Hyperemia and Hemorrhage

Question 1

describe hyperemia vs. congestion

Answer 1

• hyperemia: active increase in the volume of blood in tissues (red)
  
  • caused by arteriolar dilation
  • physiological: blushing, skeletal muscle during exercise
  • pathological: inflammation
• congestion: passive increase in the volume of blood in tissue (blue-red color); usually also accompanied by edema
  
  • impaired venous flow from tissues e.g. cardiac failure, venous obstruction
  • always pathological

Question 2

describe acute pulmonary congestions vs. chronic pulmonary congestion

Answer 2

• acute pulmonary congestion (left ventricular failure)
  
  • alveolar capillaries engorged
  • alveolar septal edema
• chronic pulmonary congestion (brown induration)
  
  • thickened fibrous septa
  • heart failure cells (hemosiderin laden macrophages)

Question 3

describe acute vs. chronic liver congestion

Answer 3

• acute passive venous congestion (right heart failure, Budd-Chiari syndrome)
  
  • central vein and sinusoids distended with blood
  • degeneration of central hepatocytes
• chronic congestion - nutmeg liver
  
  • central region of hepatic lobule is reddish brown (cirrhosis) accentuated against the surrounding zones of uncongested tan liver

Question 4

Answer 4

chronic congestion of the liver

Question 5

describe petechiae, purpura and ecchymosis

Answer 5

• petechiae: a pinpoint hemorrhage in skin or conjunctiva; represents rupture of capillary or arteriole
• purpura: diffuse superficial hemorrhage in the skin up to 1 cm in diameter
• ecchymosis: a larger superficial hemorrhage

Question 6

coughing blood = ____

Answer 6

coughing blood = hemoptysis

Question 7

vomiting blood = ____

Answer 7

vomiting blood = hemetemesis

Question 8

passing blood in stool = ____

Answer 8

passing blood in stool = melena

Question 9

describe petechiae (recurrent, severe)

Answer 9

• minor petechiae = harmless
• if recurrent = iron deficiency anemia
• if severe = hypovolemic shock
• brain stem hemorrhage: sudden death

Question 10

describe the major components of hemostasis

Answer 10

Question 11

describe disseminated intravascular coagulation (DIC)

Answer 11

• widespread small thrombi in the microcirculation throughout the body accompanied by simultaneous bleeding
• acute, subacute, chronic
• serious and often fatal
• not primary but an end point of other diseases
• recognize early and treat

Question 12

describe what is seen in the image

Answer 12

disseminated intravascular coagulation (DIC)

Question 13

describe causes of DIC

Answer 13

• idiopathic
• diffuse endothelial injury
  
  • G-ve sepsis (endotoxic)
  • viral, ricketssiae
  • immunologic injury (type II, III, SLE)
• release of thromboplastic agents in circulation → activation of coagulation
  
  • amniotic fluid embolism
  • snake bite
  • promyelocytic leukemia
  • extensive tissue necrosis, burns
  • mucin, proteolytic enzymes from carcinoma

Question 14

describe endotoxins role in DIC

Answer 14

• activate monocytes
  
  • activated monocytes release IL-1, TNFa
• IL-1 and TNF-a act on endothelial cell surface and increase the expression of tissue factor and reduce the expression of thrombomodulin
• injured endothelial cells induce platelet aggregation and activation of intrinsic pathway by exposure of collagen

Question 15

describe the effects of DIC and diagnosing DIC

Answer 15

• decreased tissue perfusion → shock, lactic acidosis, microinfarcts
• bleeding → consumptive coagulopathy
  
  • no coagulation factors left
• diagnosis:
  
  • increased FDPs
  • increased D-dimers

Question 16

describe the management of DIC

Answer 16

• heparin to prevent formation of thrombi
• replace platelets and plasma

Question 17

define shock

Answer 17

• clinical state characterized by a generalized decrease in perfusion of tissues associated with reduction in effective cardiac output
  
