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pathophysiology > MOD 5 Hematologic System > Flashcards

MOD 5 Hematologic System Flashcards

1
Q

Bone Marrow creates

A

The bone marrow stem cells differentiate into:
Red blood cell (erythrocytes)
White blood cell (leukocytes)
Platelet (thrombocytes)

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2
Q

CBC lab test do what

A

CBC lab test is a panel of tests that evaluates the red blood cells, white blood cells and platelets

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3
Q

RBC normal value

A

3.6-5.4

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4
Q

Hematocrit count

A

37-50%

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5
Q

Hemoglobin count

A

12-16.5

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6
Q

WBC

A

5,000-10,000

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7
Q

Neutrophil count

A

47-63%

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8
Q

Lymphocytes count

A

24-40%

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9
Q

Platelet count

A

150,000-400,000

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10
Q

CBC (complete blood count)

A

Helps diagnose conditions, such as anemia, infection, inflammation, bleeding disorder, or leukemia
Monitor the condition and or effectiveness of treatment after a diagnosis is established
Monitor treatment that is known to affect blood cells, such as chemotherapy or radiation

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11
Q

RBC

A

red blood cell count, a count of the actually number of RBC’s in a person’s sample of blood

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12
Q

Hematocrit

A

measures the percentage of a person’s blood that consists of red blood cells

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13
Q

Critically low HCT

A

<15% leads to heart failure
*Fluid Overload

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13
Q

Low HCT means what

A

The patient is losing blood (either internally or externally)

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14
Q

Critically high HCT

A

> 60% leads to blood clotting problems
caused by *dehydration

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15
Q

HCT is affected by what

A

the person’s fluid status

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16
Q

HCT is used to asses what

A

a person’s fluid status and how well they are responding to fluid replacement treatment

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17
Q

What test is HCT ordered with

A

HCT is often ordered with a hemoglobin test (H&H) to verify the accuracy of the HCT if BOTH the Hct and Hgb are decreased = blood loss

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18
Q

Hemoglobin measures what

A

The *amount of oxygen-carrying protein in the blood. Measured in grams.

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19
Q

Reticulocyte count measures what

A

The absolute count or percentage of *immature red blood cells in blood (if elevated it means that mature RBCs are depleted and the body is now relying on immature RBC’s

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20
Q

Red Blood cells indices are what

A

Calculations that provide information on the physical characteristics of the RBC’s (MCV, MCH, MCHC, RDW) RBC indices lab tests are used to determine if a person has anemia
-used to diagnose types of anemia

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21
Q

MCV

A

mean corpuscular volume (measurement of the average size of RBC’s

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22
Q

MCH

A

Mean corpuscular hemoglobin (calculation of the average amount of oxygen-carrying hemoglobin inside a red blood cell)

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23
Q

MCHC

A

Mean corpuscular hemoglobin concentration (calculation fo the average percentage of hemoglobin inside a red cell)

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24
Q

RDW

A

Red cell distribution width (calculation of the variation in the size of RBCs)

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25
Q

Red Blood cell count is ELEVATED in the following conditions (polycythemia)

A

Cardiovascular disease
stress
polycythemia
smokers
high altitude
hemoconcentration and dehydration
renal cell carcinoma

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26
Q

Red Blood cell count is DECREASED in the following conditions (anemia)

A

ANEMIAS
HEMORRHAGE
hemolysis
chronic renal failure
failure of marrow production

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27
Q

Anemia

A

NOT ENOUGH RBC’s

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28
Q

Clinical manifestations common to ALL anemias

A

Low hemoglobin and hematocrit levels in addition to reduced RBC’s
Plasma expansion “watery” blood, i.e., less viscous blood. This causes more turbulent blood flow, and “pale” look of blood

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29
Q

Test anemia by

A

checking inside of person’s mouth for pale colored mucosa and gums

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30
Q

S/S of anemia are a result of what

A

HYPOXIA (low oxygen levels in blood)
Causes:
Fatigue
tachypnea
tachycardia
pallor

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31
Q

Causes of anemia

A

blood loss
excessive RBC destruction
Decreased or faulty RBC production
decreased or faulty RBCs

