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INTRO TO CLINICAL > HANDOUT EXAM 2 > Flashcards

HANDOUT EXAM 2 Flashcards

1
Q

what is the leading cause of morbidity and mortality what does it account for?

A

diseases of blood vessels and heart (more than 40% of death after birth)

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2
Q

what do diseases of blood vessels and the heart impair?

A

impair circulation of blood and delivery of oxygen and nutrients (glucose) to tissues/organs

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3
Q

what do diseases of blood vessels do to cells and organs

A

decreases the function of them

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4
Q

what is impaired perfusion due to

A

due to the obstruction of blood vessels, rupture of blood vessels, or failure of the heart to pump blood

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5
Q

what is impaired perfusion particularly important for

A
  1. brain
  2. heart
  3. kidneys
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6
Q

the term “cardiovascular disease” is an umbrella term used for what 3 things

A
  1. atherosclerotic diseases of heart or blood vessels (arteries)
  2. Myocardial infarct
  3. Stroke
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7
Q

what is the most common cause of cardiovascular disease

A

atherosclerosis

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8
Q

what are some examples of less frequent causes for cardiovascular diseases

A
  1. hypertension
  2. diabetes
  3. drugs (such as cocaine)
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9
Q

what are the 9 important disease conditions of blood vessels and heart

A
  1. atherosclerosis
  2. coronary heart disease/myocardial infarct
  3. thrombosis
  4. embolism
  5. aneurysms
  6. congenital heart disease
  7. cardiomyopathy
  8. congestive heart failure
  9. hypertension
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10
Q

what are arteries and what do they carry?

A

blood vessels that carry blood away from the heart towards the peripheral tissues. normally carry oxygen-rich blood (RED)

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11
Q

what are veins and what do they carry

A

blood vessels that carry blood towards the heart. normally carry oxygen-poor (deoxygenated) blood

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12
Q

what are the two exceptions to the functional anatomy of circulatory system

A
  1. pulmonary arteries = carry oxygen-poor blood
  2. pulmonary veins = carry oxygen-rich blood
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13
Q

blood vessels have 3 layers what are they?

A
  1. intima (do not make platelets): endothelium
  2. media (layer of muscle cells): internal elastic lamina
  3. adventitia (tunica externa): external elastic lamina
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14
Q

what are the 3 major veins

A
  1. superior vena cava
  2. inferior vena cava
  3. medial cubital vein
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15
Q

what are 3 major arteries

A
  1. common carotid artery
  2. aorta
  3. femoral artery

honorable mention: heart

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16
Q

what are the ABC’s of the aortic vessels

A

A = aorta
B = brachiocephalic trunc (splits into right carotid artery and right subclavian artery)
C = carotid artery (left)
S = subclavian artery (left)

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17
Q

what coronary arteries are located on the front of the heart

A
  1. aorta
  2. left coronary artery
  3. anterior inter ventricular branch
  4. great cardiac vein
  5. right coronary artery and vein
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18
Q

what coronary arteries are located on the back of the heart

A
  1. coronary sinus
  2. posterior artery and vein
  3. small cardiac vein
  4. right coronary artery and vein
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19
Q

what are the 6 major disturbances in blood flow

A
  1. edema
  2. hemorrhage
  3. thrombosis
  4. embolism
  5. infarction
  6. shock
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20
Q

what is hemorrhage

A

bleeding

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21
Q

what is thrombosis

A

occlusion of blood vessels by local blood clot

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22
Q

what are 2 types of thrombosis and what are they associated with

A
  1. venous thrombosis = deep venous thrombosis (DVT)
  2. arterial thrombosis = stroke, myocardial infarct
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23
Q

what is embolism and what can it be due to

A

blockage of blood vessel by circulating blood clot
- can also be due to: fat embolism, air embolism, amniotic fluid

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24
Q

what are 2 types of embolism and what do they do

A
  1. venous thrombus: (right side of the heart) will end up in the LUNGS (pulmonary arteries) and lead to pulmonary embolism
  2. arterial thrombus: (left side of the heart) can result in arterial thrombosis anywhere in the body (EX: stroke)
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25
Q

what is infarction and some examples

A

tissue necrosis due to occlusion of arterial blood supply leading to tissue ischemia
- EX: myocardial infarction, stroke, gangrene

