1
Q
Basophil disorders
A
- basophilia
- basopenia
2
Q
Basophilia
A
- increased number in basophils
- rare in humans
- inflammation and immediate hypersensitivity reactions
- myeloproliferative disorders (bone marrow)
- veterinary medicine - heartworm disease
3
Q
Basopenia
A
- decreased number in basophils (normally low #s anyway)
- hyperthyroidism
- mast cells in tissues
4
Q
Monocyte issues
A
- monocytosis
- monocytopenia
- macrophages in tissues
- normal 2-8%
5
Q
Monocytosis
A
- increased number in monocytes
- often transient
- correlates poorly with disease states
- large stages of recovery when monocytes are phagocytizing leftover debris
- chronic infections
6
Q
Monocytopenia
A
- decreased number in monocytes
- rare
7
Q
Lymphocyte issues
A
- lymphocytosis
- lymphopenia
- normal is 20-30%
- viruses cause either
- B and T cells are these!
8
Q
Lymphocytosis
A
- increased number
- acute viral infections
- malignancies
9
Q
Lymphocytopenia
A
- decreased number
- immunodeficiency (AIDS)
- destruction by drugs, or radiation
- viral infections
- stress
10
Q
Common WBC diseases
A
- Infectious Mononucleosis
- leukemias
- multiple myeloma
- Lymphadenopathy
- Hodgkin Disease
11
Q
Infectious Mononucleosis
A
- not involving monocytes
- acute infection of B lymphocytes (Epstein-Barr virus is most common but also cytomegalovirus and others)
- young adults; close personal contact (kissing disease)
- 30-50 inc. time
- classic symptoms are fever, sore throat and enlarged cervical lymph nodes
- enlarged liver and spleen, neurologic and ocular manifestations can also occur
12
Q
Leukemias definition
A
- in the blood
- A malignant proliferation of WBC’s
- leads to overcrowding of the bone marrow and decreased production of the other normal hematopoietic cell lines
13
Q
Classification of leukemias
A
- type of cell line involved
- acute or chronic - depending on the point in development where normal growth was arrested
- other biological characteristics
14
Q
Leukemias exact cause is unknown but is related to:
A
- genetic predisposition
- may develop from acquired disorders
- ionizing radiation
- drugs that cause bone marrow depression (chemotherapy)
- veterinary medicine - viruses
15
Q
Multiple Myeloma
A
- B cell cancer of mature plasma cells and production of an abnormal immunoglobulin (called M-protein) -> monoclonal antibody electrophoresis (identical mutant antibodies)
- masses of malignant plasma cells scattered throughout the skeletal system causing destructive bone lesions (break easily)
- Bence Jones proteins (light chain of the M-protein) are seen in the urine and can cause damage to the renal tubular cells
16
Q
Lymphadenopathy
A
- not disease, but sign/symptom
- is enlarged lymph nodes that are palpable and tender
- localized: usually indicated drainage from an area of inflammation
- generalized: often seen with malignant diseases
- other causes: autoimmune diseases, reactions to drugs, endocrine disorders, and lipid storage diseases
17
Q
areas where lymph nodes can get enlarged
A
- submandibular
- cervical
- axillary
- inguinal
- popliteal
- hilar
18
Q
Malignant Lymphomas
A
- solid
- Hodgkin Disease
19
Q
Hodgkin Disease definition and main features
A
- responds well to chemo
- presence of Reed-Sternberg cells (RS)
- arises in a single lymph node and spreads to adjacent nodes
- malignant cells release cytokines which cause inflammatory cells to accumulate; their chemical mediators cause other malignant and non-malignant lymph cells to proliferate (~cancer w/inflammation)
- four different subtypes based on the type of cells and cytokines involved
20
Q
Three types of Hodgkin’s related to age of onset
A
- childhood form (<14 yrs)
- young adult form (15-34 years)
- older form (55-74 years)
21
Q
Risk factors for Hodgkin’s
A
- family history (partial genetics)
- prior tonsillectomy or appendectomy (lymph nodes)
- high socioeconomic status and education of mother
22
Q
Non-Hodgkin Lymphomas
A
- respons poorly to chemo
- a wide spectrum of malignancies of the lymphoid system
- many possible causes: viral, immune disorders, genetic abnormalities, environmental factors, Helicobacter pylori
