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Understanding Human Disease > exam 2 (ch. 11, 12, 14) > Flashcards

exam 2 (ch. 11, 12, 14) Flashcards

chapters 11, 12, 14

1
Q

hemostasis

A
  • hemo = blood
  • stasis = remain
  • the stopping of bleeding
  • the process is rapid and localized
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2
Q

the primary layers in hemostasis include

A
  • blood vessels
  • platelets
  • plasma proteins (coagulent proteins)
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3
Q

What are plasma proteins made by

A

liver

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4
Q

Vascular system

A

Intact endothelial cells inhibit platelet adherence and blood coagulation

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5
Q

Injury to endothelial cells promotes…

A

localized clot formation

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6
Q

Injury to endothelial cells: Phases

A

Phase 1: vasoconstriction
Phase 2: Platelets
Phase 3: Coagulation

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7
Q

First phase: Vasoconstriction

A
  1. Narrows the lumen of the vessel to minimize the loss of blood
  2. Brings the hemostatic components of the blood (platelets and plasma proteins) into closer proximity to the vessel wall
  3. Collagen = enhances contact activation of platelets
  4. Von Willebrand factor = made by endothelial cells
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8
Q

What does collagen initiate

A

vasoconstriction

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9
Q

Second phase: Platelets

A
  1. Circulate in resting state approximately 10 days

2. At rest = minimal interaction with other blood components or the vessel wall

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10
Q

When stimulated by endothelial damage, platelets function to…

A
  1. Plug the defect = round and sticky platelets, aggregate to site and build a hemostatic plug
  2. Release vasoconstrictors
  3. Cause more platelets to aggregate
  4. Secretion of active substances to initiate coagulation
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11
Q

Platelets are cells fragments of what?

A

megakarocyte

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12
Q

When platelets aggregate to site, the release what?

A
  1. ADP (recruit more platelets)
  2. Vasoconstrictive amines
    - epinephrine (vasoconstrictor)
  3. Thromboxane A2
    - amplifies the initial aggregation of platelets into a large platelet mass
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13
Q

Von Willebrand Factor

A

Secreted by endothelial cells

- important for adhesion and aggregation of platelets

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14
Q

Third phases: Coagulation

A

To go from liquid to semisolid mass.

- need calcium and vitamin K

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15
Q

what are the two pathways of coagulation

A
  1. Extrinsic
  2. Intrinsic
    - they both come together to form a common pathway; you need both for normal coagulation
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16
Q

Describe the coagulation cascade

A

Phase 1: intrinsic and extrinsic pathways come together and form common pathway

Phase 2: Prothrombin to thrombin

Phase 3: Fibrinogen to fibrin

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17
Q

Platelets and coagulation factors

A

Distinct but complimentary and mutually dependent

  • platelets interact with coagulation factors by providing binding sites
  • thrombin activates platelets
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18
Q

Coagulation Inhibitors

A 
Counterbalance coagulation factors; restrict clot by keeping it at one location. 
Substances:
- Antithrombin
- Protein C
- Plasminogen
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19
Q

Fibrinolysis

A

Plasminogen activated to plasmin

  • by Tissue plasminogen Activator (TPA), released by endothelial cells
  • plasmin dissolves fibrin
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20
Q

Fibrinolysis is activated at the same time as what?

A

Coagulation

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21
Q

Disturbances of Blood Coagulation: 4 types

A
  1. Abnormalities of small blood vessels
  2. Abnormality of platelet formation
  3. Deficiency of one or more plasma coagulation factors
  4. Liberation of thromboplastic material into circulation
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22
Q

Abnormalities of small blood vessels

A

Abnormal bleeding resulting from failure of small blood vessels to contract after tissue injury
- rare genetic disease

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23
Q

Reduced platelet numbers or function

A
  1. Thrombocytopenia (reduced platelet number in blood)
    - Causes: genetic, acquired (radiation)
    - Disease: leukemia
    - Autoimmune
    - Hypersplenism
    - Leads to petechiae
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24
Q

Petechiae

A

small pinpoint hemorrhages

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25
Q

Hypersplenism

A

Spleen normally removes platelets after about 10 days, but sometimes the spleen gets too big/active and will remove platelets before 10 days.