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26
Q

what is shock

A

dramatic drop in blood pressure leading to hypo perfusion of vital tissues

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27
Q

what is edema and examples

A

accumulation of fluid in interstitial tissues or body cavities

  • EX: edema of arms, legs, lung edema
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28
Q

what are the 3 special names for edema in body cavities

A
  1. hydrothorax (chest)
  2. ascites (abdomen): the most frequent
  3. hydropericardium (heart)
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29
Q

what are the 5 factors that can lead to edema

A
  1. increased hydrostatic pressure: impaired venous return, heart failure, venous obstruction/insufficiency
  2. reduced plasmic oncotic pressure (hypoproteinemia = decrease I blood proteins
    • kidney diseases with protein loss
    • liver cirrhosis
    • malnutrition
  3. lymphatic obstruction (lymphatic vessels drain tissue fluid)
  4. salt retention (sodium retention)
  5. inflammation
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30
Q

when is “pitting” edema present

A

when a depression remains upon pressure

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31
Q

does edema show cardinal signs of inflammation?

A

NO

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32
Q

_____ is often non-pitting

A

lymphedema

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33
Q

what is the undesired loss of blood

A

hemorrhage (can be acute or chronic)

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34
Q

hemorrhage is usually do to…

A

rupture of injury of a blood vessel (artery or vein)

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35
Q

hemorrhage less than ___% can usually be tolerated in ____ but NOT in _______

A

20% in adults NOT smaller children

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36
Q

hemorrhage may be…

A

external, internal, or into tissues (hematoma)

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37
Q

hematomas or hemorrhage can be clinically important depending on

A

size and location (EX: inside the scull = epidural hematoma = medical emergency, 20% death)

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38
Q

what is the petechiae size of a hemorrhage and some characteristics

A

very small, 1-2 mm = hemorrhage in skin, mucous surface

  1. low platelet counts (thrombocytopenia)
  2. platelet defects
  3. some milder clotting factor deficiencies
  4. increased blood pressure
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39
Q

what is the purpura size of a hemorrhage and what are some characteristics

A

> 3mm same cause as petechiae

  1. vascular inflammation (vasculitis)
  2. increased fragility of vessels
  3. thrombocytopenia purpura
  4. vascular disorders
  5. vasculitis
  6. hence-schonlein purpura (IgA vasculitis)
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40
Q

what is the ecchymosis (bruise) size of a hemorrhage

A

> 1cm = bleeding into tissues (subcutaneous), after injury, bleeding disorders

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41
Q

what are the bleedings in body cavities size of a hemorrhage

A
  1. hemothorax (chest cavity)

2 hemoperricardium (pericard)

3 hemoperitoneum (abdomen)

  1. hemarthrosis (bleeding into joints)
  2. injury
  3. bleeding disorders
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42
Q

what are 4 key points for hematoma

A
  1. pocket of blood in tissues
  2. hematoma can be felt when touched
  3. hematoma can be external or internal
  4. often pain or tenderness
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43
Q

what are key points for ecchymosis

A
  1. non-blanching purple or red discoloration of skin due to leakage of RBCs from small ruptured blood vessels
  2. cannot be felt
  3. usually not painful or tender
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44
Q

what is the most important blood vessel and what does it do

A

coronary arteries (supplies ventricle with blood)

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45
Q

75% of blood flowing through liver comes from

A

portal vein

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46
Q

what is hemostasis

A

normal mechanism of how a bleeding is terminated

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47
Q

what is primary hemostasis

A

platelets bind to damaged/inflamed vessel wall and form a platelet plug (occurs in seconds)

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48
Q

what is secondary hemostasis

A

coagulation cascade forms a fibrin clot that stabilizes (“cements”) the platelet plug (may take minutes)

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49
Q

what is thrombosis

A

the undesired activation of the coagulation system

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50
Q

what does thrombosis lead to

A

the occlusion of vessels and hypoperfusion

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51
Q

what are the most important factors that contribute to blood coagulation

A
  1. blood vessels
  2. the coagulation system
  3. blood platelets
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52
Q

what are the sequence of events for blood coagulation

A
  1. after injury arteries initially constrict
  2. the injury to blood vessels exposes extracellular matrix and tissue factors that activate blood coagulation
  3. platelets adhere to site of injury and become activated and release granules that activate even more platelets
  4. fibrin is produced by the coagulation cascade and stabilizes the platelet thrombus
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53
Q

what is the most important factor for the coagulation cascade

A

Factor Xa

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54
Q

what is factor 2 process for coagulation cascade

A

prothrombin — prothrombin activator —> thrombin

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55
Q

what is factor 1 process for coagulation cascade

A

fibrinogen (thrombin gets inserted towards it) –> fibrin

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56
Q

what are the 2 coagulation pathways and what do they do

A
  1. tissue factor (coagulation factor III) pathway TRIGGERS coagulation
  2. contact activation pathway SUSTAINS COAGULATION
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57
Q

what are coagulation factors

A

enzymes (serine proteases) that catalyze the next reaction of coagulation until fibrin is formed

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58
Q

what is the most important steps in the coagulation cascade

A

conversion of prothrombin to thrombin which then converts fibrinogen to fibrin

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59
Q

thrombus formation is a constant battle of what?