- multiple scattered peripheral lymph nodes involved (rarely localized = multi centric organ)
- may present as localized or generalized lymphadenopathy
23
Q
Causes of hemorrhage
A
trauma, atherosclerosis, or neoplastic erosion of vessel walls, toxins, inherited
24
Q
Types of hemorrhage
A
- acute or chronic or recurrent
- arterial hemorrhage
- venous hemorrhage
- capillary hemorrhages
25
Arterial hemorrhage
-spurting and pulsating
26
Venous hemorrhage
-steady flow
27
capillary hemorrhages
- petechia (minute)
- purpura (slightly larger)
- ecchymoses (large 1-2cm)
28
Hematoma
accumulation of blood enclosed in a tissue
29
hemothroax
throax
30
hemoperitoneum
peritoneum
31
hemopericardium
pericardium (aka cardiac tamponade)
32
hemoptysis
coughing up blood
33
hematemesis
vomiting blood
34
how to tell difference between hemoptysis and hematemesis
test the pH to find out
35
Hemathrosis
blood in joint capsule
36
hematochezia
anorectal bleeding
37
melena
passage of black discolored blood in the stool
38
hematuria
blood in urine (beginning of stream? end? mixed throughout?)
39
menorrhagia
menstrual bleeding
40
Normal thrombogenesis definition
-formation of a blood clot
41
Thrombogenesis steps
1. tissue damage causes defects in the endothelial calls of the vascular wall
2. a brief period of vasoconstriction slows blood flow (30 minutes)
3. Platelets rapidly adhere to damaged vessel walls (platelets aggregate and form a small plug, chemical mediators *most potent* are released by the platelets)
4. clotting factors (the coagulation cascade) become activated and act o each other to form thrombin
5. thrombin causes fibrin to be formed from fibrinogen
6. the fishnet meshwork of fibrin acts as the skeleton of the clot
7. the meshwork of fibrin strands (stabilizes, the platelet plug, traps other cells *RBC's, phagocytes, and microorganisms*, and adheres to the damaged vessel wall)
8. the process of coagulation is kept in check by natural anticoagulants (plasmin)
42
Clot retraction and lysis
- retraction: fibrin strands shorten which brings together the edges of the injured vessels and seals the site of injury
- lysis of the clot: fibrinolytic system
* plasmin splits fibrin and fibrinogen into FDP's (fibrin degradation products)
* removes clotted blood from tissues and dissolved small clots in blood vessels
43
thrombogenesis is the result of:
- coagulation proteins (clotting factors)
- platelets
- damaged endothelial cells of the vascular wall simulate clotting
44
fibrinolysis
- intact endothelial cells inhibit clotting
| - plasmin can lyse fibrin and dissolve clots
45
thrombus
an abnormal mass of clotted blood attached to the wall of a blood vessel
46
embolus
an abnormal mass of clotted blood or foreign matter moving freely in the circulation
47
infarct
localized area of ischemia or necrosis due to a thrombus or embolus
48
types of thrombi based on location
- intramural thrombi
- vavlular thrombi
- arterial thrombi
- venous thrombi
- microvascular thrombi
49
intramural thrombi
attached to the endocardium of the heart and usually overlying a myocardial infarct
50
valvular thrombi
small fibrinous thrombi on the heart valves
51
arterial thrombi
attached to an arterial wall and usually seen associated with atherosclerotic disease
52
venous thrombi
usually found in dilated veins (varicose veins)
| -long-standing venous thrombi become organized with scar tissue and may appear similar to thrombophlebitis
53
microvascular thrombi
found in arterioles, capillaries, and venues
| -typical of DIC (Disseminated Intravascular Coagulopathy)
54
Fate of small thrombi
most are lysed without consequences (normal fx of plasmin)
55
fate of larger thrombi
- remain attached, completely or partially blocking blood flow
- with time, inflammatory cells invade the clot and it develops characteristics of granulation tissue and becomes even more firmly attached
- the inflammatory cells grade the fibrin, leaving the collagenous fibrous tissue
- recanalization
- all or part of the thrombi may break off and become an emboli, which then starts to circulate
56
recanalization
blood again flows through previously obstructed lumen
