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Pathology > Circulatory Pathology > Flashcards

Circulatory Pathology Flashcards

1
Q

Edema (Definition)

A
  • Presence of excess fluid in the intercellular space
  • Anasarca is severe generalized edema
  • Effusion is fluid within body cavities
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2
Q

Edema (Causes)

A
  • Increased hydrostatic pressure: congestive heart failure, portal hypertension, renal retention of salt and water, and venous thrombosis
  • Hypoalbuminemia and decreased colloid osmotic pressure: liver disease, nephrotic syndrome, and protein deficiency like kwashiorkor
  • Lymphatic obstruction (lymphedema): tumor, following surgical removal of lymph nodes and parasitic infestation (filariasis)
  • Increased endothelial permeability: inflammation, hypersensitivity type I and some drugs like bleomycin and heroin
  • Increased interstitial sodium: increased sodium intake, primary hyperaldosteronism and renal failure
  • Increased extracellular glycosaminoglycans: pretibial myxedema and exophthalmos (Graves disease)
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3
Q

Causes of Non-pitting Edema

A
  • Lymphatic obstruction

- Pretibial myxedema

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4
Q

Exudate vs Transudate (Appearance)

A
  • E: thick and cloudy (cellular)

- T: thin and clear (hypocellular)

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5
Q

Exudate vs Transudate (Protein, LDH, and specific gravity)

A
  • E: Increased protein and LDH (vs serum) and specific gravity more than 1.020
  • T: Decreased protein and LDH (vs serum) and specific gravity less than 1.012
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6
Q

Exudate (Causes)

A
  • Lymphatic obstruction (chylous)
  • Inflammation/Infection
  • Malignancy
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7
Q

Transudate (Causes)

A
  • Increased hydrostatic pressure like HF and sodium retention
  • Decreased oncotic pressure like in cirrhosis, and nephrotic syndrome
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8
Q

Myxedema fluid contents

A
  • Hyaluronic acid

- Chondroitin sulfate

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9
Q

Active Hyperemia (Mechanism)

A
  • Active process
  • Vasodilation mediated by:
  • Vasoactive mediators
  • Hormones
  • Neurogenic reflexes
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10
Q

Active Hyperemia (Examples)

A
  • Inflammation
  • Exercise
  • Blushing
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11
Q

Congestion (Mechanism)

A
  • Passive process

- Decreased venous outflow

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12
Q

Congestion (Examples)

A
  • Congestive heart failure
  • Deep venous thrombosis
  • Budd-Chiari syndrome
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13
Q

Glycoproteins (Integrins) of platelets activation

Location and Function

A
  • GP Ib-IX-V: platelets. It’s a von Willebrand factor (vWF) receptor (Deficiency in Bernard-Soulier syndrome)
  • GP VI: platelets. It’s a collagen I, III and VI receptor
  • GP Ia/IIa: platelets. It’s a collagen I and IV receptor
  • GP IIb/IIIa: platelets. It’s a fibrinogen receptor (Deficiency in Glanzmann Thrombasthenia)
  • GP V/IIIa: mainly on endothelial cells but also on smooth muscle cells, macrophages and platelets. Adhesion of cells to the extracellular matrix components (it is activated by GP VI)
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14
Q

Extrinsic (Tissue Factor) pathway of coagulation

Initiators, Final product, Components, Testing

A
  • Tissue factor (thromboplastin or factor III)
  • VIIa which in turn activates factor X of the common pathway
  • Factors III and VII
  • Prothrombin Time (PT) and International normalized ratio (INR) which can be calculated from PT
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15
Q

Intrinsic (Contact Activation) pathway of coagulation

Initiators, Final product, Components, Testing

A
  • Collagen, platelets, high molecular weight kininogen (HMWK), prekallikerin and Hageman factor (XII)
  • Tenase complex (factor VIIIa and IXa) which in turn activates factor X of the common pathway
  • Factors XII, XI, IX, VIII
  • activated Partial Thromboplastin Time (aPTT) and Platelet Function Assay (PFT-100)
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16
Q

