Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Term 4 > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

Acute Vs Chronic Pulmonary Congestion

A

Acute:Due to left ventricular failure
Alveolar capillaries are engorged
Alveolar septal edema
Pink transudate in alveolar space

Chronic:Brown induration
Thickened fibrous septa
Heart failure cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute Vs Chronic Liver Congestion

A

Acute: Right heart failure, Budd Chiari
syndrome
Central vein and sinusoids distended
with blood
Degeneration of central hepatocytes

Chronic: Central region of hepatic lobule is
reddish brown accentuated against
surrounding areas of uncongested tan
liver – resembles Nutmeg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is hemorrhage?

A

Extravasation of blood to the exterior of the body or into non-vascular body space.Due to damage of blood vessels or defective thrombosis
* Trauma
* Atherosclerosis
* Aneurysms
* Bleeding disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hematoma

A

Hemorrhage into soft tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Petechiae

A

Pinpoint 1-2 mm hemorrhage in skin/conjunctiva- rupture of capillary or arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Purpura

A

Diffuse superficial hemorrhage up to 1 cm in diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Purpura

A

Diffuse superficial hemorrhage up to 1 cm in diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ecchymosis

A

Superficial hemorrhage >1 cm in diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Disseminated Intravascular Coagulation

A

thrombo-hemorrhagic disorder seen as a complication
of many disorders

systemic activation of coagulation which
results in the formation of thrombi throughout the microcirculation→ “consumption coagulopathy” → bleeding

DIC give rise to:
-Tissue hypoxia and microinfarcts: due to formation of
microthrombi.
-Bleeding disorder: due to pathologic activation of fibrinolysis and depletion of the clotting factors required for hemostasis

Epithelial injury can cause this, after injury thromboplastic agents are in circulation activating coagulation.

**IL-1 and TNF cause upregulation of tissue factor and down regulation of thrombomodulin = excessive clotting

Lab investigations:
- increased fibrin products and D-dimers (fibrinolysis)
- decreased fibrinogen due to excessive use
- decrease clotting factors -> increase bleeding time
- consumption of platelets and aggregation -> increase bleeding time

GIVE HEPARIN TO prevent further formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Shock

A

clinical state characterized by a generalized decrease in
perfusion of tissues associated with reduction in effective cardiac output or reduction in effective circulating blood volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cardiogenic Shock

A

results from myocardial pump failure
* Intrinsic myocardial damage (infarction), ventricular arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypovolemic Shock

A

results from loss of blood or plasma volume
* Hemorrhage
* Fluid loss from severe burns or trauma, vomiting, diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Distributive shock

A

results from excessive vasodilation causing abnormal
distribution of blood flow

Septic: caused by systemic microbial infection
* Gram- positive infections, gram-negative infections (endotoxic
shock), fungi

Neurogenic/ CNS injury: imbalance between compartments
* Anesthetic, spinal cord injury – loss of vascular tone, peripheral
pooling

Anaphylactic: generalized Ig-E mediated response
* Systemic vasodilation, increased permeability
* Reduced tissue perfusion
* Degranulation of mast cells and basophils- histamine, bradykinin, leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Obstructive Shock

A

results from extracardiac causes leading to decreased
cardiac output

Pulmonary embolism
* Tension pneumothorax
* Cardiac tamponade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Non-progressive stage (adaptation)

A

Compensated by reflex mechanisms
-Baroreceptors, release of catecholamines, renin- angiotensin, antidiuretic hormone (ADH)-> increase BP

sympathetic stimulation and aldosterone release –
tachycardia, peripheral vasoconstriction, renal conservation of fluid,
relatively maintained blood pressure.

Cutaneous vasoconstriction – cool, pale skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Progressive Stage (Reversible injury)

A

impaired tissue perfusion

*Imbalance between circulation and metabolic needs
*Intracellular aerobic respiration replaced by anaerobic
glycolysis -> low pH
*Sludging of RBCs (red blood cells)
*Blunting of vasomotor response
*Arterioles dilate and blood pools into microcirculation
*Reduced cardiac output, anoxic endothelial injury, DIC
* Patient confused, urine output decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Irriversible stage

A
  • Severe widespread cell and tissue injury
  • Leakage of lysosomal enzymes (aggravate shock)
  • Failure of multiple organ systems
  • Myocardial depressant factor reduces cardiac output
  • Perfusion of brain and myocardium at critical level
  • ATN (Acute tubular necrosis), ARF (Acute renal failure) → renal uremia
  • Ischemic bowel, entry of bacteria → endotoxic shock
  • Survival difficult even if hemodynamics are corrected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Systemic Inflammatory response syndrome

A

the body’s systemic inflammatory reaction to an infectious or non-infectious insult which is shown
clinically by changes in vital signs, such as elevations in Temperature, heart rate and respiratory rate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Sepsis