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26
Q

Deficiencies in blood coagulation: Phase 1

A
  • remember that phase 1 is when intrinsic and extrinsic pathways come together and form common pathway*
    • usually hereditary; relatively rare
    • hemophilia A or B, or Von Willebrand’s disease
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27
Q

Hemophilia

A

X-linked hereditary disease affecting males

- most common and best known

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28
Q

Hemophilia A

A

Classic hemophilia = factor 8; (antihemophilic factor); more common that Hemophilia B

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29
Q

Hemophilia B

A

Christmas disease (after affected patient) = factor 9

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30
Q

Signs / Symptoms of Hemophilia A

A
  • Spontaneous or traumatic subcutaneous bleed
  • Blood in urine
  • Bleeding in the mouth, lips, tongue
  • Bleeding in the joints, CNS, GI tract
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31
Q

Hemophilia A treatment

A

a. Transfusions (blood)

b. treated with missing factor

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32
Q

Deficiencies in blood coagulation (Phase 1): Von Willebrands disease

A

Decrease in von Willebrand factor

  • autosomal dominant (only one copy needed)
  • more common and less severe then hemophilia
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33
Q

Signs / Symptoms of Von Willebrands disease

A

bruise easily

do not bleed in joints

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34
Q

Deficiencies in blood coagulation: Phase 2

A

Deficiency of prothrombin or factors required for the conversion of prothrombin to thrombin

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35
Q

Deficiencies in blood coagulation: Phase 2 examples

A

a. liver disease (not making bile)
- bile makes some coagulant proteins
b. lack of vitamin K
- vitamin K synthesized by intestinal bacteria
- bile required for its absorption

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36
Q

Deficiencies in blood coagulation: Liberation of Thromboplastin Material into Circulation

A

Liberation of Thromboplastin Material into Circulation can start to form clot.
- this abnormal release of thromboplastin material can jumpstart the coagulation cascade

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37
Q

Liberation of Thromboplastin Material into Circulation is a result of several pathological processes such as…

A
  • snakebites
  • gram negative bacteria
  • surgery
  • disease associated with shock and tissue necrosis
  • overwhelming bacterial infections
  • other causes of tissue necrosis (burn)
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38
Q

Laboratory Tests to Evaluate Hemostasis

A
  • Platelet count
  • Bleeding time –> make small cut to see how long it takes to clog
  • Clotting time –> test tube, sample of venous blood
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39
Q

Laboratory Tests to Evaluate Hemostasis: Partial Thromboplastin time (PTT)

A

Clotting time

  • measures time it takes for blood plasma to clot after adding lipid and calcium
  • measures overall efficiency
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40
Q

Laboratory Tests to Evaluate Hemostasis: Prothrombin time (PT)

A

Measures coagulation in extrinsic pathway

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41
Q

Laboratory Tests to Evaluate Hemostasis: Thrombin time = Fibrinogen Assay

A

Measures the level of fibrinogen

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42
Q

Anti-Coagulants

A
  1. Asprin
    - inhibits Thromboxane A2 formation; acts on platelets
  2. Warfarin (aka coumadin)
    - reduced amount of Vitamin K availability; acts on coagulant proteins
    - decreased risk of clot formation
    - used chronically
  3. Heparin
    - used acutely
    - inactivates thrombin (which inhibits fibrinogen to fibrin)
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43
Q

Anatomy of Heart

A

a. 4 Chambers (2 atria that receive blood, 2 ventricles that pump blood)

b. 2 sets of valves = function to maintain unidirectional BF
- AV valves (between atria and ventricles)
- semilunar valves

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44
Q

Right side of heart

A

Receive oxygenated blood from body; pulmonary circuit

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45
Q

Left side of heart

A

Receive oxygenated blood thats been oxygenated by lungs from pulmonary veins; systemic circuit

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46
Q

What are the AV valves?

A

Tricuspid valve

Mitral valve

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47
Q

What are the semilunar valves called?

