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Foundations of Disease > Exam 2: Circulatory disturbances > Flashcards

Exam 2: Circulatory disturbances Flashcards

1
Q

Hemodynamic

Homeostasis

A

Maintaining hemostatic balance requires:

  • Normal blood circulation
  • Balance between intra- and extracellular fluid compartments
  • Normal concentrations of body fluid components
    • Proteins
    • Electrolytes
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2
Q

Hemodynamic Disturbances

A
  • Obstructive circulatory disturbances
    • Thrombosis
    • Hemorrhage
    • Edema
    • Shock
  • Blood volume and fluid distribution disburbances
    • Hyperemia
    • Hemorrhage
    • Edema
    • Shock
  • Water and electrolyte balance disturbances
    • Edema
    • Dehydration
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3
Q

Thrombus

A

Blood clot blocking blood flow.

  • Serves no useful purpose
  • Can cause vessel occlusion
    • More significant in arteries
  • Can be a site for emboli generation
    • More significant in veins
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4
Q

Virchow’s Triad

A

3 elements which can work together to ↑ risk of pathologic thrombus formation.

  1. Endothelial injury
  2. Alterations in normal blood flow
  3. Hypercoaguability
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5
Q

Endothelial Injury

A
  • Most important factor
  • Lose protective mechanisms of endothelium
    • Platelets adhere to exposed collagen
  • Common causes:
    • MI
    • Ulcerated atherosclerotic plaques
    • Traumatic injury
    • Vasculitis
    • Hemodynamic stress due to HTN
    • Injury from bacterial endotoxin
    • Smoking
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6
Q

Abnormal Blood Flow

A
  • Arteries ⇒ usually due to turbulence
  • Veins ⇒ usually due to stasis
  • Effects of ∆ blood flow
    • Disrupts laminar flow
      • Brings platelets into contact with endothelium
    • Prevents dilution of clotting factors by fresh blood
    • Retard inflow of clotting factor inhibitors
    • Promotes endothelial cell activation ⇒ local thrombosis
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7
Q

Hypercoaguability

A
  • Primary ⇒ genetic
    • Clotting factor mutations
      • Factor V Leiden
    • Lack of anticoagulants
      • Protein C & S deficiency
  • Secondary ⇒ acquired
    • Prolonged immobilization
    • Tissue damage
    • Cancer ⇒ necrotic tumor cells release procoagulant factors
    • Prosthetic heart valves
    • Atrial fibrillation
    • Hormonal imbalances
      • Oral contraceptives, estrogen therapy, pregnancy
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8
Q

Postmortem Clot

Gross Appearance

A

Shows two distinct layers:

Serum ⇒ chicken fat clot

Cells ⇒ currant jelly clot

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9
Q

Antemortum Clot

Gross Apperance

A

“Thrombus”

  • Adherent to the vessel wall
  • Multicolored layers
    • Variagated appearance
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10
Q

Thrombus

Microscopic Appearance

A
  • See integration of fibrin and cellular layers
  • Produces striped appearance ⇒ Lines of Zahn
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11
Q

Arterial Thrombi

A
  • Usually occlusive
  • Contains high [fibrin] ⇒ white thrombi
  • Common sites
    • Coronary
    • Cerebral
    • Femoral
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12
Q

Venous Thrombi

A

“Phlebothrombosis”

  • Can be occlusive
  • Sluggish flow ⇒ high [RBC] ⇒ red thrombi
  • Common sites
    • Leg veins (90%)
    • Periprostatic plexus
    • Periuterine veins
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13
Q

Mural Thrombus

A

Thrombus is attached to vessel wall

Non-occlusive

Typically see in heart or aorta

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14
Q

Occlusive Thrombus

A

Grows circumferentially in the lumen

Occludes vessel

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15
Q

Propogative Thrombus

A

Clot has a tail.

See in deep veins of extremities.

