulmonary embolus indicted by obstructed flow of injected contrast medium

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51
Q

treatment of pulmonary embolism

A
  • anticoagulants
  • thrombolytic drugs
  • angioplasty (balloon or stent)
  • thrombectomy
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52
Q

arterial thrombosis

A

development of clot in artery due to injury to vessel wall from arteriosclerosis that blocks blood flow to:

  1. coronary artery, causing Myocardial Infarction
  2. major leg artery, causing gangrene
  3. cerebral artery, causing stroke
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53
Q

in arterial thrombosis, an intracardiac thrombosis can form in 3 places:

A
  1. atrial appendages, causing heart failure
  2. surfaces of heart valves, causing valve injury
  3. wall of left ventricle, causing myocardial infarction
    - or may dislodge into circulation and cause infarction of an organ
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54
Q

thrombosis by increased coagulability

A

rise in coagulation factors following surgery or injury

-estrogen in oral contraceptives also stimulates clotting factors

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55
Q

embolism

A

blood clot, fat, air, amniotic fluid, and foreign particles

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56
Q

fat embolism

A

caused by severe bone fracture that disrupts fatty bone marrow
-fat globules sucked into veins and obstruct pulmonary capillaries

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57
Q

air embolism

A

large amount of air sucked into circulation from lung injury due to chest wound
-can get into heart chambers and prevent blood returning from body from filling heart

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58
Q

amniotic fluid embolism

A

amniotic fluid enters maternal circulation through tear in fetal membranes

  • maternal pulmonary capillaries blocked causing severe respiratory distress
  • leads to disseminated intravascular coagulation syndrome
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59
Q

foreign particulate matter embolism

A

various types of material

  • injections by substance users that crush tablets, trapped in small pulmonary blood vessels
  • causes respiratory distress
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60
Q

septic embolism

A

thrombus forms in pelvic veins after uterine infection, invaded by bacteria, travels to lungs causing infarct and lung abscess from bacteria

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61
Q

edema

A

accumulation of fluid in interstitial tissues, first noted in ankles and legs
-from disturbance of extracellular fluid circulation between capillaries and interstitial tissues

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62
Q

pitting edema

A

indentation formed when edematous tissue is pressed with fingers

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63
Q

hydrothorax

A

fluid accumulates in pleural cavity

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64
Q

ascites

A

fluid accumulates in peritoneal cavity

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65
Q

pathogenesis (development) of edema

A
  • increased capillary permeability
  • low plasma proteins
  • increased hydrostatic pressure
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66
Q

capillary hydrostatic pressure

A

force that pushes fluid from capillaries into extracellular space

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67
Q

capillary permeability

A

determines ease of fluid flow through capillary endothelium

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68
Q

osmotic pressure

A

water attracting property of a solution

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69
Q

open lymphatic channels

A

collect fluid forced out of capillaries by hydrostatic pressure and return fluid to circulation

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70
Q

shock

A

low blood flow/pressure to adequately supply body with blood

  • potentially life threatening
  • circulating blood volume
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71
Q

hypovolemic shock

A

low blood volume

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72
Q

cardiogenic shock

A

reduced cardiac output

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73
Q

septic shock

A

excessive vasodilation secondary to release of toxins and inflammatory mediators

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74
Q

anaphylactic shock

A

excessive vasodilation from release of inflammatory mediators

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75
Q

prognosis of shock depends on….

A

early recognition and rapid appropriate treatment

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76
Q

treatment for shock

A

drugs that promote vasoconstriction
IV fluids or blood to restore blood volume
treat underlying cause

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77
Q

function of heart

A

muscular pump, propels blood through the lungs and to tissues

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78
Q

heart disease

A

disturbance of heart function

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79
Q

location of heart

A

within mediastinum, 2/3 of heart lies left of midsternal line, and apex points towards left hip

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80
Q

pericardium

A

double walled sac that surrounds the heart

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81
Q

3 layers of pericardium

A

epicardium, myocardium, endocardium

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82
Q

epicardium

A

outer layer of pericardium, connective tissue, contains coronary arteries

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83
Q

myocardium

A

middle layer of pericardium, muscular layer, thickest, this layer actually pumps the heart