A

this is the body’s systemic inflammatory response (SIRS) to a source of infection in the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Septic Shock

A

this is Sepsis causing severe hypotension and organ dysfunction.
- Gram positive bacteria common cause
- localized infections can cause systemic shock w/o bloodstream
-dilation leads to hypotension and hypoperfusion
- DIC susceptible
- cellular/organ dysfunction due to hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Metabolic Abnormalities in Septic Shock

A
  • insulin resistance -> hyperglycemia
  • increase in glucose release due to increase catecholamines
  • Hyperglycemia decreases bacterial activity of neutrophils
  • strong release of glucocorticoid then no production due to necrosis of adrenal glands
  • decrease in glut 4 due to insulin resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Changes in Organs affected by hypoxic injury (septic shock)

A

-Platelet-fibrin thrombi -> found mostly in kidney
-acute tubular necrosis kidney
- aveolar damage in lungs
- cerebral watershed areas are susceptable

all areas can recover except for neurons and myoctes.

23
Q

Septic Shock Clinical Features

A

-Systemic Hypotension
-Weak rapid pulse
-Warm, Flush skin in septic shock
-Hyperventilation
-Oliguria/Anuria
-Bleeding- DIC

24
Q

Septic Shock Treatment

A
  • O2
  • insulin
  • doses of corticosteroids
  • vasopressor - maintain blood pressure
    -fluid replacement
    -antibiotics for infections
25
Q

Thrombosis

A

The formation of a solid mass from circulating blood elements in the intact circulation.

Normal role for thrombus formation is to plug defects produced by everyday activities in the vessel walls.

Thrombus formation occurring within circulation at sites of no injury or relatively mild injury

26
Q

Hemostasis

A

Hemostasis is a precisely orchestrated
physiologic process that occurs at the site of
vascular injury and culminates in the formation of
a blood clot to prevent or limit the extent of
bleeding.
-vascular wall
-platelets
-coagulation

27
Q

Virchows Triad

A

Endothelial integrity is the most important factor.

Abnormalities of procoagulants or anticoagulants can tip the balance in favor of thrombosis.

Abnormal blood flow (stasis or turbulence) can lead to
hypercoagulability directly and indirectly through endothelial dysfunction.

28
Q

Endothelial injury (Thrombosis)

A

Most important factor

  1. injury exposes VWF(platelet bindding site) -> increase tissue factor
  2. Inflammation -> increase plasminogen activator inhibitor (pro) -> decrease anticoagulant factors.
  3. platelet adhesion
  4. clots are rich in platelets
29
Q

Abnormal Blood flow (Thrombosis)

A

Turbulence can cause direct injury to endothelial cells, while pockets of stasis allows platelets and leukocytes to come in contact with endothelium.

contribute to abnormal BF:
Atherosclerotic Plaques -> turbulent flow across plaque which can damage the fibrous cap covering the atheroma, causing bleeding and exposing subendothelial collagen causing platelet adhesion and therefore thrombus formation over the ulcerated atherosclerotic
plaque. This is the pathogenesis of acute myocardial infarction.

Aneurysmsv-> aortic aneurysms cause blood to settle within the dilated lumen. Loss of blood flow in the aneurysm predispose to stasis and clot formation.

Atrial or Ventricular Fibrillation -> ineffective contraction and emptying of left atrium or ventricle causing stasis of blood and clot formation within the heart chamber.

30
Q

Hypercoagulability

A

Abnormally high tendency of activation of the clotting cascade in blood.
Very important risk factor for venous thrombosis.

31
Q

Factor V Leiden

A

Most common cause of hereditary thrombosis and most commonly presents with
veinous thromboses such as deep vein thrombosis (DVT).
Factor V Mutation produces a factor V that is resistant to inhibition by Protein C, a natural
anticoagulant. Note: PT, PTT are normal in this condition

32
Q

Prothrombin mutation

A
  • A single-nucleotide substitution (G to A) in the 3′-untranslated region. The
    result is increased transcription of prothrombin and increased levels of prothrombin in the blood.
    Clinically there’s an increased risk of veinous thromboses.
33
Q

Antithrombin Deficiency

A

Antithrombin inhibits Factors IIa (Thrombin) and factor Xa. Note: PT, PTT
are normal in this condition.

34
Q

Protein C,S Deficiency

A

Loss of inhibition of Factor Va and Factor VIIIa. Warfarin inhibits factor II,
VII, IX, X, Protein C and Protein S. Protein C and Protein S have shorter half lives than factors II, IX
and X, therefore treatment with warfarin causes a transient procoagulant state presenting with skin
necrosis in patients with protein C and protein S deficiency.