Common pathway of coagulation

Initiators, Final product, Components, Testing

A
  • Factor VIIa and Tenase complex
  • Thrombin (IIa) which in turn activates factors XI, VIII and V. also converts fibrinogen to fibrin and activates factor XIII to XIIIa
  • Factors XIII, X, V, II (Prothrombin) and I (Fibrinogen)
  • aPTT, PT and Thrombin clotting time (TCT) which is a qualitative and quantitative measurement of fibrinogen
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17
Q

Commonly used products or drugs to reduce major bleeding

A
  • Prothrombin complex concentrate
  • Cryoprecipitate
  • Fresh Frozen Plasma
  • Recombinant activated human factor VII
  • Desmopressin
  • Tranexamic acid and aminocaproic acid (inhibit fibrinolysis)
  • Aprotinin (inhibits fibrinolysis by inhibition of trypsin, chymotrypsin, plasmin and kallekrin)
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18
Q

Heparin

Mechanism of action, Pathway affected, Test affected, Antidote

A
  • Activates antithrombin III
  • Intrinsic pathway
  • aPTT (increased)
  • Protamine sulfate
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19
Q

Warfarin

Mechanism of action, Pathway affected, Test affected, Antidote

A
  • Inhibits vitamin K
  • Extrinsic pathway
  • PT (increased). The goal INR is 2.0-3.0 (2.5-3.5 in patients with mechanical valves)
  • Vitamin K
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20
Q

Enoxaparin

Mechanism of action and Important notes

A
  • It is a LMW heparin that inhibits factor Xa
  • It does not have to be monitored in most situations
  • Dosing is once or twice daily
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21
Q

Types of Bleeding

A
  • Platelet bleeding which is superficial like epistaxis, gingival, petechiae, purpura and vaginal bleeding
  • Factor bleeding which is deep like joints and muscles (hemarthrosis and hematomas)
    Note: bleeding in the brain or GI tract can be either platelet or clotting factor deficiency
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22
Q

Thrombocytopenia (Causes)

A
  • Decreased production:
  • Aplastic anemia
  • Tumor
  • Increased destruction
  • Immune thrombocytopenic purpura (ITP)
  • Thrombotic thrombocytopenic purpura (TTP)
  • Disseminated intravascular coagulation (DIC)
  • Hypersplenism
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23
Q

Platelet Qualitative Defects (Causes)

A
  • von Willebrand disease
  • Bernard-Soulier syndrome
  • Glanzmann thrombasthenia
  • Drugs (aspirin)
  • Uremia
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24
Q

Immune Thrombocytopenic Purpura (ITP)

Cause or Defect

A

IgG abs made by spleen against platelet antigens like GP IIb/IIIa and GP Ib-IX-V (hypersensitivity type II) and then the platelets are destroyed in the spleen by macrophages which have Fc receptors that bind IgG-coated platelets

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25
Q

Immune Thrombocytopenic Purpura (ITP)

Presentation

A
  • Petechiae, purpura (bruises), ecchymoses, nose bleeding and menorrhagia with no splenomegaly
  • Acute: abrupt onset following viral infection which commonly affects children 2-6 years of age. males and females are affected equally
  • Chronic: insidious onset not related to infection most commonly in women of childbearing age
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26
Q

Immune Thrombocytopenic Purpura (ITP)

Association

A
  • Lymphoma
  • Leukemia
  • SLE
  • HIV
  • HCV
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27
Q

Immune Thrombocytopenic Purpura (ITP)

Diagnosis

A
  • It’s a diagnosis of exclusion
  • Low platelet count, increased BT with normal PT and aPTT
  • Enlarged immature platelets (megathrombocytes) in peripheral blood smear
  • Increased number of megakaryocytes with immature forms in bone marrow biopsy
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28
Q