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84
Q

endocardium

A

innermost layer, visceral, smooth membrane, contains heart valves

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85
Q

right half of the heart

A

right atrium on top, right ventricle on bottom
-receives deoxygenated blood into RA from tissues from superior and inferior vena cava, goes through tricuspid valve to RV, RV pumps the blood to lungs to become oxygenated

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86
Q

left half of the heart

A

left atrium on top, left ventricle on bottom
-receives oxygenated blood into LA from lungs via pulmonary veins, goes through mitral valve (bicuspid) to LV, LV pumps blood to tissues and organs

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87
Q

semilunar valves

A

cup shaped valves at entrances of aorta and pulmonary arteries that prevent back flow of blood into ventricles during diastole (relaxation)

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88
Q

pulmonary valve

A

between right ventricle and pulmonary trunk to prevent back flow into right ventricle during diastole

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89
Q

aortic valve

A

between left ventricle and aorta to prevent back flow of blood into left ventricle during diastole

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90
Q

pulmonary circulation

A

oxygen poor blood enters the RA, goes through tricuspid valve to RV, enters pulmonary artery and goes to lungs

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91
Q

systemic circulation

A

oxygenated blood leaves lungs through pulmonary veins, enters LA, goes through mitral valve to LV, goes through aorta to rest of body

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92
Q

coronary circulation

A

supplies blood to the heart

  • aorta branches to coronary arteries, carries blood to the heart through capillary beds of myocardium
  • collected by cardiac veins, cardiac veins join to form coronary sinus that empties blood into RA
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93
Q

right coronary artery

A

supplies posterior wall and posterior part of interventricular septum

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94
Q

left coronary artery and branches

A

supplies anterior wall and anterior part of interventricular septum

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95
Q

what happens in cardiac necrosis?

A

cardiac muscle dies and it cannot proliferate to replace itself, so it is repaired with non-contractile scar tissue (doesn’t stretch)

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96
Q

angina pectoris

A

chest pain from temporary reduction in blood flow to cardiac muscles despite increased oxygen demand

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97
Q

causes of angina pectoris

A

narrowed coronary arteries-arteriosclerosis

stress induced spasm of coronary arteries

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98
Q

prolonged coronary artery blockage can lead to what?

A

myocardial infarction (MI)-heart attack

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99
Q

conduction system

A

specialized muscle cells that initiate electrical impulses in the heart, initiated in the sinoatrial node in the right atrium

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100
Q

systole

A

contraction period

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101
Q

diastole

A

relaxation period

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102
Q

cardiac cycle

A

all events associated with blood flow through heart during one heart beat
-atrial systole, atrial diastole, ventricular systole, ventricular diastole

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103
Q

cardiac output

A

5 liters/minute from each ventricle

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104
Q

blood pressure

A

blood flow in arteries results from force of ventricular contraction

  • systolic pressure is highest
  • diastolic pressure is lowest
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105
Q

electrocardiogram

A

ECG, EKG

measures electrical activity of the heart and detects disturbances in rate, rhythm, conduction, extent of muscle damage

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106
Q

cardiac arrhythmias

A

disturbances in heart rate or rhythm

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107
Q

atrial fibrillation

A

AF

the atria quiver instead of contracting, causing ventricles to beat irregularly

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108
Q

ventricular fibrillation

A

VF

ventricles don’t contract normally, incompatible with life

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109
Q

heart block

A
  • complete or incomplete

- delay or interruption of impulse transmission from atria to ventricles, from arteriosclerosis

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110
Q

congenital heart disease

A

birth defect

  • bypass channels don’t close normally
  • septal defects
  • obstruction of flow
  • abnormal formation of aorta and pulmonary artery
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111
Q

how to prevent congenital heart disease?

