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Pathology Pre-Midterm > Module 3-Path Continued > Flashcards

Module 3-Path Continued Flashcards

1
Q

What is Disseminated Intravascular Coagulation?

A

Widespread small thrombi in the microcirculation throughout the body accompanied by simultaneous bleeding.

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2
Q

DIC is the only condition where you will find petechiae, purpura and ecchymoses all three together. Explain what each are

A

Petechiae- pin point hemorrhages
Purpura-1mm -1cm diffuse superficial hemorrhages
Ecchymoses - >1cm large superficial hemorrhage

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3
Q

What syndrome involves DIC + septic shock + bilateral adrenal hemorrhages

A

Waterhouse Friderichsen Syndrome

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4
Q

There are three different etiologies of DIC, each card will go through one. 1)

A

1) Idiopathic

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5
Q

2nd etiology of DIC

A

2) Diffuse Endothelial Injury
-Gram Negative Sepsis (endotoxic) –>Activates monocytes which release IL-1 and TNF–> IL-1 and TNF act on endothelial cell surface and increase the expression of tissue factor and decrease the expression of thrombomodulin
Injured endothelial cells induce platelet aggregation and activation of intrinsic pathway by exposure of collagen
-Viral, ricketssiae
-Immunologic Injury (Type II, III, SLE)

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6
Q

3rd etiology of DIC

A

3) Release of Thromboplastic agents in circulation- activation of coagulation
- amniotic fluid embolism, fat embolism, snake bite, promyelocytic leukemia, extensive tissue necrosis and burns, mucin, proteolytic enzymes from carcinoma

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7
Q

What are the effects of DIC?

A

Decrease in tissue perfusion- shock, lactic acidosis, microinfarcts
Bleeding-consumptive coagulopathy

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8
Q

What are some investigations for DIC?

A

Bleeding times (PT and PTT) are high
D-dimer and FDP (fibrin degradation product) are high
platelet count is low as well as fibroingogen

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9
Q

How doe you manage a patient with DIC?

A

Heparin to prevent formation of thrombi

Replace platelets and plasma

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10
Q

What type of conditions give you just ecchymosis and pepura?

A 
Thrombocytopenia 
Hemophilia 
Von Wilabrand Disease 
Liver Cirrhosis 
Conditions of malabsorption of fat soluble vitamins (like chronic pancreatitis)
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11
Q

What are the chronological changes that occur to extravasated blood?

A

Hb( red-blue)
Bilirubin (blue green)
Hemosiderin (brown)

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12
Q

What are some clinical feature of hemorrhage?

A

Hemoptysis- coughing up blood
Hemetemesis- vomiting blood
Melena - passive blood in stool

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13
Q

Describe the progression of petechiae in terms of severity

A
  1. minor petechiae: harmless
  2. If recurrent: iron deficiency anemia
  3. if severe- hypovolemic shock
    Brain stem hemorrhage- sudden death
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14
Q

What is a hemorrhage?

A

Extravasation (leakage of fluid) of blood to the exterior of the body or into nonvascular body space/cavity due to rupture of blood vessels

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15
Q

Describe: hemothorax, hemopericardium, hemoperitoneum, hemarthrosis, and hematoma

A
  1. Hemothorax: collection of blood in space b/t chest wall and lung (pleural cavity)
  2. Hemopericardium: blood in pericardial sac
  3. Hemarthrosis: bleeding into joint spaces
  4. Hematoma: soft tissues, bruises, hemorrhage enclosed within a tissue
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16
Q

Clinical Case: A 65 yr old male developed severe sudden chest pain accompanied by breathlessness. The CKMB and Troponin levels were elevated. EKG showed T wave inversion. Imaging studues showed features of pulmonary edema. The BP was 60/30. What are the consequences of severe drop in the blood pressure?

A

Shock

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17
Q

What is shock?

A

Is a clinical state characterized by a generalized decrease in perfusion of tissues associated with reduction in effective cardiac output
Cardiovascular collapse

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18
Q

There are multiple causes of shock, each card will go through one. 1)

A

1) Cardiogenic: results from myocardial pump failure
- intrinsic myocardial damage (infarction), ventricular arrhythmias
- Obstructive-extrinsic compression (Cardiac tamponade)
- Outflow obstruction (PE)

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19
Q

2nd cause of shock?