  • aka cardiovascular collapse

Question 18

describe cardiogenic shock

Answer 18

• results from myocardial pump failure
  
  • intrinsic myocardial damage (infarction), ventricular arrhythmias
  • obstructive extrinsic compression (cardiac tamponade)
  • outflow obstruction (pulmonary embolism)

Question 19

describe hypovolemic shock

Answer 19

• results from loss of blood or plasma volume
  
  • hemorrhage
  • fluid loss from severe burns or trauma
  • vomiting, diarrhea

Question 20

describe septic shock

Answer 20

• caused by systemic microbial infxn
  
  • G+ve infxns, G-ve infxns (endotoxic shock), fungi

Question 21

describe neurogenic shock

Answer 21

• neurogenic
  
  • simple fainting → peripheral pooling of blood → fall down → self correct due to recumbent position → increased venous return restores CO
  • anesthetic → loss of vascular tone, peripheral pooling
  • spinal cord injury

Question 22

describe anaphylactic shock

Answer 22

• anaphylactic: generalized IgE mediated response
  
  • systemic vasodilation, increased permeability
  • reduced tissue perfusion
  • degranulation of mast cells and basophils via histamine, bradykinin, leukotrienes

Question 23

list the 3 stages of shock

Answer 23

1. initial non-progressive
2. progressive
3. irreversible

Question 24

describe the non-progressive stage

Answer 24

• stage of compensation - compensated by reflex mechanisms
• baroreceptors: release of catecholamines, renin, angiotensin, ADH
• generalized sympathetic stimulation: tachycardia, peripheral vasoconstriction, renal conservation of fluid
• cutaneous vasoconstriction: cool, pale skin
  
  • septic shock: peripheral vasodilation, flushed and warm
• coronary, cerebral vessels less sensitive to sympathetic response so maintain blood flow and oxygen delivery
• pre-renal uremia

Question 25

describe the progressive stage

Answer 25

• stage of impaired tissue perfusion
  
  • imbalance between circulation and metabolic needs
  • intracellular aerobic respiration replaced by anaerobic glycolysis
  • excess lactic acid production → low pH
  • sludging of RBCs
  • blunting of vasomotor response
  • arterioles dilate and blood pools into microcirculation
  • reduced CO, anoxic endothelial injury, DIC
• patient confused, urine output decreases

Question 26

describe irreversible shock

Answer 26

• stage of decompensation
  
  • severe widespread cell and tissue injury
  • leakage of lysosomal enzymes (aggravate shock)
  • perfusion of brain and myocardium at critical level
  • ATN, ARF (renal uremia)
  • myocardial depressant factor reduces cardiac output
• failure of multiple organ systems
• ischemic bowel, entry of bacteria → endotoxic shock
• survival difficult even if hemodynamics are corrected

Question 27

describe septic shock

Answer 27

• # 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 fxn
• net effect → hypoperfusion and multiorgan dysfunction

Question 28

____ are the most common cause of septic shock.

explain super antigens

Answer 28

G+ve bacteria are the most common cause of septic shock

• super antigens: bacterial proteins produce polyclonal T cell activation which induces T cells to release high levels of cytokines → diffuse rash, vasodilation, hypotension and death e.g. toxic shock syndrome
• infxn can be localized and still produce septic shock without detectable spread through blood stream

Question 29

describe the mechanism of septic shock

Answer 29

Question 30

describe the metabolic abnormalities seen in septic shock

Answer 30

Question 31

describe immune suppression and organ dysfunction in septic shock

Answer 31

Question 32

list treatment options in septic shock

Answer 32

• antibiotics
• intensive insulin therapy
• fluid replacement
• physiologic doses of corticosteroids
• experimental drugs to restore integrity of endothelial cells

Question 33

describe how shock affects the brain

Answer 33

• ischemic encephalopathy
  
  • edema, mottled discoloration in gray matter
  • watershed infarcts
  • pyramidal cells of hippocampus, Purkinje cells of cerebellum
  • laminar cortical necrosis
  • gray white junction blurred
  • neuronal necrosis
  • hemorrhages