A

protect the developing fetus from intrauterine injury

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112
Q

rheumatic fever

A

common in children

  • immune reaction weeks after initial strep infection
  • fever and connective tissue inflammation, especially heart and joints
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113
Q

outcomes of rheumatic fever

A
  • scarring of cardiac tissues/valves
  • death from severe inflammation and acute heart failure
  • recurs if strep infection reactivates hypersensitivity and tissue damage
114
Q

rheumatic heart disease

A

complication of rheumatic fever where heart valves are scarred
-causes valve regurgitation or stenosis (narrowing)

115
Q

non rheumatic aortic stenosis

A 
aortic stenosis (narrowing), where aortic valve has 2 cusps instead of 3
-valve thickens, calcifies from increased strain leading to heart failure
116
Q

mitral valve prolapse

A

one or both leaflets enlarge, stretch, and prolapse into left atrium and don’t fit together tightly
-click sound on systole followed by a murmur

117
Q

serotonin-related heart valve damage

A 
increased serotonin in blood, released from:
-platelets and histamine
-nerve endings
-neuroendocrine tumors in GI tract
-drugs that suppress appetite
develops thickening of heart valves
118
Q

infective endocarditis

A

affects abnormal or damaged mitral and aortic valves

  • complication of any valvular heart disease
  • platelets and fibrin deposit on damaged valves, sites for bacteria to implant and thrombi to form
119
Q

acute infective endocarditis

A

highly pathogenic organisms, commonly staph
-affects normal heart valves, those at risk include IV drug users and if unsterile materials enter the right side of the heart forming bacteria sites for thrombi to form

120
Q

coronary heart disease

A

caused by arteriosclerosis

  • cholesterol and lipids accumulate, form crystals, causing necrosis
  • arterial walls calcify
  • atheroma forms (rough, ulcerated surface predisposed to clots)
121
Q

atheroma/atheromatous plaque

A

irregular mass of yellow, mushy debris extending into muscular and elastic tissues of arterial wall

122
Q

stable plaque

A

buildup in arteries surrounded by fibrous tissue, causing permanent narrowing of vessel

123
Q

most important coronary heart disease risk factors

A 
elevated blood lipids
high blood pressure
cigarette smoking
diabetes
-1 risk factor= 2x risk
-2 risk factors=4x risk
-3 risk factors=7x risk
124
Q

manifestations of coronary heart disease

A

asymptomatic, angina pectoris, oppressive chest pain that radiates into neck/arms

125
Q

what is ischemic heart disease?

A

coronary heart disease

-decreased blood supply to heart muscle from stenosis or obstruction of coronary arteries

126
Q

myocardial ischemia

A

stenosis or obstruction of coronary arteries

127
Q

stable angina

A

midsternal pressure or discomfort on exertion

128
Q

unstable angina

A

pain lasts longer, occurs more often, and is less completely relieved

129
Q

prinzmetal’s angina

A

pain at rest rather than exertion

130
Q

severe and prolonged myocardial ischemia may lead to an acute episode manifested as:

A 
myocardial infarction (necrosis of heart muscle)
cardiac arrest (cessation of cardiac contractions
131
Q

myocardial infarction

A

necrosis of heart muscle due to insufficient blood flow through coronary arteries

132
Q

transmural infarct

A

full thickness infarct from endocardium to epicardium, usually from major coronary artery clot

133
Q

subendocardial infarct

A

part of wall undergoes necrosis

134
Q

myocardial infarction often involves which part of the heart’s muscles?

A

left ventricle and septum

135
Q

mechanisms that trigger heart attack

A
  • sudden blockage of artery from thrombus
  • hemorrhage into atheromatous plaque
  • arterial spasm
  • sudden greatly increased myocardial oxygen requirements, such as from vigorous physical activities
136
Q

cardiac arrest may result from

A
  • arrhythmia from prolonged myocardial ischemia that disrupts ventricular contraction
  • asystole (cessation of cardiac contractions)
137
Q

pericarditis

A

inflammation and fluid accumulation in pericardial sac

-complication of MI where infarct extends to epicardial surface

138
Q

cardiac rupture

A

blood leaks into pericardial sac from perforation in necrotic muscle

139
Q

papillary muscle dysfunction

A

infarcted papillary muscle can’t control mitral valve resulting in mitral valve prolapse