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32
Q

Anemia due to blood loss

A

gastrointestinal (GI) conditions, upper or lower GI bleeds
NSAID overuse (risk factor; patients with chronic pain)
Excessive menstruation or childbirth complications

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33
Q

Anemia due to excessive RBC destruction

A

Hemolytic Anemias
RBCs die quicker than the bone marrow can replace them. Causes intrinsic (inherited defective RBCs) or Extrinsic (everything else)
-inherited: sickle cell and thalassemia
-stressors: infections drugs snake or spider venom
-toxins: advanced liver or kidney disease
-autoimmune: antibody-mediated lupus cancer rh fact or drugs.
-Spleen: blood moves more slowly through an enlarged spleen, causing RBCs to become prematurely destroyed before they get through the spleen

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34
Q

Decreased or faulty RBC production

A

-Nutritional Deficiencies: Iron, Vitamin B-12, and folate are necessary components of RBC production
-Bone marrow and stem cell problems: leukemia and lymphoma are examples. Also, aplastic anemia*
-Sickle cell anemia

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35
Q

Other conditions associated with decreased or faulty RBCs

A

Advanced kidney disease
-Hypothyroidism: cause lowered iron levels in the blood
-Chronic diseases: inflammation causes production of cytokines that then destroy all blood cells including erythrocytes

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36
Q

Kidney Connection

A

Erythropoietin (made in kidneys) signals bone marrow to make ore RBCs so if kidneys are damaged erythropoietin is not excreted and RBCs are not made

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37
Q

Erythropoietin injections

A

Given to patients with severe anemia caused by kidney failure or bone marrow failure
These injections increase RBC production and may eliminate the need for a blood transfusion

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38
Q

Three vitamins/minerals required to produce RBCs

A

Iron, Vitamin B-12, Folate

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39
Q

Iron deficiencies caused by

A

lack of iron in diet or blood loss
Examples:
-metabolic demands of pregnancy and breastfeeding
-blood loss through excessive menstruation, childbirth, or blood
-digestive conditions (crohn’s) Or removal of stomach/ small intestines
-medications, excess caffeine

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40
Q

S/S of iron deficiency anemia

A

“lightheaded”, dizzy, stomatitis, difficulty swallowing, headache, confusion, memory loss

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41
Q

Iron replacement

A

Mineral supplements/ iron injections; foods - soybeans, lentils and beans, red meat, chicken, fish, fortified foods

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42
Q

Cobalamin

A

(vitamin B-12) is a necessary vitamin required to make RBCs

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43
Q

Low Vitamin B-12 levels caused by

A

Dietary: eating little or no meat may cause a lack of B-12
Lack of intrinsic factor: Intrinsic factor (protein excreted by the stomach) is needed for vitamin b12 absorption. if the stomach/upper intestine is damaged or removed, the intrinsic factor is not secreted, so there is no absorption of vit b-12.
a) conditions causing lack of IF are Crohn’s disease, gastric bypass, cancer
b) lifelong b12 replacement injections*

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44
Q

Folate Vit-B-9

A

Also called folic acid, this key element is an integral part of cell growth, especially RBCs.

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45
Q

Low folate levels are caused by

A

1- overcooking or eating too few vegetables may cause folate deficiency
2- other: pregnancy, medications, alcohol abuse, intestinal disease

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46
Q

Aplastic Anemia

A

destruction of bone marrow stem cells. Damaged BM is diagnosed as either aplastic or hypoplastic. causes pancytopenia = ALL blood cells are depressed

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47
Q

Aplastic

A

meaning that its empty

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48
Q

Hypoplastic

A

Contains very few blood cells

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49
Q

Aplastic Anemia develops because

A

of bone marrow damage. the damage may be present at birth or occur after exposure to radiation, chemotherapy, autoimmune disease, toxic chemicals, some drugs, or infection

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50
Q

Viruses linked to aplastic anemia

A

hepatitis, epstein barr, cytomegalovirus, parovirus B19 and HIV

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51
Q

S/S of Aplastic Anemia

A

may develop slowly or suddenly
-fatigue and rapid heart rate (due to low RBCs)
-frequent infections (due to low WBCs)
-Bleeding tendencies (due to low platelets) as evidenced by bleeding gums/nose bleeds/ petechiae, easy bruising, heavy, menstrual cycle, G.I. bleeding, etc.

