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Block 2 - Bugs and Drugs > Pathology > Flashcards

Pathology Flashcards

0
Q

What are the five pathophysiological causes of edema and what is an example of each?

A
  1. Increased hydrostatic pressure within the vessels due to impaired venous return or arteriolar dilation - heart failure, liver cirrhosis, venous obstruction
  2. Decreased plasma osmotic pressure - decreased production of albumin by liver, increased loss of protein by kidney, malnutrition
  3. Lymphatic obstruction - tumor
  4. Sodium and water retention
  5. Inflammation
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1
Q

What is the definition of edema?

A

Accumulation of fluid within interstitial tissue (and/or body cavities)

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2
Q

What are the three main targets of edema?

A

Soft tissues
Lungs
Brain

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3
Q

What is dependent edema?

A

Occurs in areas of body where accumulation of fluid is dependent upon gravity, most commonly associated with heart failure

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4
Q

What is anasarca?

A

Generalized edema of entire body

Most commonly associated with protein loss by kidneys in glomerular disease

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5
Q

How does heart failure lead to increased hydrostatic pressure?

A

Leads to decreased renal blood flow which leads to activation of RAAS which leads to retention of salt and water which raises blood pressure

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6
Q

What are the clinical effects of edema in soft tissue, lungs and brain?

A

Soft tissues - no significant damage but may signal underlying cause
Lungs - impair lung ability and create environment conducive to bacterial invasion
Brain - can only expand under falx cerebri, uncal herniation, or cerebellar tonsils down through foramen magnum

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7
Q

What is the difference between hyperemia and congestion?

A

H - active accumulation of blood due to increased flow

C - passive accumulation of blood due to impaired venous return

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8
Q

What is the cause and morphology of chronic passive congestion of the lung?

A

Left sided heart failure
Gross appearance - darkly pigmented, heavy and firm lungs
Hemosiderin in macrophages

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9
Q

What is the cause and morphology of chronic passive congestion of the liver?

A

Right sided heart failure
Gross appearance is nutmeg liver - shrunken and hemorrhagic centrilobar areas
Fibrosis around central veins

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10
Q

What is the definition and types of hemorrhage?

A

Extravasation of blood from vessels into extra vascular space
Petechial - pinpoint, caused by thrombocytopenia, platelet dysfunction, increased vascular pressures clotting factor deficiencies
Purpura - larger than petechiae (3-5 mm) - same causes as above, also vascular fragility or trauma
Ecchymosis - larger than purpura (>1 cm) - causes are trauma or fragility

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11
Q

How much of their blood volume must a person lose to die purely from blood loss?

A

At least 30%

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12
Q

What are the main causes of infarcts?

A 
Obstruction of vessel - thrombosis, embolism, atherosclerosis, extrinsic compression
Vessel damage
Generalized hypotension (shock)
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13
Q

What is a red infarct?

A

Blood within infarct
Venous infarcts (artery still pumping blood to tissue)
Organs with dual blood supply and or loose parenchyma (lung)
Reperfusion occurs when blood flow returned
Coagulative necrosis

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14
Q

What is a white infarct?

A

Organs with single blood supply or solid parenchyma (heart, liver, spleen)
Coagulative necrosis

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15
Q

What is a septic infarct?

A

Caused by embolization of bacterial vegetational (heart valves) or bacterial seeding of necrotic tissue
Infarct becomes an abscess

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16
Q

What are the factors determining development of an infarct?

A

Vascular supply - dual arterial supply vs. end-arterial circulation
Rate of development - time allows dev of collateral circulation
Vulnerability of cells to hypoxia - neurons more susceptible than myocytes
Oxygen content of blood - anemic patients more susceptible

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17
Q

What is a thrombus?

A

A solid intravascular mass formed from circulating blood elements during life
Mixture of platelets, leukocytes, RBCs, and fibrin

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18
Q

What is a clot as opposed to a thrombus?

A

Form outside of blood vessels when hemorrhage occurs, in vitro, or in blood vessels after death

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19
Q

What is virchows triad?