Immune Thrombocytopenic Purpura (ITP)

Treatment

A
  • No bleeding, count > 30,000: no treatment
  • Mild bleeding, count < 30,000: Glucocorticoids
  • Severe bleeding (GI/CNS), count < 10,000: IV immunoglobulins, Anti-Rho (anti-D)
  • Recurrent episodes, steroid dependent: Splenectomy
  • Splenectomy or steroids not effective: Romiplostim or Eltrombopag (both are synthetic thrombopoietin), rituximab, azathioprine, cyclosporin and mycophenolate
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29
Q

Thrombotic Thrombocytopenic Purpura (TTP)

Cause or Defect

A

Inhibition or deficiency of ADAMTS 13 (vWF metalloprotease that degrades vWF multimers) —> increase platelet adhesion, aggregation and thrombosis

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30
Q

Thrombotic Thrombocytopenic Purpura (TTP)

Association

A
  • HIV
  • Cancer
  • Drugs like cyclosporine, ticlopidine and clopidogrel
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31
Q

Thrombotic Thrombocytopenic Purpura (TTP)

Presentation

A

Pentad of signs/symptoms:
- Low platelet count
- Microangiopathic hemolytic anemia
- Neurologic symptoms (delirium, seizures, stroke)
- Impaired renal function
- Fever
Note: maintain high clinical suspicion if 3 of 5 are present especially the first 3

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32
Q

Thrombotic Thrombocytopenic Purpura (TTP)

Diagnosis

A
  • Low platelet count and increased BT
  • Schistocytes and fragmented RBCs on peripheral blood smear
  • Rising creatinine is highly suggestive
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33
Q

Thrombotic Thrombocytopenic Purpura (TTP)

Treatment

A
  • Urgent plasmapheresis

- Fresh frozen plasma

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34
Q

Hemolytic Uremic Syndrome (HUS)

Cause or Defect

A

Usually occur in children after gastroenteritis (bloody diarrhea) due to verotoxin producing E. coli 0157:H7 (EHEC) or Shigella

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35
Q

Hemolytic Uremic Syndrome (HUS)

Presentation

A

Triad of signs/symptoms:

  • Low platelet count
  • Microangiopathic hemolytic anemia
  • Impaired renal function
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36
Q

Hemolytic Uremic Syndrome (HUS)

Diagnosis

A
  • Low platelet count and increased BT
  • Schistocytes and fragmented RBCs on peripheral blood smear
  • Severe elevation in creatinine levels are more typical for HUS
  • Also note that fever and neurologic symptoms usually are not present in HUS
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37
Q

Hemolytic Uremic Syndrome (HUS)

Treatment

A
  • Most cases from E. coli will resolve spontaneously

- In severe cases urgent plasmapheresis

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38
Q

von Willebrand’s Disease (vWD)

Cause or Defect

A
  • Most common inherited bleeding disorder
    (1% of population)
  • AD
  • Deficient or defective vWF with low levels of factor VIII which is carried by vWF
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39
Q

von Willebrand’s Disease (vWD)

Presentation

A
  • Easy bruising, mucosal bleeding (epistaxis, oral bleeding), menorrhagia and postincisional bleeding
  • Platelet dysfunction is not severe enough to produce petechiae
  • Symptoms worsen with aspirin use
40
Q

von Willebrand’s Disease (vWD)

Diagnosis

A
  • Normal platelet count with increased BT and aPTT (elevated in half of patients)
  • Ristocetin cofactor assay: no platelet aggregation
41
Q

von Willebrand’s Disease (vWD)

Treatment

A
  • Desmopressin (DDAVP) which releases subendothelial stores (Weibel-Palade bodies) of vWF
  • If no response then use factor VIII replacement or vWF concentrate
42
Q