140
Q

ventricular aneurysm

A

outward bulging of healing infarct during ventricular systole and blood fills aneurysm sac

141
Q

MI mortality rates

A

6% for small infarct w/o heart failure to >50% for large infarct w/ heart failure

142
Q

enzyme test

A

diagnoses MI, because enzymes leak out from necrotic cells after an infarct, and the larger an infarct, the longer for elevated levels to return to normal

143
Q

thrombolytic therapy

A

most effective if used within one hour of first MI symptoms b/c it may not dissolve clot completely

144
Q

streptokinase

A

enzyme from strep, reduces blood coagulability and dissolves clots

145
Q

tissue plasminogen activator

A

TPA

converts plasminogen to plasmin and dissolves clots

146
Q

aspirin

A

reduces tendency of platelets to aggregate and clot within one hour of ingestion, but increases risk of brain hemorrhage with stroke

147
Q

heparin

A

reduces coagulability of blood and clot formation

148
Q

bypass surgery

A

uses segment of saphenous (leg vein) vein to bypass the obstructed artery

149
Q

coronary angioplasty

A

a balloon or stent is inserted via catheter and expanded to push plaques to the side and dilate the vein

150
Q

cocaine-induced arrhythmias and infarcts

A

intensifies effects of sympathetic nervous system

  • heart rate, muscle irritability, and peripheral vein vasoconstriction
  • leads to increased O2 demand and blood pressure
151
Q

neutral fat

A

triglyceride from ingested fat, sugar, and carbs

152
Q

c-reactive protein

A

CRP

produced in liver and released in response to tissue injury or inflammation–high level predicts high CVD risk

153
Q

metabolic syndrome

A

abdominal obesity, hypertension, abnormal lipids, insulin resistance, impaired glucose tolerance
-leads to heart disease and type 2 diabetes

154
Q

homocysteine

A

sulfur-containing amino acid that when present in high levels is a risk factor for CVD

155
Q

hypertension

A

vasoconstriction of small arterioles

  • increased force of ventricular contraction
  • increase in systolic pressure
156
Q

cardiac effects of hypertension

A

higher workload, cardiomegaly, heart failure

157
Q

vascular effects of hypertension

A

increased pressure, accelerated atherosclerosis, rupture and hemorrhage

158
Q

renal effects of hypertension

A

decreased blood supply to kidneys, renal failure

159
Q

primary/essential hypertension

A

hypertension from an unknown etiology

160
Q

secondary hypertension

A

hypertension from a known disease

161
Q

isolated systolic hypertension

A

mild/moderate rise in systolic pressure, low or normal diastolic pressure

162
Q

two types of primary myocardial disease

A

myocarditis, cardiomyopathy

163
Q

myocarditis

A

inflammation, injury, and necrosis of individual muscle fibers caused by viruses, parasites, fungi, or hypersensitivity

164
Q

cardiomyopathy

A

no evidence of inflammation, dilated cardiomyopathy and hypertrophic cardiomyopathy

165
Q

dilated cardiomyopathy

A

enlargement of heart and dilation of chambers, unknown cause and no treatment, leads to heart failure

166
Q

hypertrophic cardiomyopathy

A

hereditary, transmitted as dominant trait, marked hypertrophy of heart muscle, reduces size of ventricles

167
Q

idiopathic hypertrophic sub aortic stenosis

A

IHSS

stenosis below aortic valve, causing excessive fatigue and lightheadedness on exertion

168
Q

heart failure

A

heart is no longer able to pump adequate amount of blood and can result from any type of heart disease

169
Q

chronic heart failure

A

develops slowly and insidiously

170
Q

acute heart failure

A

rapid onset

171
Q

forward failure

A

reduced blood flow to tissues, reduced renal blood flow, salt and water retention, edema

172
Q

backward failure

A

blood backs up in veins draining to heart, leading to increased venous pressure, congestion, and edema

173
Q

diuretic drugs

A

promote excretion of excess salt and water by kidneys to lower blood pressure

174
Q

digitalis

A

drug that increases efficiency of ventricular contraction

175
Q

ACE inhibitors

A

blocks angiotensin converting enzyme (ACE) that promotes retention of salt and water, increasing blood pressure