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16
Q

Vegetation

A
  • Thrombus builds up on heart valves
  • Can also get deposition of blood borne bacteria in vegetation
  • See in cancer
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17
Q

Thrombus

Fates

A
  • Fibrinolysis by plasminogen-plasmin system
    • More common with recent thrombi d/t less fibrin polymerization
  • Central softening
    • Due to leukocyte action
  • Retraction
    • Due to thromabasthenin in platelets
  • Organization and recanalization
  • Embolization
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18
Q

Thrombus

Organization and Recanalization

A

Organization ⇒ ingrowth of endothelial cells, smooth muscle cells, and fibroblasts into thrombus

Recanalization ⇒ formation of capillary channels within thrombus which can re-create a lumen

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19
Q

Embolus

A

Detached intravascular solid (thrombus), liquid (fat), or gaseous mass that is carried by the blood to a site distant from the point of origin.

99% of all emboli are thromboemboli.

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20
Q

Arterial Thromboemboli

A
  • Originate from:
    • Mural thrombi
    • Diseased heart valves
    • Atherosclerotic plaques
    • Aneurysms
  • Main sites of embolization:
    • Legs
    • Brain
    • Intestines
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21
Q

Venous Thromboemboli

A
  • Originate from:
    • Deep veins of lower extremities ⇒ DVT (95%)
    • Pelvic venous plexus
    • Right side of heart
    • Cavernous sinus veins
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22
Q

Pulmonary Thromboemboli

Characteristics

A
  • Usually originate from a DVT
  • Very common
    • 20-25 per 100,000 hospitalized patients
  • Consequences of PE determined by size of clot
    • Determines where it will lodge
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23
Q

Pulmonary Embolism

Risk Factors

A
  • Venous stasis
    • CHF or chronic venous insufficiency
  • Injury
    • Trauma, surgery, postpartum
  • Hormonal imbalance
    • Pregnancy or OCP
  • Advanced age
  • Immobilization
  • Sickle cell disease
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24
Q

Large PE

Consequences

A
  • Usually lodges in the main pulmonary artery
  • Can straddle both sides ⇒ saddle embolism
  • Results in:
    • Severe hypoxemia
      • Interferes with return of blood to left heart
      • ↓ CO
      • Arterial hypotension
      • Shock
    • Acute right heart failure
      • See with > 60% obstruction of pulmonary circulation
      • Can result in death ⇒ acute cor pulmonale
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25
Q

Small PE

Consequences

A
  • Travels further into the pulmonary circulation
  • Causes infarction of a smaller area
  • More likely to be asymptomatic
    • 60-80% of PEs are clinically silent
  • Can leave a “web” in vessel after organization and absorption into vessel wall
  • Can be multiple clots simultaneously ⇒ shower of emboli
    • Having one increases risk of more
  • Can result in severe hypoxemia
    • Interfers with blood return to left heart
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26
Q

Paradoxical Embolism

A
  • Emboli travels from venous → arterial circulation
    • Via interarterial or interventricular defects
  • Ex. DVT causing CVA
27
Q

Fat Embolism

A
  • Common causes:
    • Trauma to fat-containing tissues
      • Long bone fx, soft tissue trauma, burns
      • Fat is suctioned into ruptured venules
    • Hyperlipidemia
  • Only produces symptoms occasionally
    • See sudden onset tachypnea and dypsnea after 24-72 hour latent period
  • Neurological involvment
    • Results in irritability and coma
    • Brain shows petechiae
      • Due to release of free FA and resultant toxic injury to vascular endothelium
28
Q

Air Embolism

A
  • Common causes:
    • Puncture wound of great vessel
    • Decompression sickness → “The bends”
      • Nitrogen gas dissolves in tissues during dive
      • If depressurize too rapidly ⇒ bubbles form in tissues
      • Chronic form ⇒ Caisson’s disease
29
Q

Atheromatous Embolism

A

Atherosclerotic plaque breaks off and travels to another site.