Hemophilias

Cause or Defect

A
  • Hemophilia A: X-linked recessive; deficiency of factor VIII
  • Hemophilia B (Christmas disease): X-linked recessive; deficiency of factor IX
  • Hemophilia C: AR; deficiency of factor XI (Ashkenazi Jews)
  • Factor VII deficiency: AR
  • Acquired: by development of antibodies against a clotting factor like in autoimmune lymphoproliferative disease, postpartum, or following blood transfusion
43
Q

Hemophilias

Presentation

A
  • It varies according to the level of deficiency
  • Spontaneous hemorrhage into tissues and joints (hemarthrosis), if left untreated can lead to arthropathy and joint destruction
  • Spontaneous intracerebral hemorrhages as well as renal, retroperitoneal, and GI bleeding may also be seen
  • Mild cases may have major bleeding after surgery or trauma but otherwise asymptomatic
44
Q

Hemophilias

Diagnosis

A
  • Normal BT, Fibrinogen and Thrombin time
  • PT is usually normal unless isolated factor VII deficiency is present
  • aPTT is prolonged (more prolonged, more severe)
  • Mixing study: mix patient’s plasma with normal plasma; if this corrects aPTT, a factor deficiency is likely. If not patient may have clotting factor inhibitor
  • Factor assay for factors VII, VIII, IX, XI and XII
  • Factor level:
  • Mild: > 5% of normal
  • Moderate: 1-3% of normal
  • Severe: < 1% of normal
45
Q

Hemophilias

Treatment

A
  • Treat bleeding episodes with immediate transfusion of clotting factors or cryoprecipitate to at least 40% of normal concentration
  • Length of Rx varies with lesion, extending up to several weeks after orthopedic surgery
  • Mild cases can be treated with DDVAP (release factor VIII from Weibel-Palade bodies), with fluid restriction to prevent hyponatremia
  • Depending on degree of loss it may be necessary to transfuse RBCs
    Note: cryoprecipitate consists mainly of factor VIII and fibrinogen and it is a more concentrated source of those than FFP
46
Q

Vitamin K Deficiency

Cause or Defect

A
  • Newborns
  • Antibiotics overuse
  • Malabsorption
  • Warfarin
  • Liver cirrhosis
    Factors II, VII, IX, X, proteins C and S will be deficient. In liver cirrhosis all factors are deficient except for factor VIII and vWF
47
Q

Vitamin K Deficiency

Presentation

A

Deep bleeding like bruises, hemarthrosis and hematomas

48
Q

Vitamin K Deficiency

Diagnosis

A

Elevated PT and aPTT, but PT goes up first cause factor VII runs out first

49
Q

Vitamin K Deficiency

Treatment

A

Give vitamin K

50
Q

Disseminated Intravascular Coagulation (DIC)

Cause or Defect

A
  • Widespread microthrombi with consumption of platelets and clotting factors causing hemorrhage and end-organ failure
  • It is always secondary to another disorder:
  • Obstetric complications (placental tissue factor)
  • Gram -ve sepsis (TNF)
  • Microorganisms (especially meningococcus and rickettsiae)
  • AML-M3 (cytoplasmic granules in neoplastic promyelocytes)
  • Adenocarcinomas (mucin)
  • Burns
  • Pancreatitis
  • Nephrotic syndrome
  • Snake bites
  • Massive tissue injury and trauma
  • Drug reactions
  • Acidosis
  • Aortic aneurysm
  • ARDS
51
Q

Disseminated Intravascular Coagulation (DIC)

Presentation

A
  • Acute: generalized bleeding from venipuncture sites and into organs, with ecchymoses and petechiae
  • Chronic: bruising and mucosal bleeding, thrombophlebitis, renal dysfunction, and transient neurologic sundromes
52
Q

Disseminated Intravascular Coagulation (DIC)

Diagnosis

A
  • Low platelet count with increased BT, PT and aPTT
  • Decreased fibrinogen level and increased D-dimer and fibrinogen degradation products
  • Microangiopathic hemolytic anemia (schistocytes)
  • DIC may be confused with severe liver disease, but unlike liver disease factor VIII is depressed in DIC
53
Q