A

2) Hypovolemic- results from loss of blood or plasma volume
- Hemorrhage
- Fluid loss from severe burns or trauma
- vomiting, diarrhea

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20
Q

3rd cause of shock?

A

3) Septic: caused by systemic microbial infection

- gram-positive infections, gram negative infections (endotoxic shock), fungi

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21
Q

What is the mechanism behind septic shock?

A
  1. Endothelial injury –> coagulation
  2. Peripheral vasodilatation and pooling of blood
  3. Fluid escapes from blood
  4. Leukocyte-induced capillaries
  5. DIC =thrombi in capillaries –> pin point cell death
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22
Q

In regards to gram negative infections in septic show, what are endotoxins?

A
  • lipopolysaccharides from walls of gram negative bacteria
  • released when cell walls are degraded by inflammatory response
  • LPS has a toxic FA (lipid A) core and a coat of complex polysaccharides (O antigen)
  • Similar molecule in cws of gram (+) bacteria, fungi and super antigen bacteria
23
Q

LPS in low doses has what affect on the system?

A
  • activates macrophages, monocytes and neutrophils
  • mononuclear phagocytes produce TNF —> IL-1 synthesis
  • IL-1 and TNF act on endothelial cells (and other) –> production of IL-6,8 –> induce adhesion molecules
24
Q

LPS in moderate doses has what effect on the patient?

A
  • Released of NO and PAF (platelet activating factor)= vasodilation
  • systemic effect of TNF and IL-1: fever, increased synthesis of acute-phase reactants, increased production of circulating neutrophils
25
Q

LPS at higher doses= septic shock syndrome, what is the effect of this?

A
  • Systemic vasodilation (hypoTN)
  • diminished myocardial contractility
  • widespread endothelial injury and activation
  • activation of the coag system-DIC
26
Q

The last cause of shock is..?

A

4) Distributive: imbalance b/t compartments

27
Q

There are two types of Distributive shock, each card will go through one. 1–>

A

1) -Neurogenic: autonomic pathways in CNS
* simple fainting: peripheral pooling in blood. Fall down-self correct due to recumbent position-increased venous return restores cardiac output
* Anesthetic -> loss of vascular tone, peripheral pooling
* Spinal Cord Injury

28
Q

2nd type of distributive shock

A

2) -Anaphylactic: generalized IgE mediated response
* systemic vasodilation, increased permeab
* Reduced tissue perfusion
* Degranulation of mast cells and basophils- histamine, bradykinin, leukotreins

29
Q

Clinical Case: A sixteen year old female had developed fever. There was evidence of leukocytosis. She was suspected to have gram negative sepsis. She subsequently developed wide spread petechiae over the trunk and limbs. The BP dropped dramatically. The chest X-ray showed an oval lesion with collection of fluid. What does this lung lesion indicate?

A

Sepsis due to the gram negative bacteria and subsequent shock

30
Q

What are some features of septic shock?

A

20% mortality
Number 1 cause of mortality in ICU
Systemic arterial and venous dilation leading to tissue hypoperfusion
Widespread activation of endothelial cells
Hypercoagulable state –> DIC
Metabolic alterations -> suppress cell and tissue function
Net effect -> hypoperfusion and multiorgan dysfunction

31
Q

Clinical Case: 25 year old male was involved in an automobile crash where he bleed profusely. The paramedics brought him to the ER. He was conscious. The pulse was 140/min. The skin was cool and he was sweating profusely. The BP was normal. Patient is in shock. What are some effects of shock? (Note this is the first stage of shock)

A
  1. Hypotension- due to peripheral pooling secondary to vasodilation
  2. Impaired tissue perfusion
  3. Cellular hypoxia
  4. Cell injury
  5. Cell death
32
Q

There are three stages of shock. The next few cards will cover them. The first stage is Initial non-progressive stage, what are some basic principles of this stage?

