Brainscape's Knowledge GenomeTM

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


See full index

Found. of Path. Processes - Block 1 > 21 - Hemodynamic Disorders > Flashcards

21 - Hemodynamic Disorders Flashcards

1
Q

What three diseases represent the most frequent causes of morbidity and mortality?

A
  1. Myocardial infarctions
  2. Pulmonary embolism
  3. Cerebral infarcts (Stroke)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Normal fluid homeostasis requires maintenance of what? What happens with failure of blood’s normal state?

A
  • Vacular wall integrity
  • Intravascular hydrostatic pressure
  • Osmolarity
  • Failure: hypercoagulable state due to mutation in factor V gene resulting in clotting when it shouldnt occur
  • Failure: hypocoagulable blood state due to platelet defect results in blood not clotting when it should
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is edema? What is anasarca?

A

Edema: accumulatio of interstitial fluid in tissues (subcutaneous and in body cavities)

Anasarca: very severe generalized edema

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

What is the normal fluid balance in the body? What factors affect fluid balance?

A
  • 2/3 intracellular
  • 1/3 extracellular (mostly interstitial) - 5% of EC fluid is in the blood plasma

Factors that affect fluid balance:
-vascular hydrostatic pressure

  • Plasma colloid osmotic pressure (due to plasma proteins)
  • Normally balanced so no loss or gan of fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does edema result from?

A

Increased hydrostatic pressure or decreased osmotic pressure that leads to accumulation of fluid in the interstitium.

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

What are some causes of increased hydrostatic pressure that result in edema? Give local and generalized examples.

A

Venous obstruction OR impaired venous return

  • Local: DVT, mass lesion, lower extremity inactivity, cirrhosis
  • Generalized: congestive heart failure

Arteriolar dilation from heat or neurohumoral dysfunciton

(These all cause incresed capillary pressure)

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

What are some causes of reduced plasma omotic (oncotic) pressure that results in edema? Give examples of disease states that lead to this?

A

Excessive loss of albumin leads to decreased volume and secondary hyperaldorsteronism.

  • Nephrotic syndrome
  • Protein-losing enteropathy (IBD)
  • Malnutrition
  • Lover disease (cirrhosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does heart failure cause edema?

A

There’s an increase in capillary hydrostatic pressure and a decrease in renal blood flow.

The decrease in renal blood flow activation the r_enin-angiotensin-aldosterone system_ causing retention of Na and H20.

This causes an i_ncrease in blood volume, leading to edema._

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

How does lymphatic obstruction cause edema? What are disease states in which this can occur?

A

Lymphatic obstruction prevents the uptake of fluid from the interstitial space, resulting in lymphedema.

Causes:

  • Inflammatory
  • Neoplastic (infiltration and obstruction by neoplastic cells)
  • Post-surgical/post radiation (scarring/removal of lymph channels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does water retention lead to edema? What disease states can lead to this?

A

Sodium and water retention cause increased hydrostatic pressure (expanded intravascular volume) and decreased colloid osmotic pressure.

Causes:

  • Excessive salt intake w/ renal insuff.
  • Acute reduction of renal function (glomerulonephritis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What isthe morphology of edema? What are three locations in which edema can occur?

A

More easily recognized grossly; microscopically subtle cell swelling and separation of ECM elements.

  1. SubQ edema: seen in CHF and renal failure
  2. Pulmonary edema: seen in left ventricular failure
  3. Edema of the brain: focally (tumors) and diffusely (viral infections)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is hyperemia and what is it caused by?

A

Increase in blood volume within a tissue due to increased blood flow and arteriolar dilation.

Active process that occurs at the site of inflammation (conjunctivitis) or in exercising skeletal muscles

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

What is congestion and what is it caused by?

A

Increased blood volume within a tissue due to decreased outflow of venous blood (backed up blood stays in liver/lungs, etc).

Passive process

May occur systemically (liver and lung due to heart failure) or lically (obstructed superior sagittal sinus).

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

What is a nutmeg liver?