35
Q

Arterial thrombi

A

Paler than venous thrombi
seen in heart and aorta
seen in other smaller arteries coronaries, carotids, femoral, mesenteric

36
Q

Venous Thrombi

A

Takes shape of the vessel
redder than arterial thrombus
superficial veins rarely embolize
deep veins -> embolize

37
Q

Clinical manifestations of Thrombus

A
  • pain, tenderness, features of necrosis such as blue/black discoloration.
  • Venous thrombi: swelling, pain, tenderness, pitting edema, warm and discolored due to
    congestion (limb).
  • aterial thrombi: Infarct (e.g. Myocardial infarct) Slow – ischemia, atrophy, fibrosis,
    collateral vessel formation (e.g. Stable angina, limb claudication); pale and cold (
    Venous embolize to lung usually
    arterial embolize to organs/tissue or lower extremeity
38
Q

Embolism

A

detached mass that is carried in the blood from point of orgin to a distant site, can cause infarction or dysfunction.

most common emboli come from the heart then to the lower extremities or brain

Most emboli were part of a dislodged thrombus

39
Q

Pulmonary Thromboembolism

A

Common origin is from the deep leg veins to the lungs

major contributor to death in hospital, when they first get out of bed.

Massive -> sudden obstruction of 60%/sudden death
Major -> medium occlusion dyspnea, pain/ infarction of 10%
minor -> small vessels obstructed/ asymptomatic

40
Q

Systemic Thromboembolism

A

arterial circulation emboli
originates from the heart (80%)
aorta from plaques
venous circulation from atrial septal defect (paradoxical)
Can lead to infarction due to embolization brain lower extremities and bowel

41
Q

Fat Embolism

A

Trauma to bone, subcutaneous tissue, burns → fat globules enter the circulation by rupture of the marrow vascular sinusoids or rupture of venules

Mechanical blockage - Globules enlarge in circulation, platelets adhere
Biochemical injury – Free fatty acids are released from adipose tissue in the circulation and are toxic to endothelial cells – DIC, clogged pulmonary and
systemic capillaries.

Pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia
* Symptoms appear 1-3 days after injury – sudden onset of tachypnea, dyspnea, tachycardia, petechiae
* Neurologic symptoms- irritability, restlessness, progression to delirium, coma

42
Q

Air Embolism

A

Air embolisms usually form via venous circulation due to lower pressure.
Arterial circulation has more pressure and is less likely to get air.
150L can cause death -> obstructive shock -> prevents outflow of blood from RV.
Tx with placing them on the left lateral decubitus so air embolism will rise to right lateral wall

43
Q

Caisson disease/ Bends? Nitrogen embolism

A

Deep diving without Caissons chamber deeper than 10m.
02 and N2 dissolve in high amount in tissue due to pressure -> sudden resurface -> releases 02 and N2 -> 02 is reabsorbed but N2 bubbles out rupturing tissue and forming embolism. -> Platelets adhere to N2-> aggravate ischemia-

Treat with slow decompression chamber

44
Q

Amniotic Fluid Embolism

A

rare sudden event after labor-> Squames, hair, meconium in mother’s pulmonary vessels

Usually fatal due to DIC or diffuse alveolar injury

45
Q

Atherosclerotic Embolism

A

autopsy finding

small dislodged fragments of plaques that obstruct end of arteries

rarely clinical symptoms

46
Q

Bone Marrow Embolism

A

Found in small pulmonary vessels are cardiac resuscitation

autopsy finding

not the cause of death

47
Q

Infarctions

A

Ischemic necrosis caused by occlusion of arterial supply or venous drainage in tissue

99% of infarcts are from embolism or thrombosis

can be caused by anything that occludes the artery or vein

48
Q

White infarcts

A

little bleeding
solid organs like kidney, spleen, heart
arterial occlusions

49
Q

Red infarcts

A

large amount of bleeding into organ
tissues with dual supply (lungs)
venous occlusion

50
Q

5 factors influencing infarcts

A
  1. nature of vascular supply. single or dual?
  2. rate of development. Sudden or slow?
  3. Tissue vulnerability. brain or muscle?
  4. Oxygen carrying capacity. anemia increases chances
51
Q

Nature of blood supply prevention

A

Dual blood supply will lessen chances of infarct

Collateral circulation -> more anastomoses the lessly likely risk of infarction.

52
Q

Pulmonary Infarction (nature of blood supply)

A

Pulmonary emboli with compromised bronchial circulation -> infarction
Pulmonary emboli with healthy circulation -> no infarction.

53
Q

Cerebral Infarction

A

Embolism is most common cause from mural thrombi

Thrombotic occlusions found in areas of carotid or middle cerebral artery.

54
Q

Myocardial Infarction

A

Coronary atherosclerosis with superimposed thrombosis

left anterior descending most common; coagulation necrosis

pale scar

increase cardiac enzymes

severe chest pain

Term 4 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions