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Med Path Fall 2020 > Hemodynamics and Shock > Flashcards

Hemodynamics and Shock Flashcards

1
Q

Thombus vs thrombosis vs embolus

A

Thrombus: Wanted blood clot
Thrombosis: Unwanted clot
Embolus/thromboembolism: Moving clot/dislodged in veins or arteries

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2
Q

Most common location of thrombosis

A

*Atherosclerotic bifurcation

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3
Q

Thrombosis causes

A

*Endothelial damage
Blood flow irregularity
Hyper coagulability

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4
Q

Result of thromosis

A

Ischemia or infarction

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5
Q

Virchow’s Triad- three categories that can increase the risk of thrombosis

A

Stasis (blood flow irregularity)
Vessel wall injury to endothelium
Hypercoaguability

*maybe inflammation (chronic and acute)

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6
Q

How does endothelial damage lead to thrombosis formation? Risk factors?

A

Endothelial breakdown/damage= exposed collagen where pro-clotting factors can bind= thrombosis formation

Risk factor: Atherosclerosis* (DM, HTN, hyperlipidemia)
Anything that damages endothelium

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7
Q

How does circulatory stasis lead to thrombosis formation? Risk factors?

A

Slow, irreg, turbulent, or stationary blood flow causes local accumulation of pro-clotting factors= thrombosis

Risk: Immobility or paralysis*, arrhythmia, heart failure, aneurysm.

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8
Q

How does hypercoagulability lead to thrombosis formation? Risk factors?

A

Predisposition towards clotting (congenital or acquired) alters blood chemistry and causes increased risk of thrombosis.

Congenital: Sickle cell
Acquired: Dehydration, pregnancy, malignancies, thombophilia, sepsis.

Risk factors: Any that promote thrombus formation. Smoking, age, obesity

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9
Q 
Arterial thrombosis 
Cause
Effect
Risk factors
Tx
A

Cause: *atherosclerosis, atrial fib, valvular disease
Effects: *MI, *Stroke, peripheral artery disease
Risk factors: *Smoking, *HTN, *high cholesterol, *Diabetes
Tx: Lifestyle changes, medications, surgery (angioplasty, graft)

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10
Q 
Venous thrombosis
Associations: 
Location: 
effects:
Treatment: 
Risk factors:
A

Associations: *Venous stasis, *hypercoagulability
Location: *deep vein. Big veins= slow flow
effects: Local pain and swelling or pulmonary edema
Treatment: Anticoagulants
Risk factors: *Immobilization, orthopedic surgery, oral contraceptives.

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11
Q

Deep veins in legs

A

Saphenous, popliteal, femoral

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12
Q

Deep vein thrombosis labs/tests

A

Elevated d dimer

ultrasound angiography

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13
Q

3 possible outcomes to venous thrombosis

A

Resolution
Embolism to lungs
Organized and recanalized–> organized and incorporated into wall.

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14
Q

Venous thrombosis can lead to-

A

Thromboembolism (dislodged thrombus) Can be fatal. Coronary or pulmonary embolism or stroke.

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15
Q

Pulmonary embolism is associated with

A

Deep vein thrombosis

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16
Q

Pulmonary embolism symptoms and tx

A

*Shortness of breath
Hemoptysis- coughing up blood
Sharp chest pain

Tx: Anticoagulation meds

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17
Q

Hemoptysis

A

Coughing up blood. Happens in pulmonary embolism

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18
Q

Venous thrombosis ocular manifestations

A

Papilledema: Venous sinus thrombosis. Bilateral swollen ON due to CSF not being able to drain.

BRVO, CRVO

19
Q

3 types of aneurysms

A

Saccular- berry (most common)
Fusiform- spindle like
Dissecting (Inner wall of blood vessel tears and forms false channel. = turbulent blood flow. Could also occur inside fusiform)

20
Q

Risk factor for aneurysm

A 
*Tobacco use
Connective tissue disorders (marfans, ehlers danlos- lots of elastic tissue= weak arteries) 
Trauma 
HTN
M>F
Age
Atherosclerosis
21
Q

Aneurysm. What is it?

A

Localized thinning of arterial wall- high pressure vessels.