A

Endothelial abnormalities
Interruption in normal flow of blood
Hypercoagulability

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20
Q

Where are endothelial abnormalities especially important in thrombi development?

A

Arteries and cardiac chambers

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21
Q

How do endothelial cells normally maintain blood in normal fluid state?

A

Preventing platelet adhesion and aggregation
Inactivation of thrombin and other components of coagulation cascade
Breaking down local fibrin deposits with tissue plasminogen activator

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22
Q

What changes occur when endothelial cells are damaged that promote thrombus formation?

A

Binding of platelets to ECM, mediated by vWF

Injury induces synthesis of pro coagulant molecules including tissue factor and inhibitors of TPA

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23
Q

What are the consequences of stasis?

A

Platelets brought into contact with endothelial surface, promoting activation
Activated coagulation factors reach high concentrations because dilution prevented
Inflow of inhibitors of coagulation reduced
Endothelial cells activated

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24
Q

What are the most important causes of arterial vs. venous thrombosis?

A

A - atherosclerosis

V - stasis, then hypercoagulable states

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25
Q

What events is platelet activation associated with?

A

Release of calcium, ADP, and thromboxane A2 - promote further aggregation and activation
Sets stage for local activation of intrinsic coagulation factors

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26
Q

What is platelet aggregation?

A

Formation of linkages between fibrinogen and platelets via GpIIb/IIIa glycoprotein receptors on surfaces of platelets
Local accumulation of leukocytes

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27
Q

What consequences does local activation of the coagulation cascade have?

A

Thrombin promotes further platelet aggregation and leukocyte adhesion - leads to formation of an irreversibly fused contracted platelet mass
Catalyzes formation of thrombin and with factor XIII results in dev of cross linked fibrin mesh work - entraps erythrocytes

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28
Q

What are lines of Zahn?

A

Gray-tan lines formed from aggregates of platelets, leukocytes, and fibrin
Helps distinguish a thrombus from a postmortem clot

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29
Q

What are clinical manifestations of venous thrombosis?

A

Majority are silent
Local mechanical obstruction of venous circulation (edema of involved extremity)
Local warmth and tenderness (more common with superficial thrombosis)
Pulmonary embolism

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30
Q

What are the different fate of thrombi?

A

Dissolution - fibrinolytic activity
Organization and recanalization - fibroblasts, smooth muscle cells, and endothelial cells can migrate into fibrin-rich matrix –> small collagen scar in wall of vessel, calcification of thrombus, dev of new vessels within substance of thrombus
Embolism
Persistent occlusion - can become calcified or propagate downstream toward heart

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31
Q

What are the different kinda of embolisms?

A 
Dislodged thrombi
Tissue fragments
Fat droplets
Gases
Foreign material
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32
Q

What are the main sources of pulmonary thromboemboli?

A

Deep veins of proximal lower extremities and pelvis
Inferior vena cava
Sometimes right cardiac chambers or other veins

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33
Q

What is massive pulmonary embolism?

A

Embolic occlusion of more than 50-60% of pulmonary arterial tree
Causes elevation of pul arterial pressure –> burden on right ventricle –> RV dysfunction and decreased output –> decreased LV output –> systemic hypotension, decreased coronary artery perfusion and decreased cerebral perfusion

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34
Q

What’s a minor pulmonary embolism?

A

Comprises less than 30% of pulmonary arterial circulation
Healthy patients - systemic perfusion pressure remains normal
Preexisting cardiac or pulmonary disease reduces tolerance for minor embolisms

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35
Q

How can a pulmonary embolism be diagnosed?

A

High index of suspicion (wells score, etc.)
Imaging techniques
Lab studies

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36
Q

What are the important clinical manifestations of pulmonary embolism?

A 
Dyspepsia
Tachycardia
Substernal chest pain
Fluctuating BP
Syncope - decreased systemic perfusion
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37
Q

What kinds of tissue fragments can cause embolism?

A

Fragments of placental tissue
Rarely amniotic fluid
Neoplastic cells

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38
Q

What is the relationship between pulmonary emboli and pulmonary infarction?