A

Chronic passive congestion of the liver, blood backed up into liver due to decreased outflow of venous blood.

May lead to tissue necrosis and fibrosis: so called “cardiac cirrhosis”

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

What would a nutmeg liver look like microscopically?

A

Centrilobular necrosis due to prolonged passive congestion causeing necrosis of the hepatocytes.

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

What would a congested lung from acute vs long-standing heart failure look like microscopically?

A

Acute congestion of capillaries in alveolar wall in acute heart failure.

Heart failure cells: macrophages containing broken down RBCs that have leaked from the capillaries in long standing heart failure

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

What is the mechanism of the change in the liver and lungs when they are congested?

A
  • Passive increased in blood volume
  • Extravasation of blood out of the sinusoids (liver) and alveoli wall capillaries (lungs)
  • Hydrostatic pressure has caused increased fluid in the interstitium
  • Lack of oxygen caused necrosis of centrol regions of liver (secondary to long-standing congestion causes stasis of blood and decreased oxygen)

NO inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the primary and secondary components of clotting (normal hemostasis)?

A

Primary: platelet plug formation

Secondar: clotting factors build upon platelet plug to strengthen it

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

What is the first step in clotting?

A

Vasculature (smooth muscle) vasoconstricts to limit blood leaking into space.

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

What occurs in primary hemostasis?

A
  1. Platelet adhesion to vWF in collagen and bind
  2. Confirmational change to expose membranes to increase SA
  3. Release granules
  4. Recruit fellow platelets via granules
  5. Plug formation (this is fairly weak)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What occurs in secondary hemostasis?

A

Clotting cascade needed to form matrix to strengthen plug

  1. Tissue factor released with endothelial damage to start clotting cascade (in vivo)
  2. Phospholipid complex expression on platelets so factors can be recruited
  3. End result: generate thrombin (factor 2a) which takes fibrinogen to fibrin (network layed down)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What labroratory screenings are done to test for primary hemostasis?

A

Platelet count

Platelet function: PFA-11, platelet aggresation studies

vWillebrand studies: vW antigen, vW activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What labroratory screenings are done to test for secondary hemostasis?

A

Prothrombin time [PT] (extrinsic + common pathway)

Activated partial thromboplastin time [aPTT] (intrinsic + common pathway)

Fibrinogen activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Bleeding disorders can come from defects in what?

A
  • Vascular integrity
  • Platelet count and/or function
  • Von Willebrand factor deficiency or dysfunction
  • Clotting factor deficiencies/inhibition: hemophilia, liver disease, anticoagulants
25
Q

What is hemorrhage? What are common causes?

A

Extravasation of blood from vessels; Accumulation within a space (hemothorax, hemoperitoneum)

Common causes: ruptured vessel, chronic congestion, predisposition to hemorrage with minimal trauma (hemorrhagic diathesis-seen with decreased ability to clot).

26
Q

What is a hematoma? What are examples?

A

Accumulation of blood within a tissue

Exp: epidural hematoma, subdural hematoma, subQ (bruise of eccymosis)

27
Q

What are petechial hemorrhages? What dysfunction are they associated with?

A

Hemorrhages into skin, mucous membranes or serosal surfaces (1-2mm).

Associated with low platelet counts (thrombocytopenia), platelet dysfunction, loss of vascular wall support, or local pressure

28
Q

What are purpura?

A

> or equal to 3mm hemorrhages associated with the same disorders as petechiae with trauma, vasculitis, and vascular fragility

29
Q

What is eccymoses? What are they associated with?

A

> or equal to 1-2 cm subcutaneous hematomas (bruises).

Associted with trauma, exacerbated by conditoins that cause purpura or petechiae.

30
Q

Name two important factors that inhibit thrombosis?

A

-AT3 (antithrombin 3) natural anti-coagulants: takes thrombin and inactivates it.

-Protein C and Protein S: natural anti-coagulants that (when activated) inhibit factors that form fibrin meshwork (factor 5 and 8) and start shutting down clotting cascade

31
Q

What are some factors that promote thrombosis?