A

factors that promote thrombus formation against factors that inhibit thrombus formation

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60
Q

what is contact activation pathway

A

activated by thrombin!
also: contact with negative charged surface )bacteria, damaged RBC) activates this pathway

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61
Q

what is the tissue factor pathway

A

“jump starts” coagulation and its primary job is to generate “thrombin burst”

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62
Q

what is the contact activation pathway tested by

A

PTT (aPTT) = activated partial thromboplastin time (only phospholipids added) which can be used to measure Heparin effects (Heparin activates antithrombin III)

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63
Q

what is the tissue factor pathway tested by

A

PT test = prothrombin time (add TF + phospholipids). it is now reported as INR value for the dosing of Warfarin (Coumadin) which inhibits vitamin K dependent factors (II, VII, IX, X)

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64
Q

what hemophilias are found in the contact activation pathway

A

hemophilia A = deficiency of factor VIII (90% of hemophilias)

hemophilia B = factor IX

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65
Q

what are the 5 hemophilia lab tests

A
  1. aPTT prolonged
  2. PT normal
  3. platelets normal
  4. bleeding time normal
  5. factor VIII or IX reduced
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66
Q

what are key points about direct-acting oral anticoagulants (DOACs) (or Novel oral anticoagulants (NOACs)

A
  1. came on the market first in 2010 including dabigatran (Pradaxa Boehringer), rivaroxaban (Xarelto, 2011), apixaban (Eliquis (2012)
  2. Target thrombin (dabigatran, Pradaxa) or factor Xa (rivaroxaban, Xarelto)
  3. As effective as warfarin (Coumadin, Vitamin K dependent inhibition of II, VII, IX, X)
  4. much more predictable effects
  5. much faster
  6. no need for routine anticoagulation monitoring
  7. problem was lack of antidotes
  8. FIRST ANTIDOTE BECAME AVAILABLE MAY 2018
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67
Q

what are some concern with direct-acting oral anticoagulants (DOACs) (or Novel oral anticoagulants (NOACs)

A
  1. DOACs are 5 to 15-fold more expensive
  2. initially no antidotes (until now)
  3. once-a-day dosing may be inefficient and not work for all
  4. bleeding risk
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68
Q

what is a thrombus

A

intravascular blood clot and the condition is called thrombosis. thrombus = blood clot

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69
Q

what 3 places can thrombi form

A
  1. veins
  2. arteries
  3. hearts
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70
Q

what can occur if a thrombus becomes dislodged

A

it can move with the blood stream until it does not fit through anymore and forms embolus

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71
Q

what are the 3 main factors contributing to thrombus formation (“Virchow’s Triad”)

A
  1. stasis of the blood flow (creates turbulence)
    • platelets are forced against vessel walls and in contact with endothelium which may activate them
    • anti-clotting factors are diluted and endothelial cells activated
  2. endothelial injury (atherosclerosis, inflammation, smoking/nicotine)
    • more important for thrombus in the arterial system
    • exposure of extracellular matrix activates platelets and clotting system
  3. blood hyper coagulability (genetic or acquired; elevated prothrombin
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72
Q

what are the 8 risk factors for thrombosis/embolism

A
  1. 350,000 - 900,000 cases of DVT per year
  2. prolonged bed rest or immobility
  3. underlying cond. (age + smoking + sitting in the same position)
  4. atrial fibrillation
  5. MI
  6. prosthetic heart valves
  7. status after surgery, fracture, burns
  8. tumors
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73
Q

what are the 3 most important clinical situations

A
  1. deep vein thrombosis (DVT)
  2. pulmonary embolism (PE)
  3. arterial thrombosis
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74
Q

what are the 3 clinical signs for DVT

A
  1. swelling
  2. pain
  3. redness
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75
Q

what 5 things can be used for diagnosis of DVT

A
  1. ultrasound
  2. elevated D-dimers levels (>300)
  3. D-dimers are fibrin breakdown products created by plasmin digesting blood clots
  4. negative D-dimers basically rule out thrombosis
  5. intravenous venography
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76
Q

what are the 5 therapy (anticoagulation) options for DVT

A
  1. short term: heparin (PTT TEST)
  2. long term: warfarin (Coumadin - PT)
  3. thrombolysis in extreme situations
  4. inferior vena cava filter (Greenfield filter) in recurrent DVT
  5. prevent by mobilizing patients
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77
Q

what is DVT with venous insufficiency

A

recently reported: not only DVT but also SUPERFICIAL VEIN THROMBOSIS is not harmless! 2 - 13% severe PE

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78
Q

what is varicose veins and what are 3 key things

A

chronic venous insufficiency = CVI)

  1. insufficiency of the venous valves
  2. increase risk for DVT ~ 4-fold
  3. 2-fold increase in PE risk
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79
Q

what is pulmonary embolus

A

clinical picture: blot clot from DVT dislodges and ends up in the lungs. major artery in the lungs is occluded (pulmonary trunk and pulmonary arteries)

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80
Q

what are the 6 clinical signs of pulmonary embolus

A
  1. SUDDEN ONSET of shortness of breath (dyspnea)
  2. rapid breathing (tachypnea)
  3. chest pain
  4. cyanosis (blue skin tint)
  5. tachycardia
  6. dizziness and risk factors
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81
Q

what are the 7 ways to diagnosis pulmonary embolism

A
  1. pulse oximetry, chest X-ray (to exclude other conditions)
  2. CT scan: CT scan with radio contrast
  3. pulmonary angiography (contrast X-ray)
  4. ventilation-perfusion scan (V/Q scan)
  5. ECG
  6. echocardiography
  7. blood tests (D-dimer, clotting status)
82
Q

what is the 5 treatments for pulmonary embolism

A
  1. thrombolysis (tPA = tissue plasminogen activator; Streptokinase)
  2. oxygen
  3. analgesia
  4. anticoagulation
  5. surgical removal of embolus

UNTREATED PE HAS > 25% MORTALITY RATE

83
Q

can smaller PE’s be survived?

A

YES

84
Q

what are the anatomy points of a thrombus

A
  1. alternating bands of pale pink platelets and fibrin (light) with red bands of RBCs (dark)
  2. Lines of Zahn mostly form in arteries (fast flowing blood), less often in veins
  3. only form when patient is alive (not post-mortem)
85
Q

what 3 location is arterial thrombus/embolus frequently located to

A
  1. brain
  2. kidneys
  3. skin
86
Q

what is the most important cause for thrombus formation

A

atherosclerosis of arterial blood vessels

87
Q

where do thrombi frequently form

A

in the heart (atrial fibrillation), heart valve disease

88
Q

if heart is dislodged what can happen

A

thrombus will enter into the arterial system

89
Q

what is ischemic necrosis caused by

A

occlusion of ARTERIAL SUPPLY (>95%) or venous drainage of an organ

90
Q

what are hemorrhagic (red ) infarcts

A

tissue is infarcted and then blood flows back in from another artery that supplies this tissue.

91
Q

what 5 places do hemorrhagic (RED) infarcts occur

A
  1. lungs
  2. tissues perfused from several sources (lungs, GI)
  3. after rupture of a vessel
  4. after re-perfusion
  5. venous infarcts
92
Q

what is anemic (white) infarct

A

arterial occlusion of organs that have only one arterial supply (heart, spleen, kidney)

93
Q

what are the 4 causes of infarction

A
  1. thrombosis
  2. embolus
  3. twisting of vessels
  4. entrapment of a vessel (EX: in a hernia sac)
94
Q

what are 4 the symptoms of infarction

A
  1. myocardial infarct
  2. cerebral infarct/stroke (hemorrhagic or ischemic stroke)
  3. bowel infarction
  4. gangrene of a limb
95
Q

what is the MAIN CAUSE of infarction

A

thrombus formation on atherosclerotic vessel

96
Q

atherosclerosis is a form of

A

arteriosclerosis

97
Q

arteriosclerosis = ?

A

hardening of arteries

98
Q

what are the 3 main types of arteriosclerosis

A
  1. atherosclerosis: MOST FREQUENT: hardening of arteries specifically due to atheromatous plaques = inflammation caused by deposition of lipoproteins (cholesterol from LDL) and inflammation
  2. Monckeberg’s medial calcific sclerosis: calcium deposits in muscular arteries
  3. Arteriolosclerosis: affects small arteries; thickening of the walls found in diabetes and hypertension
99
Q

what are the 3 other embolisms

A
  1. Fat embolism
  2. Air
  3. Amniotic Fluid
100
Q

what are key points for fat embolism

A
  1. microscopic emboli of fat droplets after fracture of large bones
  2. fat obstructs/inflames blood vessels, veins, arteries, capillaries
  3. clinically pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, petechiae in 20-50%
  • TRIAD: CONFUSION, DYSPNEA, PETECHIAE
101
Q

what are key points for air embolism

A
  1. during surgical procedures, chest wall injury
  2. arteries or veins
  3. decompression injury after diving = nitrogen bubbles in the blood
102
Q

what are key points for amniotic fluid embolism

A
  1. complication of labor and immediate postpartum
  2. sudden onset of sever dyspnea, cyanosis, shock, seizures, coma, after/during birth = 80% MATERNAL MORTALITY
  3. cause is entering of amniotic fluid or fetal tissue into maternal blood circulation due to rupture of uterine veins or tear in placental membranes
103
Q

epidural hematoma = ?