57
thrombi may:
- narrow the lumen of blood vessels and reduce blood flow (results in ischemia and therefore reduced organ function)
- occlude the lumen of the blood vessel (arterial occlusion causes hypoxia, coronary artery occlusion by thrombi is the most common cause of myocardial infarctions
- serve as a source of emboli
58
types of embolism
- thromboemboli
- liquid emboli
- gaseous emboli
- solid particle emboli
59
thromboemboli
fragments of thrombi
60
liquid emboli
includes fat emboli and amniotic fluid emboli
61
gaseous emboli
air embolism from air injected into veins or in divers
62
solid particle emboli
cholesterol crystals, tumor cells, foreign bodies
63
clinical significance of emboli
- all emboli can occult blood vessels
- thromboemboli account for most emboli
- classification based of the types of vessels:
* venous emboli
* arterial emboli
64
venous emboli classification
typically lodge in pulmonary arteries and their branches
65
arterial emboli classification
originate in the left heart or in the arterial system and are an important cause of ischemia in various organs
66
pulmonary embolism
- PE
- usually originate in veins of the legs, travel into the right side of heart and then into the pulmonary arteries
- may be fatal by causing acute anoxia if they block a main pulmonary artery
- cause pulmonary infarcts if they lodge in smaller branches
67
Arterial emboli
- mechanically fragmented due to disruption of fast arterial flow
- lodge in medium-sized or small arteries
- locations:
* cerebral circulation (stroke, CVA)
* spleen - functionally unimportant (spleen has enough other vascular paths
* kidneys - hematuria
* intestinal - can be a major surgical emergency
* coronary arteries - myocardial infarction
68
Infarction
- an acute onset of insufficient blood supply, due to thrombi or emboli that results in an area of ischemic necrosis
- often triangular in shape representing area of tissue supplied by that vessel
- gross appearance of infarcts:
* mottled infarct - when blood from collateral circulation reached an infarcted area within a few days
69
White infarct
typical of arterial occlusion in solid organs
70
red infarct
typical of venous obstruction (esp. intestines or testes)
71
the fate of infarcts
- tissues composed of post-mitotic cells:
* repaired by replacement of damaged cells with fibrous (scar) tissue
* heart - myocardial fibrosis (scarring)
* brain- liquefactive necrosis
- tissues composed of mitotic cells
* heal with relatively few residual effects (unless very large)
* e.g liver, spleen
72
septic infarcts
- have to be surgically debrided
- caused by infected thrombi or emboli
- show signs of inflammation
- may transform into an abscess
- heal poorly due to inadequate blood supply
73
perfusion
blood supply
74
hypoperfusion
ischemia (decreased blood supply)
75
Shock
- shock is a state of hypoperfusion
- three possible mechanisms:
* cardiogenic shock
* hypovolemic shock
* hypotonic shock
- all three types lead to:
* collapse of circulation, resulting in anoxia and multiple organ failure
76
Cardiogenic shock
- CHF: congestive heart failure
- pump failure of the heart, usually secondary to an infarction or CHF
- infarction destroys area of myocardium
- also: myocarditis, valvular heart disease, conduction block or arrhythmia.
77
Hypovolemic shock
massive hemorrhage, water loss due to burns, vomiting, diarrhea
78
Hypotonic shock
- due to loss of vascular tone and the pooling of blood in dilated peripheral blood vessels
* not enough blood in the body to fill all capillaries at one time!
- occurs in:
* anaphylactic shock- allergic reaction
* neurogenic shock- pain caused by trauma
* septic shock- bacterial endotoxins
Pathophysiology
flashcards
Decks in class (11)
# Cards
-
Quiz 187
-
Biology of Cancer (Quiz 2)90
-
Normal Immunology46
-
Alterations of the Immune system35
-
Autoimmune24
-
Inflammation57
-
Week 7 Quiz (Wound healing and alt. of Hematologic fx)57
-
Hematologic Alterations Cont.78
-
Alterations of cardiovascular function50
-
alterations of cardiovascular fx for week 1046
-
alterations of the heart for week 1016