A

pulmonary valve

aortic valve

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48
Q

Review of coronary circulation

A
  • main blood supply to the heart
  • myocardium is too thick for the diffusion of nutrients
  • branches off of aorta
  • venous blood collected by cardiac veins
  • empties blood into the RA
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49
Q

Review conduction system of heart

A

The heart has a normal sinus rhythm so the heart can beat as one unit

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50
Q

The main components of the cardiac conduction system

A

SA node, AV node, bundle of His, bundle branches, and Purkinje fibes

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51
Q

Electrocardiogram (ECG, EKG)

A

A tool used to examine Cv function.

- electrodes are placed on external surface around heart and they measure electrical activity of the heart

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52
Q

What is an Electrocardiogram (ECG, EKG) used for?

A
  • normal sinus rhythm
  • block in conduction system
  • rate too fast / slow
  • irregular heart beat
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53
Q

What are the waves that you see from an Electrocardiogram (ECG, EKG)

A

P wave: atria depolarization

QRS complex: ventricular depolarization

T wave: ventricular repolarization

you do not see atria repolarization because it’s hidden by QRS complex

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54
Q

Echocardiography (echo, sonogram)

A

A tool used to examine Cv function.

- ultrasound examination

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55
Q

What is Echocardiography (echo, sonogram) used for?

A
  • valve structure
  • chamber size
  • abnormal clot formation
  • looks at anatomy/structure
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56
Q

Heart Disease classifications

A

congenital
genetic
infection
environmental

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57
Q

Congenital heart disease

A

Atrial and Ventricular Septal Defects (most common)
Manifestations:
- murmur (not unidirectional, stethoscope)
- easily fatigued because oxygenated and deoxygenated blood mix
- heart failure if not discovered

usually detective at birth

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58
Q

Atrial Septal Defect

A

Left to right shunt

- oxygenated blood flowing to deoxygenated side which overloads right side of the heart (RV)

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59
Q

Atrial Septal Defect: complications

A

pulmonary hypertension

right ventricular hypertrophy

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60
Q

Atrial Septal Defect: treatment

A

surgery to close hole

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61
Q

Ventricular Septal Defect

A

Left to right shunt
- overloading blood on right side of the heart which can lead to pulmonary hypertension

  • makes left side of heart pump harder because some blood is leaving by aorta but some is mixing with deoxygenated side
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62
Q

Ventricular Septal Defect: complications

A

pulmonary hypertension

right ventricular hypertrophy

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63
Q

Ventricular Septal Defect: treatment

A

surgery to close hole

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64
Q

Congenital heart disease: Tetralogy of Fallot

A

Four heart defects:

  1. VSD (ventral septum defect)
  2. pulmonary stenosis
  3. right ventricular hypertrophy
  4. overriding aorta

Rare: 5 in 10,000 infants

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65
Q

Overriding Aorta

A

aorta is between left and right ventricles, over VSD

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66
Q

Tetralogy of Fallot: manifestations

A
  • cyanosis (blood is well oxygenated –> purple lips etc.)
  • slow growth
  • heart failure
  • variable life expectancy
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67
Q

Tetralogy of Fallot: treatment

A

surgery soon after birth

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68
Q

Valvular Heart Disease

A

There are 3 types of valvular dysfunctions

  1. Valvular Stenosis
  2. Valvular Regurgitation
  3. Mitral valve prolapse syndrome (MVPS)
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69
Q

Valvular Heart Disease: Aortic Stenosis

A

Leaflets undergo degenerative changes –> fibrotic, calcified, rigid –> restricts valve mobility, stenosis

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70
Q

Clinical outcomes of Aortic Stenosis

A

increase strain of heart –> left ventricular hypertrophy –> heart failure
*more common with aging

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71
Q

Valvular Heart Disease: Rheumatic fever (Scarlet Fever)

A

a. Commonly encountered in children
- streptococcal bacterial
b. NOT due to bacterial infection per se, but a hypersensitivity reaction
c. Antigen-antibody reaction injures CT and causes fever