Disseminated Intravascular Coagulation (DIC)

Treatment

A
  • Treat underlying cause
  • RBC transfusion
  • Platelet transfusion
  • Shock management
54
Q 
Hypercoagulative States (Thrombophilia)
(Cause or Defect)
A
  • Genetic:
  • Antithrombin III deficiency
  • Protein C or S deficiency
  • Factor V Leiden
  • Hyperhomocysteinemia
  • Dysfibrinogenemia (AD)
  • Plasminogen deficiency
  • Prothrombin G202 10A mutation
  • MTHFR gene mutation
  • Acquired:
  • Surgery, trauma and immobilization
  • Malignancy, smoking and obesity
  • Nephrotic syndrome
  • Anti-phospholipid syndrome
  • Heparin induced thrombocytopenia (HIP)
  • OCPs/hormone replacement therapy
  • Physiologic:
  • Age
  • Pregnancy
55
Q

Antithrombin III Deficiency

Cause or Defect

A
  • Inherited as AD
  • Acquired in renal failure/nephrotic syndrome —> antithrombin loss in urine —> decrease inhibition of factors IIa and Xa
56
Q

Factor V Leiden (Activated Protein C Resistance)

Cause or Defect

A

Production of mutant factor V (G to A DNA point mutation leads to Arg506Gln mutation near the cleavage site) that is resistant to degradation by activated protein C

57
Q

Protein C or S Deficiency

Cause or Defect

A
  • Protein C: AD, with homozygous patients presents as purpura fulminans in newborns . Decreased ability to inactivate factor Va and VIIIa
  • Protein S: AD with decreased ability to inactivate factor Va and VIIIa
58
Q

Prothrombin Gene Mutation

Cause or Defect

A

Mutation in 3’ untranslated region at 202 10 position replacing G with A —> increase production of prothrombin —> increase plasma levels and venous clots

59
Q

Anti-phospholipid Syndrome

Cause or Defect

A
  • Lupus anticoagulant

- Anticardiolipin antibody

60
Q 
Hypercoagulative States (Thrombophilia)
(Presentation)
A
  • Recurrent thrombotic complications including DVT, pulmonary embolism (PE), arterial thrombosis, MI, and stroke. Women may have recurrent miscarriages
  • Patients may have +ve family history
  • In protein C or S deficiency: increased risk of thrombotic skin necrosis with hemorrhage after administration of warfarin
61
Q 
Hypercoagulative States (Thrombophilia)
(Diagnosis)
A
  • Acquired causes of abnormal coagulation values should be ruled out first
  • Confirmation of hereditary abnormality requires 2 abnormal values that are obtained while patient is asymptomatic and untreated, with similar values obtained in 2 other family members
  • aPTT is only elevated in anti-phospholipid syndrome (best initial test if suspected is mixing study in which aPTT will remain elevated even after the mix. Most accurate test for lupus anticoagulant is the Russell viper venom test)
  • HIT is confirmed with ELISA for platelet factor 4 (PF4) antibodies or the serotonin release assay
62
Q 
Hypercoagulative States (Thrombophilia)
(Treatment)
A
  • Treatment should address the type of thrombotic event as well as the area of thrombosis
  • Treat DVT and PE with heparin (unfractionated or LMWH) followed by 3-6 months of oral warfarin for the first event, 6-12 months for the second and lifelong anticoagulation for subsequent events
  • Inferior vena cava filter is the best means of preventing PE in DVT patients who have contraindications to anticoagulation like recent trauma, hemorrhage or severe hypotension. also recommended for those who have recurrent DVTs on anticoagulation
  • Anti-phospholipid syndrome usually require lifelong anticoagulation after only one event of thrombosis
  • For HIT immdiately stop all heparin containing products, then administer direct thrombin inhibitors: argatroban, lepirudin and bivalirudin. Warfarin should be started after direct thrombin inhibitors
63
Q