A

Must infarcts caused by emboli but fewer than 10% of emboli produce infarcts
Due to dual blood supply of lungs - bronchial arteries can deliver sufficient blood when pulmonary arteries compromised when they are healthy
Most infarcts are hemorrhagic and can cause hemoptysis

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39
Q

What is shock?

A

Generalized decrease in perfusion of micro circulation

Also results in accumulated waste products

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40
Q

What changes in brain are associated with shock?

A

Range from occasional necrotic neurons to generalized brain parenchymal necrosis

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41
Q

What changes in heart occur with shock?

A

Areas of subendocardial myocyte necrosis - last cells to be perfumed from blood from coronary arteries

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42
Q

What changes with liver occur from shock?

A

Acute hemorrhagic centrilobular necrosis
Hepatocytes in central regions of hepatic lobules (surrounding central vein branches) last to receive oxygen and nutrient rich blood
Nutmeg appearance

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43
Q

What changes are seen in kidney with shock?

A

Acute tubular necrosis

Swelling and pallor of renal cortex and medullary congestion

44
Q

What changes are seen in lungs with shock?

A

Evidence of diffuse alveolar damage

45
Q

What is the leading cause of septic shock?

A

Infection with gram pos bacteria

46
Q

What four ways does the endothelium play an important role in hemostasis?

A
  1. Secreting tissue factor - initiates coagulation cascade and vWF (adhesive glycoprotein)
  2. Preventing platelet adhesion by coating surface with PGI2
  3. Regulating thrombin formation with thrombomodulin to activate protein c pathway
  4. Regulates fibrinolysis by secreting TPA
47
Q

What three steps does primary hemostasis consist of?

A

Platelet adhesion
Secretion
Platelet aggregation

48
Q

Platelet activation includes which three important processes?

A

Activation of phospholipase A2 - will lead to TXA2 (pro aggregate)
Fusion of cytoplasmic granules (with platelet adhesive molecules) with PM –> secretion of biochemical substances
Conformational change in GpIIb/IIIa - capable of high affinity fibrinogen binding leading to platelet aggregation

49
Q

What is secondary hemostasis?

A

Consolidation of platelet plug by formation of cross linked fibrin meshwork
Cascade of protease activity by coagulation factor proteins

50
Q

Where are coagulation factors synthesized?

A

Liver, except factor VIII - can be produced by non-hepatic tissues
Vitamin k dependent enzyme necessary for factors II, VII, IX, X

51
Q

What is the coagulation cascade?

A

Initiated by tissue factor exposed to blood by vascular injury, binds small amounts of circulating FVIIa to form complex, together with calcium and phospholipid called “extrinsic tensase” - initiates coagulation by activating FX
FXa binds FVa with calcium on phospholipids to form prothrombinase complex
Converts prothrombin (FII) to thrombin (FIIa) - cleaves fibrinogen to fibrin which can assemble into clot
Inhibited by tissue factor pathway inhibitor

52
Q

How does thrombin amplify the coagulation cascade?

A

Converts FXI to FXIa (intrinsic pathway) which activates FIX
FIXa complexes with FVIIIa, phospholipid, and calcium to form “intrinsic tenase” - further activates FX to make more thrombin
Also activates FV and FVIII (amplification phase)
Also activates FXIII - cross links fibrin polymers to stabilize clot

53
Q

What are hemophilia a and hemphilia b?

A

A - congenital deficiency of FVIII

B - congenital deficiency of FIX

54
Q

What are the natural anticoagulants?

A

Anti thrombin - binds to serine proteases to inhibit formation of fibrin clot, potentiated by heparin
Protein c - vitamin k dependent, converted to active (APC) by thrombin-thrombomodulin complex, inactivated FVa and FVIIIa
Protein s - vitamin k dependent, co factor for APC
Warfarin reduces proteins c and s

55
Q

What is tertiary hemostasis?

A

Fibrinolysis
TPA converts plasminogen to plasmin - cleaves cross linked fibrin clot -releases D dimers
Free plasmin neutralized by anti plasmin to avoid primary fibrinogenolysis
TPA regulated by PAI secreted by endothelium

56
Q

What is a stable platelet count and the recommends cutoff for prophylactic platelet transfusion?

