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
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)
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
4
Q
A
chronic congestion of the liver
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
6
Q
coughing blood = ____
A
coughing blood = hemoptysis
7
Q
vomiting blood = ____
A
vomiting blood = hemetemesis
8
Q
passing blood in stool = ____
A
passing blood in stool = melena
9
Q
describe petechiae (recurrent, severe)
A
- minor petechiae = harmless
- if recurrent = iron deficiency anemia
- if severe = hypovolemic shock
- brain stem hemorrhage: sudden death
10
Q
describe the major components of hemostasis
A
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
12
Q
describe what is seen in the image
A
disseminated intravascular coagulation (DIC)
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
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
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
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
- initial non-progressive
- progressive
- 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
describe the progressive stage
* 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
describe irreversible shock
* 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
describe septic shock
* #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
\_\_\_\_ are the most common cause of septic shock.
explain super antigens
**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
describe the mechanism of septic shock
30
describe the metabolic abnormalities seen in septic shock
31
describe immune suppression and organ dysfunction in septic shock
32
list treatment options in septic shock
* antibiotics
* intensive insulin therapy
* fluid replacement
* physiologic doses of corticosteroids
* experimental drugs to restore integrity of endothelial cells
33
describe how shock affects the brain
* 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