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72
Q

Prevention of Rheumatic fever (Scarlet Fever)

A

antibiotics as soon as streptococcal bacterial is found

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73
Q

Clinical outcomes of Rheumatic fever (Scarlet Fever)

A

a. healing with scarring of tissues (heart valves)
b. death from severe inflammation and acute heart failure
c. can recur if another streptococcal infection reactivates hypersensitivity and tissue damage

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74
Q

Valvular Heart Disease: Rheumatic Heart Disease

A

a. scarring of heart valves following rheumatic inflammation
b. primarily affects mitral and aortic valves

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75
Q

Clinical outcome of Rheumatic Heart Disease

A

valve regurgitation or stenosis –> impairs cardiac function, increases strain on heart –> eventually leads to heart failure

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76
Q

Valvular Heart Disease: Mitral valve prolapse

A

a. Common but only few develop problems
b. Leaflets enlarge, stretch, prolapse into LA –> blood leaks back into LA; mitral regurgitation
c. On auscultation: “faint systolic murmur” from reflux of blood in between closed valve leaflets

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77
Q

Causes of Mitral valve prolapse

A

genetic

CT disease

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78
Q

Cardiac Arrhythmias

A

Disturbance of the heart rhythm (irregular heart beat)

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79
Q

Cardiac arrhythmias range from…

A

They range from occasional “missed” or rapid beats to severe disturbances that affect the pumping ability of the heart

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80
Q

Cause of cardiac arrhythmias

A

an abnormal rate of impulse generation or abnormal impulse conduction

81
Q

Cardiac Arrhythmia: rate

A

a decrease or increase in heart rate

82
Q

Cardiac Arrhythmia: Premature

A

Premature = extra beats

  • flutter
  • premature atrial contraction
  • premature ventricular contraction (PVCs); common
83
Q

Cardiac Arrhythmia: Atrial fibrillation

A
  • Disorganized electrical impulses
  • Atria quiver instead of contract (incomplete emptying)
  • Common with age
84
Q

Cardiac Arrhythmia: Ventricular fibrillation

A

life threatening; paddles, quivering, blood not being distributed

85
Q

Cardiac Arrhythmia: heart block (complete or incomplete)

A

common due to athersclerosis

86
Q

What do we mean by “heart attack”? Myocardial Infarction

A

Acute Coronary Syndrome

  • blood supply is compromised to heart
  • spectrum of clinical presentations
87
Q

Categories of Acute Coronary Syndrome

A
  • stable angina
  • unstable angina
  • acute coronary syndrome
88
Q

Pathogenesis of Myocardial Infarction

A

athersclerosis

89
Q

Atherosclerosis: pathogenesis

A

Endothelial injury

  • increased permeability
  • monocyte margination, become macrophages sub-endothelial
  • induction of smooth muscle cells
90
Q

Where does Atherosclerosis occur?

A

any artery, NOT veins

91
Q

Atherosclerosis leads to…

A

Fatty streak
- lipid accumulation
and fatty streak leads to atheroma

92
Q

Atherosclerosis: lifetime development

A

Begins early in life, asymptomatic for many years

- clinical in 6th decade

93
Q

Myocardial Infarction leads to what?

A

Necrosis of the heart muscle from severe ischemia

94
Q

ischemia

A

insufficient blood flow

95
Q

Basic mechanisms that trigger heart attack

A

a. sudden blockage of a coronary artery from a thrombus
b. blockage of atherosclerotic plaque
c. sudden greatly increased myocardial oxygen requirements (vigorous PA)

96
Q

Symptoms of Acute Myocardial Infarction

A

a. Angina
b. Sympathetic Nervous system response
c. Hypotension and shock
d. May be symptomatic

97
Q

Symptoms of Acute Myocardial Infarction: Angina

A

Chest pain

- severe, crushing, constrictive OR like heartburn

98
Q

Symptoms of Acute Myocardial Infarction: Sympathetic Nervous system response

A

a. GI distress, nausea, vomiting
b. Tachycardia and vasoconstriction
c. Anxiety, restlessness, feeling of impending doom