A

Endotherlial injury: causes release of mediators that stimulate clotting

Abnormal blood flow: atherosclerosis, prolongest bed rest, A-fib, MI, prostetic heart valve, aneurysms.

32
Q

What are three different inherited hypercoagulability factors? What about acquired hypercoagulability factors?

A

Inherited:

  • Protein C deficiency
  • Protein S deficiency
  • AT3 deficiency

Acquired:

  • Malignancy
  • Estrogens
  • Antiphospholipid antibody syndrome
33
Q

What is an example of an inherited hypercoagulative disease? What causes it? How common is it?

A

Factor 5 Leiden

Caused by a single bp mutation that recults in a cleavage at a site for protein C, causing factor 5 to be resistant to active protein C (which normally degrades it factor 5). Factor 5 then contributes to clotting.

2-15% causacions are hetero. Hetero=5x risk for clotting, homo=50X risk for clotting.

34
Q

What three primary abnormalities lead to thrombus formation?

A
  1. Endothelial injury
  2. Abnormal blood flow
  3. Hypercoagulability

*Thrombosis is the formation of a clot that isnt supposed to be there.

35
Q

Define thrombosis? What are general characteristics?

A

Formation of a blood clot within intact vessel.

  • Begins at site of endothelial injury, turbulence of flow, or site of blood stasis (when blood flow is turbulentm stasis can occur).
  • Point of attachment to wall.
  • Lines of Zahn: laminations produced by alternating layers of platelets, fibrin, and RBCs.
36
Q

Where would a venous thrombosis most likely occur? What are causes?

A

90% occur in the lower extremities; can occur in upper, periprosthatic plexus, ovarian and periuterine veins, dural sinuses, and hepatic vein.

  • immobilization
  • Trauma, surgery, burns
  • Pregnancy
  • Malignancy
37
Q

What are clinical characteristics of venous thrombi?

A

No inflammation, 50% asymptomatic

Thrombi in deep veins of legs may travel to lungs (emboli).

Thrombi in superficial veins rarely embolize - may cause local swelling, pain, skin ulceration

38
Q

What is an emboli? What are the different types?

A

Detached intravascular mass carried by blood to site distant from origin.

Can be thrombus, fat, air, amniotic fluid, or tumor.

May cause ischemic necrosis (infarct) in organ to which it travels.

39
Q

What are some sources of thromboemboli?

A

Vessels

Heart: atrial or ventricular walls or valve leaflets

Atherosclerotic plaque

Paradoxical embolism: travels through heart defect into systemic circulation

40
Q

What is the most common type of embolism? What are some consequences?

A

Pulmonary embolism; usually comes from DVT of hte deep veins above the knee.

Saddle emboli (bifurcation of pulm. arteries), multiple emboli, sudden death, pulmonary hemorrhage/infarction.

41
Q

90% of emboli arise from the deep veins of the leg. What path do these take?

A

Deep veins of the leg > right atrium > right ventricle > pulmonary arteries

42
Q

What is an infarction? What are some etiologies or arterial and venous infarcts?

A

An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage of affected tissue.

Artery: thrombosis due to ruptured athero. plaque, embolism, compression

Vein (less common): venous compression, dehydration

43
Q

What are the two different morphologies of an infarct?

A

Red infarct: hemorrhagic; classic example is lung infarct secondary to embolus.

  • occurs in loose tissues, dual circulation tissues, when flow is re-established/reperfused, venous occlusions

White infarct: anemic (no blood)

  • Occurs in solid organs with end-arterial circulation like the spleen or kidney
44
Q

What type of necrosis is seen in infarction?

A

Ischemic coagulative necrosis with eventual scar formation (except in brain when it’s liquefactive).

Septic infarcts: necrosis with abscess formation (liquefactive necroses with acute inflammation and suppuration).

45
Q

What three factors affect infarct development?