30
Q

Amniotic Fluid Embolism

A
  • Rare but catastrophic complication of pregnancy
  • Desquamated cells from fetus enters amniotic fluids ⇒ maternal circulation ⇒ lungs
  • See sudden-onset of cyanosis and dyspnea
  • Can lead to disseminated intravascular coagulation (DIC)
31
Q

Ischemia

A

Decrease or loss of blood supply to a localized area of the body.

Causes loss of vital nutritional substances, especially O2, and accumulation of metabolic products.

32
Q

Infarction

A

Localized area of ischemic necrosis resulting from circulatory insufficiency.

Due to either interference of arterial flow or venous obstruction.

33
Q

Ischemia or Infarction

A

Progression from ischemia ⇒ infarction depends on:

  • Rapidity of development
  • Degree of vascular occlusion
  • Pre-existing disease in the organ
  • Sufficiency of collateral circulation
  • Tissue vulnerability to hypoxia
34
Q

Infarct

Morphology

A
  • Most are wedge shaped with base towards periphery
  • Often has 3 zones:
    1. Central ischemic necrotic zone
    2. Hyperemic zone around dead tissue
      • Where inflammation is occuring
    3. Viable zone of living tissue
35
Q

Infarct

Types

A
  • Initially ⇒ all infarcts are red
  • Subsequently ⇒ type of infarct depends on tissue blood supply
    • White infarcts
      • Seen in tissues where blood cannot seep in
      • Only one route of blood supply
    • Red infarcts
      • Tissues with dual blood supply
        • Lung & liver
      • Venous occlusion
      • Loose tissues
      • Previously congested tissue
36
Q

Pulmonary Infarct

A

Red infarct ⇒ due to dual blood supply

Wedge shape with base on pleura

37
Q

Intestinal Infarct

A

Red infarct

38
Q

Testicular Infarct

A

Red infarct ⇒ has loose CT filled with blood

Usually due to testicular torsion

39
Q

Splenic Infarct

A

White infarct

40
Q

Bone Infarct

A

White infarct

41
Q

Renal Infarct

A

White infarct

42
Q

Acute Tubular Necrosis

A

Due to renal ischemia ⇒ infarction

Renal tubular cells are very sensitive to ischemia

43
Q

Septic Infarcts

A

May occur two ways:

  1. Pre-existing bacteria present in tissue before development of ischemia necrosis
    • Ex. infarction of an area of pneumonia
  2. Bacteria brought to affected area by embolization of an infected thrombus
    • Ex. vegatation from a heart valve
44
Q

Hyperemia

A

Excess amount of blood in an organ.

Can be active or passive.

45
Q

Active Hyperemia

A
  • Caused by ↑ blood supply from arteries
    • Inflammation
      • Vasodilation in response to vasoactive substances
    • Fever
      • Vasodilation to dissipate heat
    • Neurogenic & hormonal influences
      • Hot flashes
      • Blushing
  • Can result in erythemia
46
Q

Passive Hyperemia

A

“Congestion”

  • Caused by ↓ exit of blood via veins
    • Diminished venous flow
    • Impaired venous drainage
  • Local ⇒ DVT or tumor venous obstruction
  • Systemic ⇒ CHF
  • See dilatation of veins and capillaries
47
Q

Inflammatory Breast Cancer

A
  • Groups of cancer cells lodge in subcutaneous lymphatics
  • Results in impaired fluid clearance
  • Causes passive hyperemia and edema
  • See dimpled and retracted skin
48
Q

Pulmonary Congestion

A
  • Due to left heart failure
  • Impedes exit of blood from lungs
  • Leads to chronic passive congestion in lungs
    • Capillaries engorged with blood
49
Q

Pulmonary Edema

A
  • Left heart failure ⇒ passive pulmonary congestion ⇒ ↑ capillary hydrostatic pressure
  • Fluids forced into interstitial spaces and alveolar spaces ⇒ pulmonary edema
    • ∆ gas exchange
50
Q