99
Q

Symptoms of Acute Myocardial Infarction: Hypotension and shock

A

weakness in arms and legs

100
Q

Symptoms of Acute Myocardial Infarction: men vs women

A

Men: angina
Women: Sympathetic Nervous system response
more likely

101
Q

Angina pectoris

A

chest pain due to ischemia

102
Q

Stable angina

A

Pain when heart’s O2 demand increases

- predictable

103
Q

Unstable angina

A

Medical emergency, heart attack may follow

- no pattern

104
Q

Features if Myocardial Infarction

A

a. 50% MI occur without warning
b. 50% preceded by episodes of angina
c. 80-90% MI patients arrive alive
- 10-20% die before cardiac arrhythmia
- minority recover without complications
- most develop clinical complications

105
Q

Myocardial Infarction - Diagnosis

A
  1. Physical examination:
    - usually not abnormal unless patient exhibits evidence of shock, heart failure, murmur
  2. Laboratory Data:
    - Electrocardiogram, ECG or EKG
    - Enzyme tests; enzymes leak out from necrotic cells after an infarct –> the larger the infarct, the longer for elevated levels to return to normal of enzymes
106
Q

Cardiac Enzymes

A
  • Creatine Kinase
  • Lactate Dehydrogenase
  • Troponin
107
Q

Coronary angiogram

A

Locate and determine degree of obstruction by injecting radioactive dye and using and Xray

108
Q

Long term Complications of MI

A
  • arrhythmia
  • heart failure
  • cardiogenic shock
  • pericarditis
  • thromboemboli
  • cardiac rupture
  • ventricular aneurysm
109
Q

Coronary heart disease risk factors

A
  • elevated blood lipids (high cholesterol/LDL/triglycerides)
  • high BP
  • Cig smoking
  • diabetes
  • obesity
  • gender
  • homocysteine
110
Q

Likelihood of coronary heart disease and heart attack

A

a. 1 risk factor = 2x risk
b. 2 risk factors = 4x risk
c. 3 risk factors = 7x risk

111
Q

Treatment for CAD: goal

A

restore blood flow

112
Q

Treatment for CAD

A

a. destroy clot
- angioplasty
b. cardiac bypass
c. stent (brace lumen open)

113
Q

what is cad

A

coronary artery disease

114
Q

myocardial infarction treatment: Thrombolytic therapy

A

a. Thrombolytic therapy = tissue plasminogen activator
- reduces blood coagulability, dissolves clots
- effective but clot may not completely dissolve
- better outcome sooner the clot is dissolved (1 hr of MI symptoms)
- may cause bleeding issues

115
Q

Explain the action of aspirin and how it reduces CVD risks

A

Action: Reduces platelet aggregation

  • rapidly absorbed from stomach and SI
  • inhibits platelet function within 1 hr of ingestion
  • reduces risk of CVD and stroke
  • increases risk of bleeding
116
Q

myocardial infarction treatment: medical treatment

A

a. Medical treatment: control or eliminate risk factors
- stop smoking
- control hypertension
- anti-coronary diet: low cholesterol and fat (sat./trans)
- weight reduction
- exercise program

117
Q

Cocaine-Induced Arrhythmia’s and Infarcts

A

Prolongs and intensifies effects of sympathetic nervous system:

a. increases heart rate: increased O2 demand
b. increased muscle irritability: predisposes to arrhythmia
c. increased peripheral vasoconstriction and coronary artery spasm: high BP
d. fatal arrhythmia’s and MI can occur even among those with normal coronary arteries

118
Q

cardiomyopathy: causes

A

genetic mutations

environment

119
Q

types of cardiomyopathy

A
  1. Dilated cardiomyopathy (congestive cardiomyopathy)
    - weakened, enlarged (all chambers), poor pumping, problem in systole
  2. Hypertrophic cardiomyopathy
    - can lead to sudden cardiac arrest
    - leading cause of death in young athletes
    - diminished outflow
    - less room for heart to fill (problem in diastole)
  3. Restrictive cardiomyopathy
    - heart is rigid, restricted from stretching
    - decrease in diastole
    - decreased outflow
120
Q

complications of cardiomyopathy

A
  • heart failure
  • blood clots - pulmonary embolism
  • valves problems
  • cardiac arrest
  • sudden death
121
Q

Heart failure

A

General term used to describe several types of cardiac dysfunction that result in inadequate perfusion of tissues with blood-borne nutrients

122
Q

Heart failure: types

A

Left Heart failure
Right Heart failure
usually you have both

123
Q

Is damage to heart muscle reversible?