A

5x10^9/L
10x10^9/L
Patient with bleeding risks or co morbid conditions may need more

57
Q

What is the platelet function analyzer?

A

Measures time required for blood to occlude aperture in membrane of collagen/Epi or collagen/ADP coated test cartridge = closure time
Screens patients for platelet function disorders, monitors some anti platelet therapy

58
Q

What are PT and PTT?

A

Tests developed to diagnose patients with bleeding disorders
Never shown to assess bleeding risk in a non bleeding patient
Good personal and family history of bleeding is the best test

59
Q

What is the international normalized ratio (INR)?

A

Calculated by comparing patiens PT to mean normal PT and applying international sensitivity index (measure of PT reagents sensitivity as compared to WHO standard
Not reliable as primary measure

60
Q

What is TT?

A

Assesses final step in coagulation, conversion of fibrinogen to fibrin
Time required to form clot after bovine thrombin added to patient plasma
Useful in distinguishing effect of heparin from other causes of prolonged PTT and detection of dysfibrinogenemia common in chronic liver disease

61
Q

What are gamma delta T cells?

A

Form of T cell associated with mucosal surfaces

Negative for cd 4 or 8 and recognize non protein molecules

62
Q

What is the normal innate immune response?

A

TLR recognizes PAMP - signaling via myD88 or TRIF results in inflammatory cytokines and upregulation of MHC and co stimulatory molecules (activation of trans. Factors like NFkappaB)

63
Q

What are the three signals for T cell activation?

A
  1. Peptide presented with MHC
  2. CD28 on T cell to CD 80/86 on APC
  3. Cytokines like IL-2
64
Q

What are the two signals for B cell activation?

A
  1. Antigen binding to surface antibody

2. CD40 on B cell to CD40L on T cell (appear after T cell gets signal 1)

65
Q

What do th1 cells produce?

A

Interferon gamma - activates macrophages and antibody production by B cells

66
Q

What do th2 cells produce?

A

IL-4 - stimulates B cells to class switch into IgE

67
Q

What do th17 cells produce?

A

IL-17 - inflammatory cytokine that plays role in inflammatory disorders

68
Q

What are four ways antibodies participate in the immune response?

A
  1. Neutralize microbes and toxins
  2. Opsonization
  3. ADCC
  4. Initiate complement cascade
69
Q

What are the four types of hypersensitivity reactions?

A

Type 1 - immediate
Type 2 - antibody mediated
Type 3 - immune complex
Type 4 - T cell mediated/delayed type

70
Q

What is the sequence of events in type 1 hypersensitivity?

A

Activation of th2 cells and production of IgE
Th2 produce IL-4, 5 (activates eosinophils), 13 (stimulates epithelial cells to secrete mucus)
Binding of IgE to Fc receptors on mast cells, basophils, eosinophils
Activation of these cells and release of mediators

71
Q

What three groups of mediators are released from mast cells?

A
  1. Vasoactive amines - histamine, adenosine (bronchoconstriction and inhibits platelet aggregation), chemo tactic factors that recruit eosinophils and neutrophils, proteases and acidic proteoglycans like heparin
  2. Lipid mediators - prostaglandin (bronchospasm and mucus secretion) and leukotriene
  3. Cytokines (inc. TNF)
72
Q

What are the immediate and late phases of a type 1 hypersensitivity response?

A

Immediate occurs within minutes due to release of mediators from basophils/mast cells. Late phase 4-8 hrs after exposure from leukocytes

73
Q

What is atopy?

A

Familial predisposition to type 1 hypersensitivity reactions

There is a genetic component

74
Q

What causes a type 2 hypersensitivity response?

A

Binding of antibodies to cellular component of tissues

75
Q

What are the three processes involved in type 2 hypersensitivity responses and what are examples of each?

A
  1. Opsonization and phagocytosis - opsonized cells typically eliminated in spleen - ex. Hemolytic anemia, thrombocytopenic purpura
  2. Inflammation - antibodies can activate complement - ex. Good pasture
  3. Antibody mediates cellular dysfunction - myasthenia gravis, Graves’ disease
76
Q

What are the three phases of a type 3 hypersensitivity response?