22
Q

Location of aneurysms

A

*cerebral arteries
*Brain stem
Aortic arch
Thoracic artery
Abdominal arteries

High pressure arteries. Not so much veins

23
Q

3 complications to aneuryssms

A

Rupture –> Hemorrhagic (bleeding) stroke
Dissection (tear/false valve in vessel) –> ischemic stroke
Thrombus –> secondary turbulent blood flow–> Clotting –> ishchemic stroke

24
Q

Tx of aneursysm

A

Stent
Clip- stops bleeding.
Coiling-fill out pouching so blood can’t enter. Promotes clotting that seals off.
Liquid embolic agents- fill out pouching with “glue” so blood can’t enter.
Blood thinner
HTN meds

25
Q

aneurysms are more likely to form where?

A

In high pressure vessels. Usually arteries over veins.

26
Q

Ocular manifestations of aneurysms

A

Aneurysmal 3rd nerve palsy. Could lead to hemorrhagic stroke and death. Life threatening. Posterior communicating artery has 20% of aneurysm that compresses CN III.

VF changes

27
Q

3 required functioning organ systems for life

A

Cardiovascular
Respiratory
Renal

28
Q

Primary circulatory system component

A

Heart pump, fluid volume, closed circulatory system. Ideally no addition or removal.

29
Q

Shared feature of all shock

A

inadequate tissue perfusion (not enough O2 to necessary organs) Causes homeostasis to become compromised

Result: Body wide shift to anaerobic metabolism.

Fatal if untreated.

30
Q

Inadequate cell o2 –> anaerobic metabolism. What other two paths?

A
  1. Inadequate energy production –> Metabolic failure of pumps –> Cell death
  2. Lactic acid production –> Metabolic acidosis –> cell death.
31
Q

shock MOA (3)

A
  1. Inadequate oxygen deliver*
    - respiratory failure
    - Anemia or hemorrhage
    - Fluid loss: vomit, diarrhea, dehydration
    - Cardiac pump failure
  2. Impaired oxygen uptake due to biochem poisoning
  3. Inadequate nutrient delivery
    - Malnutrition
    - GI absorption disorder
    - Lack of insulin (diabetes mellitus)
32
Q

Final common pathway of shock

A

Metabolic acidosis and cell death

33
Q

5 main types of shock

What do they all have in common

A 
Hypovolemic shock *
Cardiogenic shock 
Septic shock 
Hypotonic/anaphylactic 
Neurogenic

All involve reduced blood oxygen

34
Q

Hypovolemic shock *

A

Decreased blood volume due to trauma, child birth, dehydration.

35
Q

Cardiogenic shock

A

Ineffective cardiac pumping

MI, pulmonary embolus, cardiac tamponade

36
Q

Septic shock

A

Blood infection- systemic inflam response to secondary infection.
Exo or endo toxin mediated

**Fever and peripheral thrombosis
Ex: Candidia

May lead to cariogenic or hypovolemic shock

37
Q

Hypotonic shock/ anaphylactic

A

Decreased peripheral vascular tone = Vasodilation = blood pools in peripheral tissues

Due to type 1 hypersensitivity reaction

38
Q

Neurogenic shock

A

Brain and or spinal cord damage

39
Q

Two main signs of septic shock

A

Fever and peripheral thrombosis

40
Q

3 stages of shock

A

compensatory
Progressive
Refractory

41
Q

Stage 1 of shock: Compensatory. What happens?

Mechanisms to fix? Presents as what?

A

Normal BP
Adequate tissue person
No permanent damage

Mechanisms to fix: vasoconstriction. Increase blood flow to major organs. Increase CO. Decrease urine.

Presents as decreased skin perfusion, tachycardia.

42
Q

Stage 2 of shock: Progressive. What happens?

A 
Body's mechanism starts to fail 
Failing BP, hypotension --> Tachycardia and tachypnea 
Acidosis 
reduced tissue perfusion 
Tissue damage
43
Q

Stage 3 of shock: Refractory period. What happens?

A

Very low BP
Inadequate tissue perfusion
Widespread organ failure

Death occurs even with homeostasis restoration.

44
Q

Septic shock may lead to what other forms of shock?

A

May lead to cariogenic (loss of pumping power) or hypovolemic shock (Decreased blood vol and vasodilation)

Med Path Fall 2020 (20 decks)

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