A

LUCID INTERVAL

104
Q

what are 2 clinical presentations of epidural hematoma

A
  1. preceding trauma
  2. INTIAL LOSS OF CONSCIOUSNESS > LUCID INTERVAL > FOLLWED BY DECLINE IN MENTAL STATUS
105
Q

can presentation for epidural hematoma be variable? if so what are some examples

A

YES
1. headache
2. nausea/vomiting
3. seizures
4. focal neurologic deficits: visual dropouts, aphasia, weakness, numbness

106
Q

what are the differences in the general appearance between arteries and veins

A

arteries: THICK walls with SMALL lumens (appear rounded)

veins: THIN walls with LARGE lumens (appear flattened

107
Q

what is the difference of the tunica intimacy between arteries and veins

A

arteries: endothelium appears WAVY due to CONSTRICTION of smooth muscle. internal elastic membrane present in LARGER vessels

veins: endothelium appears SMOOTH. internal elastic membrane ABSENT

108
Q

what are the differences in the tunica media between arteries and veins

A

arteries: normally the THICKEST layer. smooth muscle cells and ELASTIC fibers predominate (proportions of these vary with distance from heart). external elastic membrane present in LARGER vessels

veins: normally THINNER than the tunica external. smooth muscle cells and COLLAGENOUS fibers predominate. Nervi vasorum and vasa vasorum present. external elastic membrane ABSENT

109
Q

what are the differences in the tunica external between arteries and veins

A

arteries: normally THINNER than tunica media in all but the LARGEST arteries. COLLAGENOUS and ELASTIC FIBERS. Nervi vasorum and vasa vasorum present

veins: normally the THICKEST layer. COLLAGENOUS AND SMOOTH FIBERS predominate. some smooth muscle fibers. Nervi vasorum and vasa vasorum present

110
Q

what do the symptoms of infarction depend on

A

on the tissue and its blood supply: how much oxygen does it need; does it have another blood supply

111
Q

CASE OF THE DAY: what are the 8 key points for neurofibromatosis type 1

A
  1. 90% cases
  2. neurofibromas = tissues in and around nerve grows: Schwann cells, fibroblasts, melanocytes
  3. gliomas, meningiomas
  4. CAFE-AU-LAIT SPOTS (6 OR MORE)
  5. abnormal bones (bowing)
  6. neurofibromin gen Chr. 17
  7. autosomal dominant
  8. increased cancer risk (~7%)
112
Q

CASE OF THE DAY: what are the 2 key points for neurofibromatosis type 2

A
  1. bilateral acoustic neuromas
  2. meningiomas
113
Q

neurofibromatosis type 1 (NF 1) also known as ?

A

Recklinghausen disease

114
Q

what are the 5 major diseases affecting the heart

A
  1. coronary artery disease
  2. hypertensive heart disease
  3. congenital heart diseases
  4. heart valve diseases
  5. cardiomyopathies
115
Q

what are 3 key points for coronary artery disease

A
  1. stable angina pectoris
  2. unstable angina pectoris
  3. myocardial infarction
116
Q

what are the 2 key points for hypertension heart disease

A
  1. cor pulmonale
  2. systemic hypertension
117
Q

what is normal heart weight for males and females

A

250 - 300 g = females
300 - 350 g = males

118
Q

what are the values for wall thickness in right and left ventricle

A

0.3 - 0.5 cm = right ventricle
1.3 - 1.5 cm = left ventricle

119
Q

what is the percentage of myocytes (heart muscle cells)

A

25% of the cells of the heart, but 90% of the mass of the heart

120
Q

what are the four chambers of the heart

A
  1. right atrium
  2. left atrium
  3. right ventricle
  4. left ventricle
121
Q

what are the 4 valves of the heart

A
  1. pulmonary valve (b/w right ventricle and pulmonary artery)
  2. tricuspid valve (b/w right atrium and right vent)
  3. mitral valve (b/w left atrium and left ventricle)
  4. aortic valve (b/w left ventricle and aorta)
122
Q

what is ventricular systole and what happens during it

A

time period of the contraction of the ventricle (left and right). beginning of the QRS by ECG