A
  1. Compensated by reflex mechanisms : attempt to increased CO and blood volume
  2. Baroreceptors: release of catecholamines, renin, angiotensin, and ADH
  3. Generalized SNS: tachycardia, peripheral vasoconstriction, renal conservation of fluid (remember that vasoconstriction is due to hypovalemia)
  4. Cutaneous vasoconstriction =cool, clamy, pale skin
  5. Coronary, cerebral vessels: less sensitive to SNS response so they maintain blood flow and O2 delivery
  6. Pre-renal uremia (renal failure)
33
Q

what is the difference between hypovolemic shock and septic shock?

A

Hypovolemic: vasoconstriction, cool, pale skin

Septic Shock: vasodilation, flushed and warm skin

34
Q

Clinical Case: a 25 year old male was involved in an automobile crash where he bled profusely. The paramedics brought him to the ER. He was conscious. The pulse was 140/min. The skin was cool and he was sweating profusely. The BP was normal.
He stared becoming confused. The urine output dropped. The blood pH became acidic. What stage of shock is the patient in?

A

Stage 2: Progressive Stage = impaired tissue perfusion

  • imbalance between circulation and metabolic needs
  • Intracellular aerobic respiration replaced by anaerobic glycolysis (shift is the key to the symptoms that follow)
  • Excess lactic acid production=low pH=lactic acidosis
  • Decreased pH=sludging of RBCs
  • Blunting of vasomotor response
  • Arterioles dilate and blood pools in microcirculation
  • Decreased CO, anoxic endothelial Injury, DIC
  • patient confused; decreased urine output
35
Q

A 25 year old male was involved in an automobile crash where he bled profusely. The paramedics brought him to the ER. He was conscious. The pulse was 140/min. The skin was cool and he was sweating profusely. The BP was normal. He started becoming confused. The urine output dropped. The blood pH became acidic.
He went into a coma. The serum LDH was elevated. Urine production ceased. BP became unrecordable. What stage of shock is this patient in?

A

Stage 3: Irreversible Shock= decompensation
-severe widespread cell and tissue injury
-leakage of lysosomal enzymes
-perfusion of brain and myocardium at critical level
-Acute Tubular Necrosis –> Acute Renal Failure (renal uremia)
-Myocardial depressant factor: decreased CO
-Failure of multiple organ system
-Ischemic Bowel= entry/movement of flora bacteria to other regions of body
->endotoxic shock aka septic shock
(hypovolemic shock shifts to septic shock:movement of flora bacteria )
-survival difficult if hemodynamics are corrected

36
Q

What type of bacteria is septic shock due to?

A
  1. Gram Positive Bacteria–> most common cause
  2. Others -> Gram Negative bacteria, fungi
  3. Super antigens
    (infection can be localized and still produce septic shock without detectable spread through the blood stream)
37
Q

What is a super antigen?

A

Bacterial Proteins produce polyclonal T cell activation which induces T cells to release high levels of cytokines –> diffuse rash, vasodilation, hypotension and death (toxic shock syndrome)
again is localized

38
Q

What is the pathogenesis of septic shock? This is quite long, so its broken up between cards

A
  1. Microorganism release a variety of substances
  2. Activate PMN, macrophages, dendritic cells, endothelial cells and complement
  3. Activated cells and complement initiate inflammatory responses
  4. Systemic Inflammatory response syndrome -SIRS
    (SIRS can also be triggers by non infectious conditions like trauma, burns, pancreatitis, global ischemia)
39
Q

Septic Shock pathogenesis continued

A
  1. Products of microbes -> Pathogen Associated Molecular patterns (PAMP)
  2. PAMPs activate inflammatory cells and complement
  3. Inflammatory cells produce cytokines - TNF and IL1 and cytokine like mediators: high mobility group box 1 (HMGV1) and free oxy radicals and lipid mediators like Prostaglandins (PG), Platelet activating factor (PAF)
    These lead to activation of endothelial cells
40
Q

Septic shock pathogenesis continued

A
  1. Endothelial cells start expressing adhesion molecule, release procoagulants and secondary wave of cytokines
  2. Complement activation (by PAMPs and through proteolytic activity of plasmin) leads to production of anaphylotoxins (C3a and C5a), Chemotaxic fragments (C5a) and opsonins (C3b). This leads to pro inflammatory state
    Endothelial activation leads to thrombosis, DIC, increased vascular permeability and vasodilation
41
Q

Septic Shock in DIC is caused because…?

