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.Pathology 1 > Hyperemia and Hemorrhage > Flashcards

Hyperemia and Hemorrhage Flashcards

1
Q

describe hyperemia vs. congestion

A
  • 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
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2
Q

describe acute pulmonary congestions vs. chronic pulmonary congestion

A
  • 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)
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3
Q

describe acute vs. chronic liver congestion

A
  • 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
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4
Q
A

chronic congestion of the liver

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5
Q

describe petechiae, purpura and ecchymosis

A
  • 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
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6
Q

coughing blood = ____

A

coughing blood = hemoptysis

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7
Q

vomiting blood = ____

A

vomiting blood = hemetemesis

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8
Q

passing blood in stool = ____

A

passing blood in stool = melena

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9
Q

describe petechiae (recurrent, severe)

A
  • minor petechiae = harmless
  • if recurrent = iron deficiency anemia
  • if severe = hypovolemic shock
  • brain stem hemorrhage: sudden death
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10
Q

describe the major components of hemostasis

A
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11
Q

describe disseminated intravascular coagulation (DIC)

A
  • 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
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12
Q

describe what is seen in the image

A

disseminated intravascular coagulation (DIC)

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13
Q

describe causes of DIC

A
  • 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
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14
Q

describe endotoxins role in DIC

A
  • 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
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15
Q

describe the effects of DIC and diagnosing DIC

A
  • decreased tissue perfusion → shock, lactic acidosis, microinfarcts
  • bleeding → consumptive coagulopathy
    • no coagulation factors left
  • diagnosis:
    • increased FDPs
    • increased D-dimers
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16
Q

describe the management of DIC

A
  • heparin to prevent formation of thrombi
  • replace platelets and plasma
17
Q

define shock

A
  • clinical state characterized by a generalized decrease in perfusion of tissues associated with reduction in effective cardiac output
    • aka cardiovascular collapse
18
Q

describe cardiogenic shock

A
  • results from myocardial pump failure
    • intrinsic myocardial damage (infarction), ventricular arrhythmias
    • obstructive extrinsic compression (cardiac tamponade)
    • outflow obstruction (pulmonary embolism)
19
Q

describe hypovolemic shock

A
  • results from loss of blood or plasma volume
    • hemorrhage
    • fluid loss from severe burns or trauma
    • vomiting, diarrhea
20
Q

describe septic shock

A
  • caused by systemic microbial infxn
    • G+ve infxns, G-ve infxns (endotoxic shock), fungi
21
Q

describe neurogenic shock

A
  • 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
22
Q

describe anaphylactic shock

A
  • anaphylactic: generalized IgE mediated response
    • systemic vasodilation, increased permeability
    • reduced tissue perfusion
    • degranulation of mast cells and basophils via histamine, bradykinin, leukotrienes
23
Q

list the 3 stages of shock

A
  1. initial non-progressive
  2. progressive
  3. irreversible
24
Q

describe the non-progressive stage

A
  • 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
25
Q

describe the progressive stage

A
  • 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
26
Q

describe irreversible shock

A
  • 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
27
Q

describe septic shock

A
  • # 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
28
Q

____ are the most common cause of septic shock.

explain super antigens

A

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
29
Q

describe the mechanism of septic shock

A
30
Q

describe the metabolic abnormalities seen in septic shock

A
31
Q

describe immune suppression and organ dysfunction in septic shock

A
32
Q

list treatment options in septic shock

A
  • antibiotics
  • intensive insulin therapy
  • fluid replacement
  • physiologic doses of corticosteroids
  • experimental drugs to restore integrity of endothelial cells
33
Q

describe how shock affects the brain

A
  • 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

.Pathology 1 (15 decks)

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