Hemostasis Flashcards
(41 cards)
Symptoms of Pulmonary Edema
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Heart Failure Cells
Hemosiderin-laden macrophages in the alveolar spaces that can be seen w/ chronic pulmonary congestion
Process of ecchymosis healing
Hemoglobin (red-blue) =» Bilirubin (blue-green) =» Hemosiderin (gold-brown)
Hemorrage
Can manage up to 20% loss before shock occurs
Sentinal Node Biopsy
Reduces the number of axillary dissections needed for breast-cancer staging =» reduced comorbidity of breast cancer
PFA
Prolonged collagen/EDI; normal collagen/ADP =» Drug induced issue
Prolonged both =» platelet abnormality (possible vWF)
Leukocytoclastic vasculitis
Destruction of the vascular wall due to the deposition of drug-induced immune complexes
Henoch-Schonlein Purpura
Systemic hypersensitivity disease in which immune complexes deposit in the vascular wall
*Colicky abdominal pain, AGN, polyarthralgia
Immune Thrombocytopenic Purpura
Chronic: IgG autoab against platelet that are prominently removed by the spleen (will be congested and have fulminant macros)
*BM will have increased megakaryocytes w/ left-shifted maturation
Treatment: Immunosuppression, rituximab
Acute: Abrupt, normally self-limiting but can progress to acute
Heparin Induced Thrombocytopenia
Type I: Direct platelet aggregation caused by heparin a couple days after administration; common and clinically insignificant
Type II: Abs directed against Platelet Factor 4 complex result in agglutination and thrombosis; **can be life-threatening
-LMW heparin is LESS LIKELY to cause but cannot cure it
TTP
Caused by an ADAMTS deficiency =» accumulation of HMW multimers of vWF and aggregation
Classic pentad: 1. Fever
2. Thrombocytopenia
3. Microangiopathic hemolytic anemia
4. Renal failure
* 5. Neurologic symptoms
Treatment: Plasma exchange to remove antibody
*DO NOT GIVE PLATELETS; MAKES IT WORSE
Hemolytic Uremic Syndrome
Presents as bloody diarrhea and subsequent renal failure following an infection by E.coli 0157:H7
Treatment: Supportive care; plasma exchange
Can suffer irreparable renal damage
Bernard-Soulier Syndrome
Deficiency of platelet Gp-Ib complex where platelets bind to vWF; AR inheritance
*Giant platelets
Labs: Everything can cause aggregation except ristocetin
Glanzmann’s Thrombasthenia
Deficiency of Gp-IIIb-IIa where fibrinogen crosslinks platelets
Labs: Only ristocetin can cause aggregation
vonWillebrand Disease
Most common bleeding disorder that presents as prolonged bleeding from cuts, menorrhagia, and GI bleeding
-Abnormal PFA and PTT
Type I and III =» quantitative (III more severe)
Hemophilia A
Factor VIII deficiency that presents w/ easy bruising, menorrhagia, and *hemarthrosis
Labs: Prolonged PTT
-Will not see mucous membrane bleeding or petechiae
Treatment: Humate P/ recombinant Factor VIII
Christmas Disease
Clinically identical to Hemophilia A but is due to altered/deficient Factor IX
-Prolonged PTT
Treatment: recombinant Factor IX
DIC
Presents as a microangiopathic hemolytic anemia that progresses to SOB, respiratory failure, **RENAL FAILURE, circulatory shock (all related to hypoxia of areas affected)
-Can originate from meningococcemia, APML, Adenocarcinoma, placenta abruption, massive tissue injury
=»Tissue injury and massive Thrombin release cause excessive activation of coag cascade and fibrin deposits in vasculature
Labs: Decreased platelets, fibrinogen
Prolonged PTT and PT
Increased D-dimer
PB: Schistocytes, reticulocytosis, leukocytosis, left shift, thrombocytopenia
*Can cause Waterhouse-Friedrichson Syndrome (meningococcemia) and Sheehan Syndrome along w/ thrombi affecting other areas
Sheehan Sydrome
Postpartum pituitary necrosis; can be caused by DIC
SIRS
“Systemic Inflammatory Response Syndrome”
Exaggerated response of a local inflammatory reaction mediated by TNF-a, IL-1, IL-6 and excessive endothelial cell activation
-Diagnosed by two or more signs of the following: fever, tachcardia, tacypnea, leukocytosis, leukopenia
Trigger for septic shock
Bacterial products that activate TLRs on PMNs
Endothelial Cell Activation during Septic Shock
3 major effects
- Thrombosis (DIC)- Inflammatory mediators stimulate PAI-1 and TF prod.; also decrease TFPI, Protein C, thrombomodulin
- Increased Vascular Permeability- Increases interstitial fluid decreasing the amount of fluid available to the tissues =» hypoxia
- Vasodilation- Increased NA and TXA2
Adult Respiratory Distress Syndrome (Shock)
Can be induced by septic shock when decreased perfusion of the heart =» decreased contractility =» increased pulmonary edema =» lung damage
*Septic shock also damages the kidneys, liver, lungs
Stages of Shock
Nonprogressive- Tissue perfusion is maintained after reflex mechanisms compensate (SIRS)
Progressive- Worsening circulator and metabolic imbalances cause acidosis and organ/tissue damage
Irreversible- Extent of tissue damage is too bad and pt. is done for