  • blood is ejected from the LV into the aorta, and from RV into pulmonary arteries
123
Q

what is ventricular systole and what happens during it

A

time period AFTER contraction when the ventricles relax

  • pressure in the ventricles drops until below pressure in the atrium
  • blood flows from the left atrium in LV, and from right atrium into RV
124
Q

what does heart function depend on

A

conduction of electrical impulses

125
Q

where is the sinoatrial (SA) node located and what does it do

A

located in the right atrium and is the pacemaker of the heart
- will discharge at 70 - 80 times/minute

126
Q

what is the SA node innervated by

A

vagal and sympathetic nerve fibers

127
Q

what happens if SA node fails

A

the next lower system will take over (EC: AV node)

128
Q

what is the AV not and what does it do

A

GATEKEEPER to prevent fast depolarization of the heart

129
Q

what does a P wave represent on a ECG/EKG

A

atrial depolarization (contraction) = small hump

130
Q

what does the QRS complex represent on ECG/EKG

A

ventricular depolarization (contraction) = sharp (tall) signal

131
Q

what does a T wave represent on an ECG/EKG

A

repolarization of the ventricle (relaxation) = jumps a little then falls

132
Q

what are 4 tips for easy ECG interpretation

A
  1. normal ECG strip is 10 seconds
  2. for heart rate multiply QRS/10 sec by 6
  3. check if “p” is there followed by QRS
  4. check how ST waves behave
133
Q

what is junctional bradycardia? how many beats/min is it

A

“junctional rhythm” = only AV node fires
- 40 - 60 beats/min

134
Q

what is the heart sound

A

“lub-dub”

135
Q

what is the first heart tone

A

S1 or “lub”: sound is due to vibration of the blood thrust against the closed atrial valves. sudden pressure increase in the ventricles at the beginning of systole reverses blood flow towards atria and closes atrial valves (left: mitral valve; right: tricuspid valve)

136
Q

what is the second heart tone

A

S2 or “dub”: caused by the closure of the aortic and pulmonary valves at the end of the systole. Sound is due to vibration of the blood thrust against the aortic or pulmonary valves
- S2 can sometimes be split into P2 (pulmonary valve sound) and A2 (aortic valve sound) during inspiration (inhaling of air)

137
Q

what are the 8 characteristics of congestive heart failure

A
  1. cyanosis
  2. jugular vein distension
  3. hepatomegalie
  4. ascites
  5. edemas
  6. increased venous pressure
  7. exhaustion
  8. tiredness
138
Q

what is heart failure

A

inability of the heart to pump sufficient blood through the body

139
Q

what can heart failure be caused by

A

anything that impairs the pump function of the heart

  1. MI
  2. hypertension
  3. arrhythmias
  4. valve defects
  5. pulmonary hypertension
140
Q

what is the MAIN cause of heart failure

A

volume overload = heart must pump too much blood

141
Q

what are the 7 symptoms of heart failrue

A
  1. shortness of breath on light exercise (dyspnea) or at rest (orthopnea)
  2. fatique
  3. pulmonary edema
  4. peripheral edema
  5. ascites
  6. nocturnia (urinating at night)
  7. jugular vein distention
142
Q

what are the 6 treatments for heart failure

A
  1. resolve underlying cause
  2. weight reduction
  3. decrease fluid overload
  4. sodium restriction
  5. fluid restriction
  6. drug treatment: reduce blood pressure, diuretics, beta blockers, treat arrhythmias
143
Q

general causes of heart failure for the left side of heart

A
  1. hypertensive heart disease (peripheral arterial hypertension
    • left ventricle works harder to overcome increased pressure in the aorta
  2. left ventricular hypertrophy
  3. coronary heart disease
  4. arrhythmias
144
Q

general causes of heart failure for the left side of heart

A
  1. cor pulmonale: hypertrophy or dilation of the right ventricle because of impaired perfusion of the lungs
  2. acute cor pulmonale = PE (pulmonary embolism)
  3. chronic cor pulmonale: chronic obstructive lung disease, loss of lung tissue (Tb, cancer surgery)
  4. Mechanism: right ventricle works harder to move blood through the lungs - right heart tries to compensate
145
Q

the heart tries to compensate until it…

A

FAILS

146
Q

what is concentric hypertrophy

A

pressure overload

147
Q

what is eccentric hypertrophy

A

dilation of the heart = volume overload

148
Q

how big can the heart grow up to

A

1000 g

149
Q

what is right ventricle hypertrophy

A

cor pulmonale

150
Q

what is hypertrophy of the right ventricle caused by

A

changes in the pulmonary blood vessels

151
Q

what are the most frequent causes for right ventricular hypertrophy

A

COPD: chronic obstructive pulmonary disease (chronic bronchitis/emphysema)
- loss of lung tissue