A

Antigen antibody complex formation
Deposition of immune complexes
Inflammatory reactions at various sites (systemic)

77
Q

What are three examples of a type 3 hypersensitivity?

A

SLE
Polyarteritis nodosa
Serum sickness

78
Q

How does size of immune complexes determine pathogenicity?

A

Large - rapidly removed by macrophages via binding to Fc

Small and intermediate - occur when there is antigen excess, harder to clear

79
Q

What is athus reaction?

A

Involves formation of antigen antibody complexes resulting in vasculitis
Can occur following intradermal injection of antigen 4-12 hrs later
Commonly caused by diphtheria and tetanus vaccine
Results in severe pain, swelling, edema, hemorrhage and sometimes necrosis

80
Q

What is the difference between type 4 and type 1 hypersensitivity responses?

A

Type 4 involves T cells and is slower - 12-48 hrs after antigenic challenge

81
Q

What are two examples of type 4 hypersensitivity?

A

Injection of tuberculin challenge - mediated by th1

Contact dermatitis

82
Q

What are the two types of tolerance?

A
  1. Central - selection of b and T cells unresponsive to self antigens during maturation in thymus and bone marrow
  2. Peripheral - anergy when signal 1 but no costimulatory, regulatory T cells have CD25 and FOXP3 that suppress immune responses, secrete tgf-beta and IL-10 and express inhibitory ligand For cd80/86 on APC, apoptosis of activated immune cells
83
Q

What are four common causes of autoimmunity?

A

Mutations of genes involved in tolerance (FAS or AIRE)
Genetic predisposition - HLA types
Molecular mimicry - exposure to bacteria/viruses
Environment - can modify self antigens

84
Q

What are the basics of SLE?

A

Production of IgG autoantibodies to nuclear constituents
Primarily women between 15-40
Common symptoms are fatigue, fever, weight loss, anorexia
Diagnosis requires 4 of 11 criteria
Formation of immune complexes main cause of organ damage

85
Q

What are the 11 possibly criteria of manifestations of SLE?

A 
Skin - malar rashes 
Serositis - inflammation of pleura and pericardium 
Kidney (lupus nephritis) - renal disease
Neurological 
Hematological - anemia from systemic inflammation, leukopenia and mild thrombocytopenia
Pulmonary 
Cardiac - pericarditis
Lymphadenopathy
Splenomegaly
Hepatomegaly
Spontaneous abortion and still birth
86
Q

How are RA patients identified?

A

Anti CCP test

87
Q

What is sjogren syndrome?

A

Autoimmune disease characterized by dry eyes and mouth from immune destruction of lacrimal and salivary glands
Isolated or in combo with another autoimmune disease
Glands infiltrated with cd4 T cells that release th1 type cytokines
Antibodies directed to ss-a and ss-b and Fc component of IgG

88
Q

What is systemic sclerosis and what are the two subsets?

A

Excessive fibrosis of tissues and production of autoantibodies

  1. Limited cutaneous - most common, skin involvement limited to face, neck and extremities, patient with CREST (sclerodactyly with skin fibrosis confined to fingers, anti centromere antibodies)
  2. Diffuse cutaneous - skin involvement of trunk and extremities, autoantibodies target topoisomerase 1 and RNA polymerase III, poor prognosis
89
Q

What is the sequence of progression in scleroderma?

A

Injury to endothelial cells, activation of endothelium and recruitment of immune cells
T cells responding to self antigen produce type II cytokines that activate fibroblasts
Endothelial cell proliferation and intimal fibrosis leading to ischemic injury
B cell activation resulting in production of antibodies to DNA topoisomerase I or anti centromere antibodies

90
Q

What do patients with mixed connective tissue disease have high titers of?

A

Autoantibodies to U1RNP

91
Q

How does polyarteritis nodosa manifest?

A

Necrotizing inflammation of blood vessel wall due to deposition of immune complexes

92
Q

What is the hallmark of immunodeficiencies?