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52
Q

Treatment for Aplastic anemia

A

Medications, blood transfusions, and stem-cell transplants

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53
Q

Sickle Cell anemia

A

An autosomal recessive defect of hemoglobin
is the most common inherited blood disorder in the US. Individuals with a single defective gene have sickle cell “trait” while those with 2 defective genes have sickle cell “disease”

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54
Q

treatment options for sickle cell anemia

A

There are several drug therapies and bone marrow transplants available (with complications of rejection i.e. septicemia or host vs graft disease)

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55
Q

3 types of sickle cell crisis can occur

A

Vaso-occlusive
Sequestration
aplastic

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56
Q

Vaso-occluisve

A

Occurs when the SICKLED RED BLOOD cells trigger the formation of blood cloths within circulation. Tissue damage is minor and can resolve within a week DEHYDRATION AND INFECTION are an initiating
cause: Stroke, pulmonary infarction, myocardial infarction, gangrene

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57
Q

Sequestration

A

When the sickled red blood cells are removed from the general circulation by the spleen the severity depends on the amount o f blood removed and held in the spleen and liver thereby reducing the amount of circulating red blood cells. CAN PRODUCE HYPOVOLEMIA SHOCK.

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58
Q

Aplastic

A

caused by exhaustion of the bone marrow. Erythropoiesis cannot keep up with the constant need to replace red blood cells. SICKLED RED BLOOD CELLS HAVE A LIFESPAN OF 10-20 DAYS this constant stress on bone marrow stem cells can eventually lead to bone marrow failure

59
Q

Treatment for sickle cell crisis

A

Give OXYGEN (to relieve hypoxia)
IV FLUIDS (to treat dehydration and prevent sickle cells sticking together)
PAIN MEDS (patient will develop painful clotting throughout the body and go into shock)

60
Q

SC crisis

A

Considered physiological and not psychosocial on NCLEX

61
Q

ABC priorities sickle cell crisis

A

Circulation issue

62
Q

Polycythemia

A

too many RBC’s
opposite of anemia can cause hyperviscosity or thrombosis

63
Q

Primary polycythemia

A

absolute
polycythemia vera is an INHERITED condition affecting primarily Caucasians with European Jewish ancestry. The onset of S/S could occur at any age but usually over 60 years. Mostly men

64
Q

Secondary polycythemia

A

Relative
physiologic response to CHRONIC HYPOXIA that triggers the body to make more RBCs for oxygen transport in an effort to get more oxygen to the cells of the body

65
Q

Cause of polycythemia

A

Sleep Apnea
COPD
Heart Failure
Pulmonary Disease
High Altitude
EPO (erythropoietin) shots

66
Q

Sleep apnea and polycythemia

A

due to either obstructive sleep apnea or central sleep apnea (the brain does not signal the lungs to breathe). Both types result in oxygen deprivation

67
Q

COPD and polycythemia

A

Chronic obstructive pulmonary disease (asthma and emphysema) that hamper gas exchange in the lungs

68
Q

Heart failure and polycythemia

A

reduces tissue profusion, which create hypoxic tissue even if the blood volume and concentrations are normal. The low oxygenation will trigger an increase in production of RBCs

69
Q

Pulmonary disease

A

gas exchange between lungs and vasculature may be impaired. The decrease in O2 exchange will produce hypoxia and trigger an increase in production of RBCs

70
Q

High altitude

A

body compensates for lower O2 levels at higher altitudes by making more RBCs to carry oxygen. Takes 6-8 weeks to build up enough erythrocytes

71
Q

EPO

A

EX: blood doping by athletes for performance enhancement or who abuse anabolic steroids

72
Q

S/S of polycythemia

A

caused by reduced blood flow of viscous blood and clotting- PLETHORA: RUDDY COMPLEXION; FATIGUE; DIZZINESS; HEADACHE. Thick blood increases the workload on the heart and leads to High blood pressure which leads to decreased perfusion to the brain due to sluggish blood flow of thick blood