A

No. It is either turned into scar tissue or fibrosis

124
Q

Sudden cardiac death

A

Natural death from cardiac causes within one hour of acute symptoms (not a heart attack per se)

125
Q

Sudden cardiac death may be due to

A
  • arrhythmia
  • MI
  • aortic aneurysm
  • electrocution
  • drugs (coke)
126
Q

Fluid compartments in the body

A

ICF, Interstitial fluid, plasma

interstitial fluid and plasma are ECF

127
Q

Factors that regulate fluid flow

A
  • hydrostatic pressure
  • capillary permeability
  • osmotic (colloid) pressure
  • open lymphatic channels
128
Q

osmotic (colloid) pressure

A

pressure exerted by proteins

129
Q

What are some things that influence circulatory disturbances?

A
  1. Blockage
    - Thrombus
    - Atherosclerosis
  2. Dilation
    - varicose veins
  3. Damage to wall
  4. Alterations in permeability
    - edema
  5. Pressure changes
    - increase (hypertension)
    - decrease (shock)
130
Q

Thrombus vs blood clots

A

Normally, blood does not clot within the vascular system without injury.
Thrombus = pathological
Blood clot = physiological; normal response when you have external injury

131
Q

Thrombus

A

Hemostasis activated without external vessel injury; abnormal intravascular blood clot

  • can occur in any vessel or within the heart
  • stationary
132
Q

Thrombosis

A

formation of thrombus

133
Q

Pathogenesis of thrombus: Virchow’s Triangle

A
  1. Slowing or stasis of blood flow (abnormal blood flow)
  2. Blood vessel wall damage (intrinsic endothelial damage)
  3. Increased coagulability of blood
134
Q

Embolus

A

A detached clot carried into pulmonary or systemic circulation; plugs vessel of smaller caliber than diameter of clot, blocking blood flow and causing necrosis

135
Q

Infarct

A

Tissue necrosis from interruption in blood flow

136
Q

Thrombus formation: common sites

A

bifurcation of artery or veins

137
Q

Venous Thrombosis: Thrombophlebitis

A

Clot formed in vein which leads to inflammation; typically in leg

138
Q

Predisposing factors leading to clot formation in leg veins

A
  • prolonged bed rest
  • cramped position for long period (impaired “milking action”)
  • genetic factors
139
Q

Venous Thrombosis outcome

A
  • Leg swelling from partial blockage of venous return in leg

- pulmonary embolism

140
Q

For a Pulmonary Embolism, clinical manifestations depend on what?

A

Clinical manifestations depend on size of embolus and where it lodges in the pulmonary artery

141
Q

Explain potential risks of a large pulmonary embolism

A

Large pulmonary emboli may completely block main pulmonary artery or major branches obstructing blood flow to lungs

142
Q

Symptoms of a large pulmonary emboli

A

a. cyanosis and shortness of breath due to inadequate oxygenation of blood
b. right ventricular dysfunction
c. decreased return of blood to left heart
- systemic BP falls and patient may go into shock

143
Q

Explain a small pulmonary emboli

A

a. small emboli may pass through main pulmonary arteries, becoming stuck in peripheral arteries supplying lower lobes of the lungs
b. raises pulmonary pressure and inadequate collateral circulation
c. affected lung segment undergoes necrosis; pulmonary infarct

144
Q

General symptoms of a pulmonary embolism

A

a. dyspnea - shortness in breath
b. chest pain
c. cough and expectoration of bloody sputum due to leakage of blood from infarcted lung tissue into bronchi