A

Recurrent infection

93
Q

What are six causes of immunodeficiencies?

A

Abnormal immune cell development
Abnormal cell to cell communication
Abnormal embryonic differentiation
Enzymatic defects
Absence of cell surface adhesion molecules
Defective synthesis of proteins including complement or Ig

94
Q

What causes primary antibody deficiencies?

A

Defects in genes involved in B cell differentiation or Ig genes

95
Q

What are the key clinical findings of primary antibody deficiencies?

A

Recurrent infections due to encapsulated pyogenic bacteria
Infected with gram- rods, staph, and flu causing damage to mucosal surfaces
Normal immune responses (normal t cells) but protective immunity doesn’t develop
Other defects in immune regulation

96
Q

What is x linked agammaglobulinemia?

A

Loss of function mutation in Bruton tyrosine kinase
Block in B cell maturation at pre-b cell stage
Can produce IgM heavy chain but not light chains
Resp inf, diarrhea from giardia, osteomyelitis, skin inf, do NOT give live polio vaccine

97
Q

What is hyper IgM syndrome?

A

Defect in CD40/CD40L signaling
X linked or mutations in ligand, receptor, or other genes for class switching
Cannot undergo class switching
Normal or elevated IgM with low everything else
Normal T cell and B cell counts

98
Q

What is IgA deficiency?

A

Low IgA, normal IgM, with or without low IgG
Sometime high level of IgE
Often develop autoimmune diseases
Risk with transfusion - will see IgA as foreign

99
Q

What is common variable immunodeficiency?

A

Normal levels of Ig but later levels consistent with IgA deficiency
Most patients have IgA deficiency with low level of IgG and IgM and IgE
Normal numbers of B cells

100
Q

What is severe combined immunodeficiency and what are the four main types?

A

Defective T cell differentiation with or without abnormal B cell differentiation

  1. Reticular dysgenesis - affects t, b, nk, leukocytes, platelets
  2. Alymphocytosis - affects t and b due to mutations in RAG
  3. Absence of t lymphocytes - t and nk cells
  4. Adenosine deaminase deficiency - t, b, nk
101
Q

What is DiGeorge syndrome?

A

Thymic hypoplasia
T cell deficiency from improper development of third and fourth branchial arches
Facial defects, cardiovascular defects, mental retardation, feeding difficulties
Sometimes thymus transplant restores normal function

102
Q

What is wiscott-Aldrich syndrome?

A

Mutation in wiscott-Aldrich protein
Eczema, thrombocytopenia, recurrent infections, short life expectancy without bone marrow transplant
Age related depletion of T cells in periphery

103
Q

What are the four types of transplant?

A

Autologous
Syngeneic
Allogeneic
Xenogeneic

104
Q

What are the two mechanisms for recognition of allo-MHC?

A
  1. Direct allorecognition - recipient T cells recognize foreign MHC displayed on donor APC, short period of time after transplantation - donor APC rapidly depleted from graft
  2. Indirect - recipient T cells recognize recipient APC presenting donor derived peptide from donor MHC, long term grafts
105
Q

What are the three types of organ rejection?

A

Hyper acute - preformed antibodies
Acute - cell or antibody mediated, treated w immunosuppressives
Chronic

106
Q

What three strategies are used for improving graft survival?

A

HLA matching
Testing for donor specific antibodies
Immunosuppressive therapies

107
Q

What are seven common immunosuppressive agents?

A

Corticosteroids
Cytotoxic drug
Antimetabolites - interfere with synthesis of nucleic acid
Calcineurin inhibitors
Mycophenolate mofetil - blocks guanine nucleotides
Anti il2 receptor
Antithymocyte globulin

108
Q

How are hematopoietic stem cell transplants used?

A

Autologous and allogeneic for leukemia and lymphoma
Only allogeneic for immunodeficiencies
Humoral rejection generally not seen - mostly t and nk cells
GVHD from T cells is a concern - skin rashes, destruction of gut epithelium and bile duct, and jaundice

Block 2 - Bugs and Drugs (9 decks)

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