A
  1. Anatomy of vascular supply (is ther an alternative blood supply or is it end arterial like the kidney and spleen?)
  2. Rate of occlusion - slowly developing occlusions allw development of collateral supply
  3. Tissue vulnerability to hypoxia (neurons die faster than cardiac myofibers)
46
Q

What is the difference between a hemorrhagic infarct and a hematoma?

A

In a hemorrhagic infarct, blood is mixed with necrotic tissue.

In a hematoma, blood is collected and forms a solid mass.

47
Q

What is disseminated intravascular coagulation (DIC)? What illnesses is it associated with?

A

Initial clotting (microangiopathy), resulting in organ ischemia, followed by bleeding tendencies.

“consumptive coagulopathy”: widespread clotting leads to consumption of clotting factors and platelets >>> bleeding occurs

Severe illness such as sepsis, trauma, cancer, burns, ischemia.

48
Q

What is shock (CV collapse)?

A

Systemic hypoperfusion caused by reduced CO and decrease in effective circulating blood.

Hypotension > impaired perfusion and cellular hypoxia >tissue injury > death

49
Q

What are the three major types of shock? What are some examples of each?

A
  1. Cardiogenic: MI, PE, Arrhythmia
  2. Hypovolemic: hemorrhage, fluid loss
  3. Septic: overwhelming microbial infection
50
Q

Other than the three major types of chock (cardiogenic, hypovolemic, and septic), what are two other types? Describe each.

A

Neurogenic shock: interruption of sympathetic vasomotor input with spinal cord injury, results in art and venous dilation and decreased CO

Anaphylactic shock: IgG mediated hypersensitivity response causeing systemic vasodilation and increased vascular permeability.

51
Q

What are the three phases of shock and what occurs during each?

A
  1. Nonprogressive phase (initial): Tachy, peripheral vasocontriction, renal fluid conservation, perfusion of organs maintained
  2. Progressive phase: tissue hypoxia and lactic acidosis, lowering of tissue pH and blunting of vasomotor response. Tissue hypoperfusion.
  3. Irreversible phase: Cellular and organ injury present preventing survival; excessive production of lactic acid from anaerobic glycolysis.
52
Q

What is the morphology of shock?

A

Multi-organ failure, primarily due to hypoxia.

53
Q

What are the clinical manifestations of shock?

A

Hypovolemic and cardiogenic shock: hypotension, tachy, tachypnea - cool, clammy, cyanotic skin

Septic shock: hypotenesion tachy, tachypnea, peripheral vasodilation initially. Skin initially feels warm and flushed.

54
Q

How common is septic shock and what are the main causes? What is the mortality?

A

Up to 20% mortality, main cause of deaths in the ICU. (Young healthy people without other diseases have >90% chance of survival from hypovolemic shock)

Most often gram POSITIVE bacteria, followed by gram negative bacteria and fungi.

*cardiogenic shock with extensive MI or gram-negative sepsis have significantly worse mortality rate*

55
Q

Someone comes into the hospital and you suspect shock due to the warm and flushed skin, what is a likely cause?

A

Warm and flushed indicates septic shock, which is most likely caused by bacteria (particularly gram negative).

You may suspect something like strep pneumonia.

56
Q

Where might an abdominal aortic aneurysm travel to?

A

It would travel distally and would remain on the arterial side - for example it could travel to the popliteal artery and cause occlusion.

57
Q

On CT, you see accumulation of blood beneath the dura compressing the cerebral hemisphere. What is the best term to describe this abnormality?

A

Hematoma.

58
Q

Is someone has congestive heart failure, what is the mechanism by which their edema occurs?

A

Hypoperfusion of the kidneys causes secondary hyperaldosteronism (LV not pumping enough to perfuse kidneys)

Incresed hydrostatic pressure

59
Q

What lab tests would you have done if you think someone has a problem inhibiting thrombosis?

A

Anticoagulants: look for how much and how functional they are

  • Protein C and S activity and antigen
  • ATLL activity and antigen

Molecular abnormalities in factor 5 or PT gene

Lupus anticoagulant and antiphospholipid antibodies

Found. of Path. Processes - Block 1 (18 decks)

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