145
Q

Diagnosis of pulmonary embolism

A 
Pulmonary angiogram (gold standard): detects blocked pulmonary artery 
- inject dye and look with XRAY
146
Q

Treatment of pulmonary embolism

A
  1. Anticoagulants: heparin initially followed by Warfarin
  2. Angioplasty
  3. Thrombectomy (clot extraction surgery)
  4. General supportive care
147
Q

Varicose veins

A 
Dilated tortuous (twisty) veins. 
- common, tend to run in families
148
Q

Varicose veins Etiology

A

incompetent valves

149
Q

Complications of Varicose veins

A
  • pain
  • thinning of skin fed by vein
  • thrombophlebitis (not risk for PE)
150
Q

Treatment for Varicose veins

A

small incision and pull vein out

151
Q

Arterial thrombosis

A

Can happen in artery or vein

a. blood stasis is not a factor due to rapid blood flow and high BP
b. can grow to occlude vessel

152
Q

Main cause of Arterial thrombosis

A

Injury to vessel wall from arteriosclerosis, smoking, hypertension

153
Q

Explain how and where Arterial thrombosis may affect and individual

A
  1. Coronary artery: myocardial infarction
  2. Major leg artery: gangrene
  3. Cerebral artery: stroke
154
Q

Arterial thrombosis: Intracardiac thrombosis

A

Within chambers of heart.

  1. Clot forms
    a. within atrial –> heart failure
    b. surfaces of heart valves –> valve injury (stenosis)
    c. wall of left ventricle –> MI
    d. chambers –> may dislodge into systemic circulation and cause infarction in spleen, kidneys, or brain
155
Q

Thrombosis due to increased coagulability

A

A rise in coagulation factors following surgery or injury

156
Q

What is a chemical that my stimulate the synthesis of clotting factors ?

A

Estrogen in contraceptive pills because it stimulates the liver to make coagulants

157
Q

Thrombosis due to increased coagulability: hereditary gene mutations

A

There is a mutation in the gene regulating prothrombin synthesis
- risk for venous thrombosis increases as prothrombin level rises

158
Q

Why might patients with cancer be likely to develop a thrombosis?

A

Due to rapid release of thromboplastic materials into circulation from tumor

159
Q

What are some sources of an embolism?

A
  • thrombus
  • atherosclerotic debris
  • bone marrow fat
  • air
  • amniotic fluid
160
Q

Amniotic Fluid embolism

A

Complication of pregnancy
a. amniotic fluid enters maternal circulation through a tear in fetal membranes

b. fetal cells, hair, fat, and amniotic debris fluid blocks maternal pulmonary capillaries causing severe respiratory distress
c. Thromboplastic material in fluid activates coagulation mechanism leading to disseminated intravascular coagulation syndrome (DIC)

161
Q

Air embolism

A

Large amount of suck sucked into circulation from lung injury due to chest wound
- may be accidentally injected into circulation

  • air carried into right heart chambers and prevents filling of heart by returning venous blood
  • heart is unable to pump blood and person dies rapidly of circulatory failure
162
Q

Arteriosclerosis

A

Thickening and hardening of arteries

163
Q

what is one cause of Arteriosclerosis

A

atherosclerosis

164
Q

Risk factors for developing atherosclerosis

A

High levels of blood lipids

  • hypertension
  • smoking
  • diabetes
  • physical inactivity
  • age
  • overweight
  • family history
  • gender
165
Q

dyslipidemia

A

high LDL, low HDL

166
Q

Low-density Lipoprotein (LDL)

A

bad cholesterol

167
Q

High-density Lipoprotein (HDL)

A

good cholesterol; protective; increases with regular exercise, smoking cessation, modest alcohol intake

168
Q

Hypertension is due to

A

due to excessive vasoconstriction of small arterioles

169
Q

Explain how hypertension results in cardiac effects

A

Increased peripheral resistance –> higher workload –> heart enlarges –> heart failure

170
Q

Explain how hypertension results in vascular effects

A

Increased pressure –> premature wearing out of vessels; accelerates atherosclerosis; injury to vessels –> rupture and hemorrhage

171
Q

Explain how hypertension results in renal effects

A

Narrowed renal arterioles –> decreased blood supply to kidneys –> injury and degenerative changes in glomeruli and tubules –> renal failure

172
Q

Criteria for BP vs high BP

A

good: 120/80
high: 140/90

173
Q

How do you treat hypertension?