A

Pro-inflammatory cytokines result in increased production of tissue factor and reduce fibrinolysis by increasing the PAI expression, tissue factor pathway inhibitor, Thrombomodulin and Protein C
The reduced blood flow enhances the pro coagulant tendency because the activated coagulation factors are not washed out

42
Q

Septic Shock and DIC, what results do you find?

A
  1. Systemic deposition of fibrin rich thrombi in small blood vessels
  2. Exaggerate the already existing tissue hypoperfusion
  3. Consumption of coagulation factors –>bleeding
  4. Widespread vascular leakage and edema
  5. Deficient nutrition and waste removal in tissues
43
Q

What is one of the reasons for edema and hypotension in septic shock?

A

Pro-inflammatory cytokines loosen the endothelial tight junctions by displacing adhesion molecule VE-Cadherin –> leads to leaky vessel walls

44
Q

What is the second reason for edema and hypotension in septic shock?

A

Vasodilation: caused by expression of vasoactive inflammatory mediators (C3a, C5a, PAF, and increased production of NO)

  • > relaxation of vascular smooth muscle
  • -> hypotension and reduction in tissue perfusion
45
Q

During septic shock the patient becomes hyperglycemic due to insulin resistance and therefore needs to be given insulin. What is the mechanism for the insulin resistance?

A

Gluconeogenesis: cytokines like TNF, IL1, Stress induced hormones like glucagon, GH, Glucocorticoids and catecholamines
Suppression of insulin release and increase insulin resistance in skeletal muscle and peripheral tissues: pro-inflammatory cytokines

46
Q

Hyperglycemia in septic shock suppresses bacterial activity of PMN and increases the expression of what?

A

adhesion molecules on endothelial cells

47
Q

The initial surge in glucocorticoid release is followed by later depression in their production –> further exaggerated by what syndrome?

A

Waterhouse Fridericken syndrome (Adrenal necrosis due to DIC)

48
Q

What are some treatment options for septic shock?

A
  1. ABX
  2. Intensive insulin therapy
  3. Fluid replacement
  4. Physiologic doses of corticosteroids
  5. Experimental drugs to restore integrity of endothelial cells
49
Q

Morphological changes occur in shock. in different organs, each card will go through an organ. 1) Brain

A
  1. Ischemic Encephalopathy
    - of all organs damaged in shock, neurons die first
    - edema, mottle discoloration on gray matter
    - watershed infarcts: areas farthest from vessels die 1st
    - laminar necrosis: cell death in cortex in a band like pattern with preservation of cells immediately adjacent to meninges/blood supply
    - most susceptible: pyramidal cell of hippocampus purkinje cells of cerebellum
50
Q

The next organ affected by shock is the heart. Explain some features you will find

A
  1. Heart:
    - focal and widespread necrosis
    - contraction band necrosis
51
Q

The next organ affected by shock is the liver. Explain some features you will find

A
  1. Liver:
    - fatty change
    - central hemorrhagic necrosis
52
Q

The last organ affected by shock is the pancreas. Explain some features

A
  1. Pancreas:
    - necrosis
    - pancreatitis: enzyme releases damages neighboring tissues; including pancreas
53
Q

All organ can recover from shock except what?

A

Neurons and myocytes

54
Q

What are clinical features of shock?

A
  1. Weak, rapid pulse
  2. Tachypnea
  3. Cool, clammy cyanotic skin (w/hypovolemic shock: septic shock=flushed warm)
  4. gradual loss of function: cardiac, cerebral and pulmonary
  5. Electrolyte disturbances, metabolic acidosis
  6. Renal Failure
  7. Life threatening: MI, bleeding, sepsis

Pathology Pre-Midterm (35 decks)

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