Heparin induced thrombocytopenia (HIP)

Cause or Defect

A
  • More common with use of unfractionated heparin
  • Presents after 5 to 10 days after start of heparin with marked drop in platelet count (more than 30%)
  • Venous clots are more common
64
Q

Bernard-Soulier Syndrome

Diagnosis

A
  • Normal or decreased platelet count with increased BT
  • Giant platelets
  • Abnormal ristocetin test
65
Q

Virchow’s Triad

A
  • Endothelial injury can be due to atherosclerosis, vasculitis, or many other causes
  • Alteration in laminar blood flow predisposing for DIC occur with blood stasis (e.g., immobilization), turbulence (e.g., aneurysms), and hyperviscosity of blood (e.g., polycythemia vera)
  • Hypercoagulative states (thrombophilia)
66
Q

Common locations of thrombus formation

A
  • Coronary and cerebral arteries
  • Heart chambers in atrial fibrillation or post-MI (mural-thrombus)
  • Aortic aneurysms
  • Heart valves (vegetations)
  • Proximal deep leg veins (DVTs)
67
Q

Outcomes of thrombosis

A
  • Vascular occlusion and infarctions
  • Embolism
  • Thrombolysis
  • Organization and recanalization
68
Q

Thrombus vs Blood clot

A
  • T: Intravascular / BC: Extravascular or intravascular (post-mortem)
  • T: platelets, fibrin, RBCs and WBCs / BC: fibrin, RBCs and WBCs
  • T: lines of Zahn present / BC: lines of Zahn absent
  • T: has shape / BC: lacks shape
69
Q

Causes of Infarction

A
  • Thrombotic or embolic occlusion of an artery or vein (99%)
  • Vasospasm
  • Torsion of arteries and veins (e.g., volvulus, ovarian and testicular torsion)
70
Q

Red Infarcts (Grossly)

A
  • Occur in venous occlusion and tissues with multiple blood supplies like liver, lungs, intestine, testes and in reperfusion (e.g. after angioplasty)
  • Reperfusion injury is due damage by free radicals
71
Q

Pale Infarcts (Grossly)

A

Occur in solid organs with single (end-arterial) blood supply like heart, kidney and spleen

72
Q

Microscopic Pathology of infarction (Sequence)

A
  • Ischemia
  • Coagulative necrosis (most organs)
  • Inflammation (neutrophils and macrophages)
  • Granulation tissue (capillaries, fibroblasts and type III collagen)
  • Fibrous tissue (type I collagen)
73
Q

Regions most vulnerable to hypoxia/ischemia in Brain

A
  • ACA, MCA, and PCA boundary areas (Watershed areas which receive blood supply from most distal branches of 2 arteries with limited collateral vascularity)
  • Most vulnerable neurons include Purkinje cells of the cerebellum and pyramidal cells of the hippocampus and neocortex
74
Q

Regions most vulnerable to hypoxia/ischemia in Heart

A

Subendocardium (LV)

75
Q

Regions most vulnerable to hypoxia/ischemia in Kidney

A
  • Straight segment of proximal tubule (medulla)

- Thick ascending limb (medulla)

76
Q

Regions most vulnerable to hypoxia/ischemia in Liver

A

Area around central vein (zone III)

77
Q

Regions most vulnerable to hypoxia/ischemia in Colon

A

Splenic flexure and rectum (Watershed areas which receive blood supply from most distal branches of 2 arteries with limited collateral vascularity)

78
Q

Shock

Definition and Causes

A
  • Vascular collapse and widespread hypoperfusion of cells and tissues
  • Due to:
  • Reduced blood volume
  • Reduced cardiac output
  • Reduced vascular tone
79
Q

Shock

Types

A
  • Hypovolemic shock
  • Cardiogenic shock
  • Septic shock
  • Neurogenic shock
  • Anaphylactic shock
80
Q