73
Q

Treatment for polycythemia

A

periodic phlebotomy i.e. blood letting to siphon off some excess blood also O2

CPAP

aspirin to prevent blood clotting.

radioactive phosphate also used

74
Q

Total WBC

A

5,000-10,000

75
Q

Neutrophil count

A

47-63%

76
Q

Lymphocyte count

A

24-40%

77
Q

Associated organs with leukocytes

A

Bone marrow
thymus
spleens

78
Q

White blood cell differential

A

Identifies counts the number of the varioius types of white blood cells present.
neutrophils
lymphocytes
monocytes
eosinophils
basophils

79
Q

Elevated white blood cell count

A

leukocytosis
-neutrophils = acute bacterial infection
-lymphocytes = viral infection and or chronic bacterial infection
-eosinophils = allergies or parasitic infection

80
Q

Decreased white blood cell count caused by:

A

leukopenia
-steroids (or medications that contain them aka prednisone)
-chemotherapy
-bone marrow failure (aplastic anemia or cancer such as leukemia)
-use of antiseizure medication such as Tegretol

81
Q

Cancers affecting WBCs

A

Leukemias
lymphomas
multiple myelomas

82
Q

Leukemia is cancer of what

A

cancer of white blood cells

83
Q

Lymphoma is a cancer of what

A

Cancer originating in the lymphatic system

84
Q

Myelomas is a cancer of what

A

cancer that affects the type of B-cell (that make antibodies)

85
Q

Leukemia’s main cause is what

A

malignant growth of lymphocytes leading to overproduction of nonfunctioning white blood cells that grow faster than the functioning cells.

86
Q

how is leukemia classified?

A

speed and progression and the type of cells involved

87
Q

4 main types of leukemia

A

How fast it progresses:
acute leukemia
chronic leukemia

type of blood cell effected:
lymphocytic leukemia
myelogenous leukemia

88
Q

Acute leukemia

A

the abnormal blood cells are immature blood cells (blasts). They can’t carry out their normal functions, and they multiply rapidly, so the disease worsens quickly. Acute leukemia requires aggressive, timely treatment.

89
Q

Chronic Leukemia

A

some produce too many cells and some cause too few cells to be produced.
Chronic leukemia involves more mature blood cells.

These blood cells replicate or accumulate more slowly and can function normally for a period of time.

Some forms of chronic leukemia initially produce no early symptoms and can go unnoticed or undiagnosed for years.

90
Q

Lymphocytic leukemia

A

This type of leukemia affects the lymphoid cells (lymphocytes) which form lymphoid or lymphatic tissue. Lymphatic tissue makes up your immune system.

91
Q

Myelogenous leukemia

A

this type of leukemia affects the myeloid cells. Myeloid cells give rise to red blood cells, white blood cells, and platelet-producing cells.

92
Q

Leukemia S/S

A

fatigue, low fever, night sweats, weight loss

Specific to leukemia:
lymphadenopathy
anemia, infection, bleeding problems
pallor

93
Q

Lymphadenopathy

A

S/S specific to leukemia
swelling lymph nodes. may swell without any other s/s or well in random patterns.

94
Q

Anemia, infection, bleeding problems

A

Specific to leukemia
due to bone marrow damage that affects all blood cells

95
Q

Pallor

A

specific to leukemia
malignant leukocytes crowding the bone marrow and leading to decreased erythrocyte and thrombocyte production (causing pale skin color)

96
Q

Lymphomas

A

Blood cancer that affects the lymphatic system, causes an overproduction of malfunctioning lymphocytes this overload compromises the immune system. Lymphoma can develop in many parts of the body, including lymph nodes, bone marrow, blood, spleen, and other organs

97
Q

There are two main types of lymphoma

A

Hodgkin’s and Non-hodgkin’s

98
Q

Hodgkin’s lymphoma

A

Cell affected: B-cell lymphocytes, REED-STERNBERG CELLS PRESENT

Age of onset: 20-30 years old (more common in younger) and 60-70 years old

Node involvement: cervical, inguinal, axillary, and retroperitoneal

Extra-nodal involvement: uncommon

Symptoms: PAINLESS SWOLLEN LYMPH NODES, WEIGHT LOSS, BONE MARROW DAMAGE (BLOOD DYSCRASIAS)