Pulmonary Exudates

A
  • Left-sided CHF ⇒ pulmonary congestion ⇒ pulmonary edema
  • Progresses to microhemorrhages of pulmonary capillaries
    • Releases RBCs into alveolar spaces
    • Mφ phagocytize RBCs
    • Results in hemosiderin-laden Mφ ⇒ “heart failure cells”
  • Can stimulate lung fibrosis and lead to pulmonary HTN
51
Q

Liver Congestion

A

Chronic passive congestion of liver:

  • Seen with right heart failure or hepatic vein/IVC obstruction
  • Liver is enlarged and firm
  • See dilated central veins & sinusoids
    • Causes pressure on hepatocytes in the centrilobular area
  • Grossly, congested area appear dark red & alternates with normal brown liver ⇒ nutmeg pattern
52
Q

Cardiac Cirrhosis

A
  • Right-sided CHF ⇒ chronic passive liver congestion ⇒ eventual progression to centrilobular fibrosis
  • Caused by pressure atrophy of centrilobular hepatocytes
53
Q

Edema

A

Accumulation of abnormal amounts of fluid in interstitial tissue space or body cavities.

Pleural space ⇒ pleural effusion

Pericardial space ⇒ pericardial effusion

Peritoneal space ⇒ ascites

Fluid is usually non-inflammatory ⇒ transudate

54
Q

Edema

Pathogenesis

A
  • Caused by hemodynamic derangements
    • ↑ forces which move fluids from intravascular to interstitial spaces
  • Can be due to:
    • ↑ intravascular hydrostatic pressure
    • ↓ colloid osmotic pressure of plasma
    • ↑ vascular permeability
    • Impaired lymph flow
55
Q

Localized Edema

Mechanisms

A
  • ↓ venous drainage ⇒ ↑ venous hydrostatic pressure
    • DVT, incompetent valves/varicose veins, tumors
  • ↑ vascular permeability
    • Allows escape of colloid proteins from vessels ⇒ ↓ colloidal osmotic pressure
    • Allergic rxn, burns, infection
  • Lymphatic obstruction ⇒ lymphedema
    • Filariasis infection
      • Worms in lymphatics
      • Get elephatiasis
    • Congenital
      • Milroy’s disease
    • Post surgical s/p lymph node resection
56
Q

Generalized Edema

Mechanisms

A
  • ↑ capillary hydrostatic pressure
    • See in cardiac edema
    • Affects dependent parts of the body, liver, lungs, spleen
  • ↓ plasma proteins
    • Mostly albumin
    • ↓ plasma oncotic pressure
    • Neprhotic syndrome ⇒ loss albumin in urine
    • Cirrhosis ⇒ ↓ albumin synthesis
  • Sodium and water retention
    • Due to abnormality of tubular reabsorption, aldosterone secretion, ADH secretion
57
Q

Hemorrhage

A

Extravasation of blood due to vessel rupture.

58
Q

Hematoma

A

Extravasated blood within tissue

59
Q

Petechiae

A

Pinpoint hemorrhages

Causes:

Areas of increased intravascular pressure

Low platelet count or abnormal platelet function

60
Q

Ecchymosis

A

Larger subcutaneous hemorrhages

( > 1-2 cm)

61
Q

Larger Hemorrhages

A
  • Hemothorax
  • Hemoperitoneum
  • Hemathrosis
  • Hemorrhagic stroke
62
Q

Shock

A

Critical condition caused by a sudden drop of blood flow throughout the body.

63
Q

Adult Respiratory Distress Syndrome

(ARDS)

A

“Shock lung”

  • Caused by diffuse alveolar damage
  • Results in extravasation of large amounts of fluid into alveolar spaces
  • See hyaline membranes lining alveoli
    • Impairs gas exchange
64
Q

Acute Pancreatitis

A
  • Due to release of catalytic enzymes from exocrine pancreas
  • See fat necrosis
  • White, chalky deposits in gross speciment
  • Dead adipose tissue on micro

Foundations of Disease (46 decks)

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