Cardiogenic Shock

Causes

A
  • MI
  • Arrhythmias
  • PE
  • Cardiac tamponade
81
Q

Hypovolemic Shock

Causes

A
  • Hemorrhage
  • Severe burns
  • Severe dehydration
82
Q

Septic Shock

Causes

A
  • Could be due to any bacterial infection but most commonly gram -ve bacteria
  • Lipid A component of LPS which binds to CD14 on macrophages resulting in release of TNF, IL-1, IL-6, and IL-8
  • The cytokines can trigger vasodilatation and hypotension, ARDS, and multiple organ dysfunction
  • Mortality rate is 50%
83
Q

Neurogenic Shock

Causes

A
  • Anesthesia

- Brain or spinal cord injury

84
Q

Anaphylactic Shock

Causes

A
  • Insect bites and stings
  • Food
  • Medications
  • Others like latex exposure and exercise
    It is a type I hypersensitivity reaction
85
Q

Baroreceptor Reflex in Shock

A
  • Baroreceptors in carotid sinus and aortic arch responds rapidly to decrease in blood pressure
  • Send signals via cranial nerves IX and X to th brain stem vasomotor center in medulla oblongata which will increase sympathetic output
  • Leading to increase heart rate, ejection fraction and total peripheral resistance of vessels
86
Q

Stages of Shock

A
  • Stage I (compensation): perfusion of vital organs is maintained by reflex mechanisms (baroreceptor reflex) and activation of RAAS
  • Stage II (decompensation): progressive decrease in tissue perfusion which leads to potentially reversible injury with metabolic (lactic) acidosis, electrolyte imbalances and renal insufficiency
  • Stage III (irreversible): irreversible tissue injury and organ failure, ultimately resulting in death
87
Q

Pathology of Shock for specific organs

Kidneys, Lungs, Intestines, Liver, and Adrenals

A
  • Kidneys: acute tubular necrosis (acute renal failure) with oliguria and electrolyte imbalances
  • Lungs: diffuse alveolar damage
  • Intestines: superficial mucosal ischemic necrosis and hemorrhages, and with prolonged injury may develop sepsis with bowel flora
  • Liver: centrilobular necrosis
  • Adrenals: Waterhouse-Friderichsen syndrome (meningococcal septic shock with bilateral hemorrhagic infarction and acute adrenal insufficiency)
88
Q

Embolism

Definition

A

Any intravascular mass that has been carried down the blood stream from its site of origin, resulting in the occlusion of a vessel

89
Q

Embolism

Types

A
  • Thromboemboli (98%) (DVT —> PE or Mural thrombus and atrial fibrillation —> CNS emboli)
  • Atheromatous emboli (severe atherosclerosis)
  • Fat emboli (bone fractures, soft tissue injury and liposuction. classic triad: hypoxemia, neurologic abnormalities and petechial rash)
  • Bone marrow emboli (bone fractures and CPR)
  • Air emboli (“bends” or Caisson disease which may lead to avascular necrosis of hips)
  • Amniotic fluid emboli (in labor and may lead to DIC). fetal squamous cells are seen in maternal pulmonary vessels
  • Tumor emboli (metastasis)
  • Talc emboli (IV drug abuse)
  • Bacterial/septic emboli (infectious endocarditis)
90
Q 
Pulmonary Embolism (PE)
(Causes)
A
  • 70% from DVTs