176
Q

acute pulmonary edema

A

manifestation of acute heart failure from temporary disproportion in ventricle output

  • right heart pumps blood into lungs faster than left heart delivers blood to tissues
  • lungs fill with blood
177
Q

aneurysms

A

dilation or out pouching of portion of arterial wall

-caused by arteriosclerosis and congenital causes

178
Q

arteriosclerotic aneurysm

A

narrowing, thrombosis, and weakening of vessel wall

-can occur in aorta, can rupture and lead to fatal hemorrhaging

179
Q

venous thrombosis

A

blockage of vein by clots

180
Q

phlebitis

A

inflammation of veins

181
Q

varices/varicosities

A

excessive dilation of veins

182
Q

stem cells

A

precursor cells in bone marrow that form red cells, white cells, and platelets

183
Q

red cells

A

transport oxygen, most numerous cells, can survive 4 months

184
Q

erythroblast

A

precursor red cell in bone marrow

185
Q

hemoglobin

A

oxygen-carrying protein formed by developing red call

186
Q

leukocytes

A

less numerous, survival rate is several hours to several days

187
Q

lymphocytes

A

can last several years, 2nd most common leukocyte

  • mostly located in lymph nodes, spleen
  • cell mediated defense reactions
188
Q

types of leukocytes

A

neutrophils, monocytes, eosinophils, and lymphocytes

189
Q

neutrophils

A

most numerous in adults, 70% of total circulating white cells
-predominant in inflammatory reactions

190
Q

monocytes

A

phagocytic, increased in certain chronic infections

191
Q

eosinophils

A

increased in allergic reactions or presence of animal-parasite infections

192
Q

platelets

A

essential for blood coagulation, smaller than leukocytes, survive for 10 days

193
Q

megakaryocytes

A

largest precursor cells in bone marrow that produce platelets

194
Q

hematopoiesis

A

formation and development of blood cells, bone marrow replenishes blood cells

195
Q

4 substances necessary for hematopoiesis

A

protein, vitamin B12, folic acid, iron

196
Q

reticulocyte

A

young red cell w/o nucleus but retains some organelles

197
Q

anemia

A

reduction in RBC or subnormal level of hemoglobin and deficiency of iron, vitamin B12, folic acid

198
Q

normocytic anemia

A

RBC have normal size and appearance

199
Q

macrocytic anemia

A

RBC larger than normal, show folic acid and vitamin B12 deficiency

200
Q

microcytic anemia

A

RBC smaller than normal

201
Q

hypochromic anemia

A

reduced hemoglobin content

202
Q

hypochromic microcytic anemia

A

smaller than normal RBC and reduced hemoglobin

203
Q

iron deficiency anemia

A
  • most common type
  • hypochromic microcytic
  • inadequate iron intake, menstruation, infants during rapid growth all susceptible
204
Q

characteristic lab profile of iron deficiency anemia

A
  • low serum ferritin and serum iron
  • high serum iron binding protein
  • low percent iron saturation
205
Q

treatment of iron deficiency anemia

A

primary focus is to learn the cause and direct treatment towards the cause, and administer iron supplement

206
Q

vitamin B12 deficiency anemia

A

leads to neurologic disturbance b/c it is required for structural and functional integrity of nervous system

207
Q

pernicious anemia

A

lack of intrinsic factor results in macrocytic anemia (intrinsic factor is in vitamin B12)

208
Q

folic acid deficiency anemia

A

relatively common, body has very limited stores which much be replenished continually
-inadequate diet, poor absorption from intestinal disease, and pregnancy all cause it

209
Q

complete blood count

A

assesses degree of anemia, leukopenia (reduced WBC), and thrombocytopenia (low platelets)

210
Q

blood smear

A

determine if blood cell size ir normal, macro, micro

211
Q

reticulocyte count

A

assesses rate of production of new red cells

212
Q

lab tests

A

determine iron, vitamin B12, and folic acid levels

213
Q

bone marrow study

A

studies abnormalities in bone marrow cells

214
Q

hemolytic anemia

A

hereditary, spherical, hemoglobin S and C, defective hemoglobin synthesis, and enzyme defects (G6PD)

