GP 28 - Hemodynamic Disorders 2 Flashcards

1
Q

Define and differentiate hyperemia and congestion. What is the morphology of these conditions? Are these conditions physiological or pathological?

A

Hyperemia - active increase in the volume of blood in tissues caused by arterioloar dilation. The area experiencing this will appear red. This can be either physiological (blushing, exercise) or pathological (inflammation)

Congestion - passive increase in the volume of blood in tissues caused by impaired venous flow from those tissues. The area experiencing this will appear a red-blue color and may have edema. This is always pathological

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2
Q

Describe the key morphological differences between acute and chronic pulmonary congestion. Describe what causes these morphologies.

A

Acute pulmonary congestion will have engorged alveolar capillaries and septa due to the increased hydrostatic pressure (usually from left HF).

Chronic Pulmonary Congestion - after some time, the engorged alveolar capillaries will develop micro-hemorrhages, spilling RBCs into the alveolar spaces which macrophages will then digest and become hemosiderin laden. The alveolar septa will also thicken and become fibrotic. These characteristic appearances are referred to as brown induration

Refer to image

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3
Q
A
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4
Q

Describe the key morphological differences between acute and chronic hepatic congestion. Describe what causes these morphologies.

A
  • Acute liver congestion is caused by passive venous congestion (usually RVHF) of the central veins in the hepatic lobules. This leads to the sinusoids distending with blood and degeneration of the central hepatocytes
  • In chronic liver congestion, the central region of hepatic lobule is reddish brown and surrounded by zones tan colored uncongested liver lobules. This gives the liver a nutmeg appearance. There may also be some hemorrhage, hemosiderin laden macrophages, and fibrosis.
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5
Q
A

Chronic hepatic congestion

Note the nutmeg appearance caused by the central region of the hepatic lobule becoming necrotic

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6
Q
A

Chronic liver congestion

Note the dead hepatocytes around the central vein and the live hepatocytes on the periphery (aka - centrilobular necrosis)

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7
Q

List and describe the major types of hemorrhage we need to know.

A
  • Hemothorax, Hemopericardium, Hemoperitoneum, hemarthrosis - bleeding into the pleural space, pericardial space, peritoneal space, and joint spaces, respectively.
  • Hematoma - bleeding into the soft tissues
    • Petechiae - a pin point hemorrhage from a ruptured capillary or arteriole
    • Purpura - diffuse superficial hemorrhage up to 1cm in diameter
    • Ecchymosis - a >1cm superficial hemorrhage
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8
Q

Describe the chronological changes that occur to extravasated blood.

A
  1. Hb - bruise appears red/blue
  2. Bilirubin - bruise appears blue/green
  3. Hemosiderin - bruise appears brown
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9
Q

What are the medical terms for:

  • coughing blood
  • vomiting blood
  • passing blood in stool
A

Coughing Blood - hemoptysis

Vomiting Blood - hemetemesis

Passing Blood in Stool - melena

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10
Q

What is DIC? What are it’s most common causes?

A

Disseminated intravascular coagulation (DIC) is a condition in which blood clots form throughout the body, blocking small blood vessels.

Most Common Causes are:

  • Idiopathic
  • Diffuse Endothelial Injury - gram negative sepsis (rickettsia), viral infection, immunologic injury (type II, III, SLE)
  • Release of thromboplastic agents - amniotic fluid embolism, snake bite, promyelocytic anemia, extensive tissue necrosis (burns), mucin, proteolytic enzymes from carcinoma
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11
Q

How can gram negative bacterial infections cause DIC?

A

Endotoxins from the bacteria activate monocytes, which then release IL-1 and TNFα. These cytokines then cause the endothelium to increase the expression of tissue factor and reduce the expression of thrombomodulin.

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12
Q

What are the clinically important effects of DIC? How is it usually diagnosed?

A

Adverse Effects:

  • Decreased tissue perfusion possibly leading to shock, lactic acidosis, and microinfarcts
  • Consumptive coagulopathy leading to excessive bleeding on injury

Diagnostic Tests:

  • Fibrin degredation products (FDPs), specifically D-dimer
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13
Q

How is DIC managed?

A

Heparin to prevent formation of thrombi

Platelet and plasma infusions

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14
Q

What is the definition of shock? Use the MAP equation to further explain

A

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

MAP = CO * SVR

If there is a drop in either CO or SVR (systemic vascular resistance) the other variable will increase to maintain MAP. This increase has a limit, however. If that limit is exceeded, shock begins.

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15
Q

What is sepsis?

A

A condition that arises when the body’s response to infection causes injury to its own tissues and organs.

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16
Q

Define and differentiate the different types of shock.

A
  • Cardiogenic - shock caused by a decrease in CO as a result of decreased HR or Contractility. Typically MI, tamponade, or outflow obstruction
  • Hypovolemic Shock - shock caused by a decrease in CO as a result of decreased preload (volume loss). Typically hemorrhage, vomiting, diarrhea
  • Septic - shock caused by a decrease in SVR as a reult of sepsis due to a bacterial (endotoxic shock) or fungal infection
  • Neurogenic - shock caused by a decrease in SVR as a result of a loss in vascular tone due to a decrease SNS activity. Typically from standing still too long, anesthesia, or a spinal cord injury
  • Anaphylactic - shock caused by a decrease in SVR as a result of systemic vasodilation and increased membrane permeability due to an IgE mediated allergic reaction (usually Type 1).
17
Q

What is distributive shock?

A

A condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate supply of blood to the body’s tissues and organs.

Neurogenic and Anaphylactic shock are examples of distributive shock