152
Q

what does right ventricular hypertrophy lead to

A

congestive heart failure

153
Q

what is coronary heart disease also called

A

ischemic heart disease

154
Q

what is the most important cause for coronary heart disease

A

obstruction of coronary arteries by atherosclerosis (atheroma = lump of porridge in Greek)

155
Q

what is atherosclerosis caused by

A

deposits of cholesterol crystals between intima and media and subsequent proliferation of macrophages and other cells

156
Q

what does the fibrous cap consist of

A
  1. smooth muscle cells
  2. macrophages
  3. foam cells
  4. lymphocytes
  5. collagen
  6. elastin
  7. proteoglycans
  8. neovascularization
157
Q

what does the necrotic center consist of

A
  1. cell debris
  2. cholesterol crystals
  3. foam cells
  4. calcium
158
Q

what are the 2 phases for the progression of atherosclerosis

A
  1. pre-clinical phase (usually young age)
  2. clinical phase (usually middle age to elderly
159
Q

what is the order for the pre-clinical phase

A

Normal artery -> fatty streak -> fibrofatty plaque -> advanced/vulnerable plaque

160
Q

what is the order for the clinical phase

A

aneurysm and rupture -> occlusion by thrombus -> critical stenosis

161
Q

what does L/F/C stand for in the atheromatous plaque in coronary artery

A

L = lumen
F = fibrous cap
C = core

162
Q

what are the major risk factors for atherosclerosis

A
  1. Increasing age
  2. male gender
  3. family history
  4. genetic abnormalities
  5. hyperlipidemia (hypercholesterolemia)
  6. hypertension
  7. smoking
  8. diabetes
  9. BAD cholesterol: LDL (low-density lipoproteins)
    • delivers cholesterol to tissues
  10. GOOD cholesterol: HDL (high-density lipoproteins)
    - transports cholesterol from plaques to the liver for excretion
163
Q

what are potential risk factors for atherosclerosis

A
  1. obesity
  2. physical inactivity
  3. stress
  4. high carbohydrate intake
  5. postmenopausal
164
Q

what do the 3 different types of cholesterol levels indicate

A

< 200 = desirable level. lower risk for heart disease

200 -239 = borderline high risk

> 240 = high risk

165
Q

what is the generally desirable level for the total cholesterol test

A

under 200 mg/dL

166
Q

what is the generally desirable level for the LDL (bad) cholesterol test

A

under 100 mg/dL

167
Q

what is the generally desirable level for the HDL (good) cholesterol test

A

over 40 mg/dL for a man, over 60 mg/dL for a woman

168
Q

what is the generally desirable level for the triglycerides test

A

under 150 mg/dL

169
Q

if the t(total) cholesterol/HDL = 5 what does it interpret

A

average risk for heart disease

170
Q

if the t(total) cholesterol/HDL = 3.4 what does it interpret

A

approx. half the average risk

171
Q

if the t(total) cholesterol/HDL = 9.6 what does it interpret

A

double the average risk

172
Q

what are the 5 well-known risk factors for cardiovascular disease

A
  1. overweight
  2. high blood pressure
  3. high cholesterol
  4. smoking
  5. diabetes
173
Q

what is coronary heart disease also referred to

A

CAD; ischemic heart disease

174
Q

what is coronary heart disease

A

sudden severe narrowing of the large coronary arteries

175
Q

what is coronary heart disease normally due to

A

atherosclerosis

176
Q

what are the 3 major clinical manifestations for coronary heart disease

A
  1. stable angina pectoris
  2. unstable angina pectoris
  3. myocardial infarction (MI)
177
Q

what is angina pectoris

A

ischemia leads to clinical symptoms, but not to death of heart muscle cells

178
Q

what is myocardial infarct

A

ischemia so sever that it leads to clinical symptoms and death of heart muscle cells