215
Q

polycythemia

A

primary and secondary polycythemia

216
Q

secondary polycythemia

A

reduced oxygen saturation leads to increase in RBC

217
Q

primary polycythemia

A

overproduction of red cells, white cells, and platelets

218
Q

complications of polycythemia

A

clot formation due to increased blood viscosity and platelet count

219
Q

hemochromatosis

A

common genetic disease, transmitted as recessive trait

  • iron overload but hard to excrete
  • iron buildup leads to organ damage, scarring and derangement of organ function
220
Q

manifestations of hemochromatosis

A

take years to develop

  • tan to brown skin
  • diabetes
  • cirrhosis
  • heart failure
221
Q

treatment of hemochromatosis

A

periodic removal of blood (phlebotomy) until iron stores depleted

222
Q

thrombocytopenia

A

primary and secondary thrombocytopenia, where there is allow platelet count

223
Q

secondary thrombocytopenia

A

damage to bone marrow from drugs or chemicals, where bone marrow is infiltrated by leukemic cells

224
Q

primary thrombocytopenia

A

bone marrow produces platelets but are rapidly destroyed

225
Q

lymphatic system

A

provides immunologic defenses against foreign material via cell mediated defense mechanisms, made of lymph nodes and lymph veins

226
Q

lymph nodes

A

bean shaped structure consisting of mass of lymphocytes supported by meshwork of reticular fibers and phagocytic cells-phagocytic cells destroy microorganisms

227
Q

spleen

A

mass of lymphocytes that filters blood and forms antibodies

228
Q

lymphoid tissue

A

in thymus, tonsils, and adenoids. lymphoid aggregates in intestinal mucosa, respiratory tract, and bone marrow

229
Q

thymus

A

overlies base of heart–large during infancy and childhood, but atrophies during adolescence

230
Q

lymphadenitis

A

inflamed and enlarged lymph nodes

231
Q

infectious mononucleosis

A

caused by Epstein-Barr virus (EBV)

-infection of B lymphocytes, enlargement of spleen, lymph nodes, and lymphoid tissues

232
Q

neoplasms

A

metastatic tumors in breasts, lung, colon, and other sites

-spreads to more distant lymph nodes through lymph channels

233
Q

malignant lymphoma

A

hodgkin’s and non hodgkin’s

234
Q

lymphocytic leukemia

A

from lymphoid precursor cells

-can be acute or chronic

235
Q

effects of speed removal

A
  • less efficient elimination of bacteria
  • impaired antibody production
  • predisposed to systemic infections
236
Q

oxygen delivery

A

respiratory system oxygenates blood, removes CO2

-circulatory system transports gases in bloodstream

237
Q

how many lobes in each lung?

A

2-left

3-right

238
Q

bronchi

A

largest conducting tube for lungs

239
Q

bronchioles

A

less than 1mm, connected to bronchi

240
Q

terminal bronchioles

A

smallest tubes conducting air in and out of lungs

241
Q

respiratory bronchioles

A

distal to terminal bronchioles with alveoli, participate in gas exchange

242
Q

two functions of respiration

A

ventilation and gas exchange between alveolar air and pulmonary capillaries

243
Q

atmospheric pressure

A

760 mmHg

244
Q

requirements for efficient gas exchange

A
  • large capillary surface in contact with alveoli
  • uninterrupted diffusion across alveolar membrane
  • normal pulmonary blood flow
  • normal alveoli
245
Q

pulmonary function tests

A

evaluate efficiency of pulmonary ventilation and pulmonary gas exchange-measure volume of air moved in and out under normal conditions

246
Q

vital capacity

A

max volume of air expelled after max inspiration

247
Q

one-second forced expiratory volume (FEV)

A

max volume of air expelled in 1 sec.