A
  1. increase PA
  2. diet
    - reduce salt
    - increase fruits and veggies
  3. medication
    - diuretics (decrease blood vol)
    - angiotensin-converting enzyme (ACE) inhibitors
174
Q

Aneurysm

A

Dilation or out-pouching of portion of arterial wall

175
Q

causes of Aneurysm

A
  1. Arteriosclerosis
    a. causes narrowing, thrombosis, and weakening of vessel wall
  2. Congenital
176
Q

Explain and Aneurysm in the aorta

A

most common in distal part of aorta; may rupture, leading to massive and fatal hemorrhage

177
Q

Dissecting Aneurysm of aorta

A

Spitting of elastic and muscle tissues

178
Q

What are some symptoms of Aneurysm in aorta?

A

severe chest and back pain

179
Q

What are risk factors for developing an Aneurysm

A

hypertension, atherosclerosis

180
Q

Ischemia is due to

A
  1. Obstruction
  2. Vascular occlusion
    a. torsion (twisting of BV)
    b. drowning
    c. CO
181
Q

long periods of ischemia lead to

A

infarct

182
Q

Factors influencing the development of an infarct

A
  1. Single or dual vascular supply (more the better)
  2. Rate at which obstruction develops (atherosclerosis or embolus)
  3. Sensitivity of downstream tissue to oxygen deprivation
  4. oxygen content in blood
183
Q

Edema

A

Shift of water from vascular space into another compartment (usually interstitial)
- result of underlying condition

184
Q

Two types of edema

A

Exudate: fluid w protein
Transudate: fluid w low protein

185
Q

How can edema be fatal?

A

Cerebral edema

Pulmonary edema

186
Q

Pathogenesis of Edema

A
  1. Increased capillary permeability
    a. causes swelling of tissues with acute inflammation
    b. increase in capillary permeability from some systemic diseases
  2. Low plasma proteins
    a. excess protein loss (kidney disease)
    b. inadequate synthesis (malnutrition)
  3. Increased hydrostatic pressure
    a. heart failure
    b. localized venous obstruction
  4. Lymphatic obstruction
187
Q

Lymphedema

A

Edema of Lymphatic Obstruction

  • build up of fluid when lymphatics damaged or blocked
  • high protein edema
  • most common cause is due to removal of lymph nodes (secondary lymphedema)
188
Q

Why would you need to remove lymphnodes

A

cancer

189
Q

Shock

A

Inability to meet the O2 demands of the body

190
Q

Shock could be the final stage of what?

A
  • severe hemorrhage
  • bacterial sepsis
  • burns
  • MI
  • severe soft tissue damage
191
Q

What is the end result of shock?

A

often times the end result is multi-organ failure and death

192
Q

Cardiogenic shock

A

Pump failure

Cannot maintain perfusion pressure

193
Q

Hypovolemic Shock

A

decreased blood volume

194
Q

Anaphylactic shock

A

A severe, potentially life-threatening allergic reaction.

195
Q

Septic (sepsis) shock

A

Systemic bacterial infection

- gram negatives

196
Q

Septic (sepsis) shock leads to

A
  • vasodilation
  • decreased myocardial contractility
  • endothelial cell damage which may start DIC
197
Q

Effects of irreversible shock

A
  • circulatory collapse
  • marked hypo-perfusion of vital organs
  • loss of vital functions
  • multi-organ failure
  • death
198
Q

Prognosis of shock

A

Prognosis of shock depends on early recognition and rapid appropriate treatment

199
Q

How could you treat shock?

A
  1. Drugs that promote vasoconstriction
  2. Use of intravenous fluids or blood to restore blood volume secondary to fluid loss or hemorrhage
  3. Treat underlying cause

Understanding Human Disease (4 decks)

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