179
Q

what are 8 key points for angina pectoris

A
  1. sudden onset of chest discomfort: pressure, heaviness, burning, choking sensation, pain
  2. typically radiates from left chest and arm
  3. frequently precipitated: after heavy meals, going from warm to cold, emotional or physical stress
  4. usually lasts a few minutes
  5. relieved by nitrites (vasodilators)
  6. can radiate to abdomen = indigestion
  7. ECG typically normal, but stress ECG may show changes
  8. coronary angiogram
180
Q

what is Prinzmetal’s angina

A

looks like angina pectoris but is caused by vasospasm of coronary arteries

181
Q

what are 3 key points for stable angina

A
  1. predictable, triggered by activity, exertion, stress
  2. usually resolves quickly when resting (5 - 20 minutes)
  3. pattern stays stable for > 1 month
182
Q

what are 4 key points for unstable angina

A
  1. angina occurs at rest, no trigger, pattern of angina changes
  2. may not go away
  3. symptoms more severe than in previous angina
  4. symptoms for the first time or less than a few weeks
183
Q

stable angina can convert to…

A

unstable angina

184
Q

what is unstable angina sometimes called

A

preinfarction angina

185
Q

what is the next step for unstable angina

A

myocardial infarct

186
Q

what are the 8 symptoms for MI

A
  1. chest pain
  2. discomfort
  3. nausea
  4. vomiting
  5. arrhythmia
  6. loss of consciousness
  7. possibly sudden death
  8. pain radiates to left arm, jaw, back, epigastrium (stomach area)
187
Q

what are the symptoms of MI in women

A
  1. dyspnea
  2. weakness
  3. fatigue
188
Q

how much MI’s are silent

A

1/3

189
Q

what is used to diagnose MI

A
  1. ECG = ST-elevation MI (STEMI)
    • cardiac enzymes:
      creatine phosphokinase
      MB; troponin I or T
  2. Non-ST elevation MI (NSTEMI) = ST not elevated, but cardiac enzymes elevated
190
Q

what are the 3 key points for STEMI

A
  1. ST- elevation MI
  2. complete occlusion of coronary artery , myocardial damage
  3. cardiac enzymes elevated (CK-MB, I-troponin)
191
Q

what are the 5 key points for NSTEMI = mild heart attack

A
  1. non-ST-elevation MI
  2. partial/intermittent occlusion of coronary artery, myocardial damage
  3. cardiac enzymes elevated
  4. 30% of all MI
  5. often STEMI MI happens hours or days later
192
Q

what is the sequence of histopathologic events after MI

A
  1. Ischemia for > 20 - 40 minutes leads to myocyte death
  2. 4-12 hours: myocyte death becomes histologically visible: coagulation necrosis, edema hemorrhage
  3. 12-24 hours: necrosis with infiltration of neutrophils
  4. 2-3 days: necrosis with even more inflammation
  5. 5-10 days: macrophages remove dead tissue and scar formation - THIS IS DANGER TIME FOR MYOCARDIAL RUPTURE because this tissue is the weakest (proliferation phase of wound repair)
  6. 2-4 weeks - granulation tissue
193
Q

what are treatments for MI

A
  1. MI is an emergency
  2. rest, half sitting
  3. upon recognition of MI: immediately 325 mg Aspirin
  4. MONA: morphina, oxygen, nitroglycerin
  5. thrombolysis (recombinant tPA, stretokinase, urokinase)
  6. cardiac catheter, angioplasty
  7. door to balloon time = 90 mins. until opening of artery
    • 2005-2010 nationwide gone from median 96 mins. to 64 mins.
    • under 90 min: from 44.2% to 91.4%
    • under 75 min: 27.3% to 70.4%
194
Q

what is the TTC for acute MI

A

triphenyltetrazolium chloride staining

195
Q

what are the 3 most frequent types of shock

A
  1. cardiogenic shock
  2. hypovolemic shock
  3. septic shock
196
Q

what is cardiogenic shock

A

failure of the heart to pump blood (MI, aarythmias, PE, heart tamponade

197
Q

what is hypovolemic shock

A

loss of blood volume (bleeding, burns, trauma)

198
Q

what is septic shock

A

systemic infarction (mostly gram negative organisms - endotoxic shock)

  • peripheral vasodilation, endothelial injury, disseminated intravascular coagulation, cytokine release (TNF, IL-1, IL-6)
  • multi-organ system failure
199
Q

what are other types of shock

A
  1. anaphylactic shock
  2. neurogenic shock (after spinal cord injury)
200
Q

what are the 6 symptoms of shock

A
  1. anxiety, restlessness, disorientation
  2. hypotension
  3. rapid pulse (tachycardia)
  4. cool, clammy, mottled skin
  5. decreased urine production (oliguria)
  6. rapid breathing (hyperventilation)
201
Q

what do other symptoms of shock depend on

A

THE TYPE OF SHOCK (EX: cardiogenic shock, septic shock, hypovolemic shock)

INTRO TO CLINICAL (2 decks)

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