- 30% from right side heart or pelvic venous plexuses of prostate and uterus

91
Q 
Pulmonary Embolism (PE)
(Presentation)
A
  • Classic presentation (20% of cases): hemoptysis, dyspnea and chest pain
  • Look for sudden onset of shortness of breath with clear lungs on examination and a normal chest x-ray
  • Other possible findings are:
  • Tachypnea, tachycardia, and cough
  • Unilateral leg pain from DVT
  • Pleuritic chest pain from lung infarction
  • Fever can arise from any cause of clot or hematoma
  • Excessively severe emboli will produce hypotension
92
Q 
Pulmonary Embolism (PE)
(Diagnosis)
A
  • Best initial tests are chest x-ray, EKG, and ABG
  • Chest x-ray: usually normal. Most common abnormality is atelectasis. Wedge shaped infarction, pleural based lesion (Hampton hump), and oligemia of one lobe (Westermark sign) are much less common
  • EKG: usually normal with sinus tachycardia. Most common abnormality is non-specific ST-T wave changes. only 5% will show right axis deviation, RV hypertrophy or RBBB. Classic triad of S1Q3T3 (acute heart strain with an S wave in lead I; Q wave in lead III; and inverted T wave in lead III) is uncommon
  • ABG: hypoxia (PO2 < 80 mmHg) and respiratory alkalosis (high pH and low p CO2) with a normal chest x-ray is extremely suggestive of PE
  • CT angiogram (Spiral CT scan): to confirm the diagnosis of PE if highly suspected
  • Ventilation/Perfusion (V/Q) scan: reported as high probability of PE (FP is 15%), intermediate or low probability (FN is 15%). A normal scan essentially exclude a clot. Used first only in pregnancy
  • D-dimer: do it only if low suspicion. used to rule out PE
  • Lower extremity Doppler study: if +ve no need for further CT or V/Q cause Rx is the same
  • Angiography: is the most accurate nearly 100% specificity, but with 0.5% mortality rate, so it is rarely done
    Note: Chest x-ray must be normal for the V/Q scan to have any degree of accuracy. Do spiral CT if chest x-ray is abnormal
93
Q 
Pulmonary Embolism (PE)
(Treatment)
A
  • Heparin is the best initial therapy. LMWH also can be used (Enoxaparin, Fondaparinux, dalteparin, tinzaparin)
  • Warfarin should be started at same time with heparin (the goal is INR 2-3) and continued for at least 6 months after the event or as long as risk factors exist
  • Inferior vena cava filter
  • Contraindications to the use of anticoagulants (e.g., melena, CNS bleeding)
  • Recurrent emboli while on heparin or fully therapeutic warfarin (INR of 2-3)
  • Right ventricular dysfunction with enlarged RV on echo. This means severe disease, so the next embolus even if seemingly small, could be potentially fatal
  • Thrombolytics:
  • Hemodynamically unstable patients (systolic Bp < 90 and tachycardia
  • Acute RV dysfunction
  • Direct acting thrombin inhibitors (argatroban, lepirudin): in heparin induced thrombocytopenia
94
Q

DVT and PE Prophylaxis

A
  • Treat all immobile patients
  • Heparin or LMWH
  • Intermittent compression of lower extremities (less effective)
  • Early ambulation (most effective)
95
Q 
Pulmonary Embolism (PE)
(Outcomes)
A
  • No sequelae (75%)
  • Infarction (15%)
  • Sudden death (5%): large emboli lodge in the bifurcation (saddle embolus) or large pulmonary artery branches and obstruct more than 50% of pulmonary circulation
  • Chronic secondary pulmonary hypertension (3%): recurrent PEs which will increase pulmonary resistance
    Note: Paradoxical Emboli are venous emboli that gain access to systemic circulation by crossing from right to left side of heart through a septal defect most commonly patent foramen ovale
96
Q

Elevated ESR Causes

A
  • Most anemias
  • Infections
  • Inflammation like temporal arteritis and polymyalgia rheumatica
  • Cancer like metastasis and multiple myeloma
  • Renal disease (end-stage or nephrotic syndrome)
  • Pregnancy
97
Q

Low ESR Causes

A
  • Sickle cell anemia
  • Polycythemia (increased RBCs “dilute” aggregation factors)
  • Heart failure
  • Microcytosis
  • Hypofibrinogenemia

Pathology (9 decks)

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