248
Q

pleura

A

thin membrane covering lungs (visceral) and internal surface of chest wall (parietal)

249
Q

pleural cavity

A

potential space between lungs and chest wall

250
Q

intrapleural pressure

A

pressure within pleural cavity

251
Q

intrapleural (pleural cavity) pressure is lower or higher than intrapulmonary (within lungs) pressure?

A

less. aka negative pressure b/c it is less than atmospheric pressure

252
Q

pneumothorax

A

escape of air into pleural space due to lung injury or disease

253
Q

spontaneous pneumothorax

A

no apparent cause, rupture of a small air filled sac at lung apex

254
Q

manifestations of pneumothorax

A

chest pain, shortness of breath, reduced breath sounds

255
Q

tension pneumothorax

A

positive pressure develops in pleural cavity (higher than pressure within lungs), cured with chest tube

256
Q

atelectasis

A

lung collapse, can be caused by a bronchial obstruction

257
Q

compression atelectasis

A

caused by external compression of lung by fluid, air, or blood in pleural cavity

258
Q

pneumonia

A

inflammation of the lung

-exudate spread through lungs and alveoli, reaching pleural surface causing irritation and inflammation

259
Q

lobar

A

infection of entire lung by pathogenic bacteria

260
Q

bronchopneumonia

A

infection of parts of lobes or lobules adjacent to bronchi

261
Q

clinical features of pneumonia

A

fever, cough, purulent sputum (pus in sputum), pain on respiration, shortness of breath

262
Q

COPD

A

emphysema and chronic bronchitis

263
Q

pulmonary emphysema

A

destruction of alveolar structure, destruction begins in upper lobes, begins with dyspnea on exertion

264
Q

chronic bronchitis

A

chronic inflammation of terminal bronchioles; cough and purulent sputum

265
Q

3 main anatomic derangements in COPD

A
  1. inflammation and narrowing of terminal bronchioles
  2. dilation of pulmonary air spaces
  3. loss of lung elasticity, lungs no longer recoil normally following inspiration
266
Q

bronchial asthma

A

spasmodic contraction of smooth muscle walls of bronchi and bronchioles; dyspnea and wheezing on expiration

267
Q

neonatal respiratory distress syndrome

A

progressive respiratory distress soon after birth-alveoli don’t expand normally
-premature, c section, and diabetic mothers

268
Q

adult respiratory distress syndrome

A

shock is major manifestation, blood pressure falls and blood flow to lungs reduced

269
Q

traumatic shock

A

results from severe injury

270
Q

septic shock

A

results from systemic infection

271
Q

pulmonary fibrosis

A

fibrous thickening of alveoli from irritant gases, organic and inorganic particles
-makes lungs rigid, gas exchange hampered, progressive respiratory disability

272
Q

pneumoconiosis

A

lung injury from inhalation of injurious dust

273
Q

lung carcinoma

A

usually smoking related neoplasm, common malignant tumor in both genders
-aka bronchogenic carcinoma, cancer usually arises from bronchial mucosa

274
Q

squamous cell carcinoma

A

lung carcinoma that is very common

275
Q

adenocarcinoma

A

lung carcinoma that is very common

276
Q

large cell carcinoma

A

lung carcinoma with large, bizarre epithelial cells

277
Q

small cell carcinoma

A

lung carcinoma with small, irregular dark cells with scanty cytoplasm resembling lymphocytes, very poor prognosis

278
Q

prognosis of lung carcinoma

A

generally poor due to early spread

279
Q

MTB

A

multiple drug resistant tuberculosis-resistant to at least two drugs

280
Q

XDR-TB

A

extremely drug resistant tuberculosis-no longer controlled by many TB drugs

281
Q

arterial blood gases

A

pH=7.35-7.45 (acidic-below, basic-above)
oxygen= >80-100, hypoxemia if below
carbon dioxide= 35-45, respiratory cause if below
bicarbonate (HCO3)= 22-26, metabolic cause if high

282
Q 
ex) 7.48 pH
      78 O2
      32 CO2
      24 HCO3 
identify imbalance?
A 
basic/alkaline
hypoxemia
respiratory cause
normal value
respiratory alkalosis with hypoxemia

Intro to Disease (4 decks)

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