9th lecture (hemorrhage and shock) Flashcards

1
Q

define hemorrhage?

A

extravasation of blood. It can get into the tissues forming a hematoma. Chronic bleeding may create iron insufficiency anemia. Jaundice may be a symptom of bleeding since RBC are broken down making bilirubin and later hemosiderin.

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2
Q

Shock definition?

A

lack of circulatory volume.

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3
Q

what are the 3 classes/categories of bleeding?

A
A/ hemorrhage per rexine (rexine = rupture of vessels)
1. Apoplexia (bleeding within organs and accompanying symptoms)
2. hematoma epidurale
3. hematoma subdural 
4. hematoma subarachnoidal bleeding.
5. Rupture of varicositas esophagi 
B/ hemorrhage per arrorionem 
ulcus chronicum pepticum ventriculi (stomach ulcer)
tumor arroia (tumor growth erodes the vessel = bleeding)
C/ hemorrhage per-diapedesim 
1. petechiae; 1-2 mm blood spot
2. purpura; larger diameter blood spot
3. suphuria; massive blood spot.
a/ thrombopathia
b/ coagulopathies 
c/ vasculopathies
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4
Q

describe apoplexia?

A

brain bleeding is related to high blood pressure. The bleeding occurs mostly in the basal ganglions. There are 2 morphological alterations to vessels predispose to vessel rupture;
1. charcot bouchard aneurysm.
2. hyalinic atherosclerosis
the increased intracranial pressure actually presses the cerebellum into the foreman magnum. and the patient dies from the cardio-respiratory failure since the brain coordination centers for them are impeded.

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5
Q

Hematoma epidural description?

A

Hemmatoma epidural: fracture of the temporal bone may rupture the arterial meningeal media. The bleeding is between the dura matter and the skull, peeling the dura matter away from the skull. This is an intracranial but extra-cerebellar bleeding.
lucidum intervallum: a temporary improvement of the patient’s condition after a traumatic brain injury followed by a second deterioration.
So the process is as follows:
-head hit and conciousness is lost
-regain consciousness
-the blood separates dura from skull
-inter-cranial pressure increase
-patient becomes unconscious again.
TYPICALLY seen in people who fall over when drunk and hit their head on a hard surface.

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6
Q

hematoma subdural description?

A

bleeding between the pia and dural matter. between the pia and dura there are bridging veins which drain the arachnoid blood to the sinuses.
The brain is anchored in the fluid. The rotation of the brain may tear the bridging veins making a subdural hematoma.
TYPICALLY seen in a car crash when the passengers inside the vehicle hit their head on the windshield.
Old age can also be a factor as the brain atrophy/shrinking may cause tension in the bridging veins. People engaged in Boxing may experience chronic bleeding.

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7
Q

hematoma subarachnoidal bleeding description?

A

In the circle of willis in the brain there could be a subarchnoidal aneurysm that may develop near the outbranching from the circle of willis. This aneurysm could rupture leading to subarachnoidal bleeding. if someone has a aneurysm it could rupture at around above the age of 40, its rupture is linked to hypertension. If an aneurysm develops in the brain, several years could go by before it rupture.
Minor clinical symptoms could be visual problems and headache.
To treat the aneurysm a coil could be placed in it to slow down the blood flow, encouraging coagulation, and healing occurs.

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8
Q

Describe Rupture of varicositas esophagi?

A

cirrhotic liver causes a increased pressure in the portal system resulting backpressure of the blood through the portacaval anastomosis. The dilated veins in the esophagus varicosities that may rupture.

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9
Q

hemorrhage perarrorionem definition?

A

when bleeding occurs as the vessels are eroded. For example an ulcer forming in the stomach can erode the wall of the stomach, and bleeding can occur if the ulcer goes deep enough to reach vessels.

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10
Q

C/ hemorrhage peridiapedium description?

A

penetrating through the vessel, the vessels themselves stay intact.

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11
Q

thrombopathia description?

A

bleeding because the number of platelets is below 20000/cubic mm (low platelet count)

  1. aplastic anemia (bone marrow stem cells disease)
  2. bone marrow infiltration by tumors (cancer destroy the normal bone marrow hematopoiesis)
  3. Immune thrombocytopenia: Autoantibodies against the platelets
  4. infection: any septic states and inflammatory reaction decreased the number of platelets.
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12
Q

Define coagulopathies?

A

The patient is able to thrombocytes cannot form since the factors that are needed to for the coagulation cascade are decreased or lost.

  1. cirrhosis hepatis: (liver cannot produce factors)
  2. DIC: (consumption of factors and platelets (thrombopathies))
  3. hemophilia: genetic factors insufficiency Hemophilia A = factor 8 is missing, Hemophilia B when factor 9 is missing
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13
Q

Describe vasculopathies?

A

The patient has proper coagulation and normal platelet count bu the capillaries are leaky.

  1. hypoxia (endothelial cells are damaged)
  2. infections disease (sepsis)
  3. vasculitis (autoimmune diseases destroy integrity of the vessels)
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14
Q

Shock definition?

A

systemic hypoperfusion, do to

  • cardiac output
  • reduced circulatory blood volume
  • impaired tissue perfusion
  • tissue hypoxia.
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15
Q

Types of shock?

A

A/ Caridac shock
1. pump failure
-acute myocardial infraction (AMI)
-Arrhythmias
-Rupture of the heart
2. Diastolic failure
-cardiac tamponade
3. Outflow failure
-pulmonary embolisim
-atrial thrombosis (flow to ventricle blocked)
B/ hypovolemic shock
-hemorrhage
-loss of plasma volume (for example: burns)
C/ Anaphylactic shock (hypersensitive reaction that causes systemic vasodilation, drop in pressure and loss of fluid into interstitial tissues)
D/ Neurogenic shock (spinal cord injury, the vascular structure tone is lost)
E/ Septic shock: (related to gram negative bacteria getting into the blood) also called endotoxin shocks generated by the lipoprotein saccharides that have a toxic fatty acids)

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16
Q

Pathogenesis of septic shock?

A

endothelial damages, which are related to the monocyte-macrophage system. since the macrophages have a PAM receptor (pathogen associated molecules) which are a group of endotoxins that are binded by the monocytes that release cytokines (IL1, TNFa, PG, PAF, ROS) all of these effect on the endothelial cells which increase the platelet activation, and increase the extravasation of the fluid = EDEMA, and also cause vasodialtion.
THE RESULT: low oxygenation and hypoperfusion of tissue.

17
Q

the metabolic effect of septic shock?

A

IL1 and TNF (tumor necrosis factor) generate reduced insulin secretion. They also generate insulin resistance at the peripheral tissues. This results in hyperglycemia.
There is an increased secretion of corticosteroid and depletion of the adrenal cortex.

18
Q

Morphological consequences of shock?

A
  1. Multiorgan failure (MOF) (fibrin thrombi plugging arteries do to platelet aggregation on endothelium)
  2. acute tubular necrosis: (for example in the kidney the vessels going to the glomeruli from where they go to the medulla, causing a decreasing oxygen gradient. This gradient causes the tubular cells to die off and plug the outflow tubes causing renal failure.
  3. ARDS (adult respiratory distress syndrome) capillary damage causes plasma leakage into the alveoli forming the hyalinic membrane disease.
  4. GI tract: (mucus membrane of the intestine is very sensitive, thus during hypoxia and hypoperfusion bleeding into the mucous membrane could occur.
19
Q

what are the stages of shock?

A
  1. compensatory phase (baroreceptors detects hypoperfusion)

2. progressive phase (the compensatory systems cannot compensate and thus hypoperfusion occurs)