Curability: 90%

Treatment: RADIATION THERAPY (localized), CHEMOTHERAPY (generalized), IMMUNOTHERAPY (MAB), BONE MARROW (stem cell) TRANSPLANT

99
Q

Non-Hodgkin’s Lymphoma

A

Cell affected: B AND T LYMPHOCYTES

Age of onset: 50 years old (95% are adults)

Node involvement: cervical, axillary, inguinal, femoral

Extra-nodal involvement: common

Symptoms: same as Hodgkin’s plus
pleural effusion, abdominal pain, splenomegaly

Curability: LESS THAN 25%

Treatment: same general treatments as Hodgkin’s disease but specific chemo and drugs are different

100
Q

multiple myelomas

A

MM is a cancer that starts in a type B-cell lymphocyte called plasma cells in the bone marrow. These are protein-making cells which normally make all the different kinds of proteins that comprise the antibodies of the immune system.

101
Q

How are myelomas classified

A

they are classified by the type of immunoglobulin being attacked

102
Q

What happens with MM

A

bone marrow stops making different forms of immunoglobulin and instead starts to produce a single abnormal type of protein referred to as a MONOCLONAL OR M PROTEIN.

Collection of MM cells called plasmacytomas can ERODE THE HARD OUTER SHELL OR CORTEX OF THE BONE that normally surrounds the marrow. causing bone lesions

103
Q

Bone lesions cause what

A

pain and PATHOLOGICAL (SPONTANEOUS) FRACTURES of the bones affected by the cancer.

104
Q

Multiple myeloma signs and symptoms

A

High calcium levels in the blood (hypercalcemia) due to calcium moving from damaged bone into the blood

Renal failure myeloma nephrosis caused by damage to kidneys by paraproteins that cause hyperviscosity of body fluids a distinctive feature of myeloma.

Tumor markers are M-PROTEINS (found in serum) and BENCE-JONES PROTEIN found in urine

Anemia: BM not functioning and kidney not producing Erythropoietin leads to blood dyscrasias

Bone pain: The first symptom, and pathological fractures (occur spontaneously w/o an injury

105
Q

Platelets normal range

A

150,000-400,000

106
Q

Platelets defined as

A

also called thrombocytes
they are CELL FRAGMENTS (NOT CELLS) that are vital for normal blood clotting

107
Q

Associated organs with platelets

A

LIVER
platelet production is regulated by thrombopoietin

108
Q

Low platelet count occurs because

A

The body’s bone marrow doesn’t make enough platelets

the bone marrow makes enough platelets, but the body destroys them or uses them up

the spleen holds on to too many platelets

109
Q

Platelet count increased in what conditions

A

Thrombocytosis

-some cancers
-inflammatory conditions
-birth control pills
-recover phase of trauma/surgery

110
Q

Platelet count is decreased what conditions

A

Thrombocytopenia

-Medications such as aspirin, ibuprofen, and acetaminophen (damages liver leads to bleeding problems)

-“G” herbs (garlic, ginger, ginkoba, ginseng)

-DIC (disseminated intravascular coagulation)

111
Q

S/S of bleeding

A

Hemorrhage- blood leaving the blood vessel (internal or external bleeding)

Menorrhagia- Heavier than normal menstrual bleeding

Epistaxis- bleeding from the nose

112
Q

Petechiae

A

Pinpoint hemorrhages of small capillaries in the skin, conjunctiva of the eyes or mucous membranes

113
Q

Purpura

A

red or purple discolorations on the skin that do not black on applying pressure

114
Q

Ecchymosis

A

blood leaks into tissues under the skin causing bruising

115
Q

Hematoma

A

collection of blood usually clotted, in organs, body spaces or under the skin

116
Q

Causes of thrombocytopenia

A

idiopathic thrombocytopenia purpura - ITP

Thrombotic thrombocytopenia purpura - TTP

Drug-induced Thrombocytopenia

117
Q

idiopathic thrombocytopenia purpura - ITP

A

Autoimmune disorder that causes an IgG antibody to bind with platelets destroying their function. Results in low platelet count and s.s of bleeding

Idiopathic = arising spontaneously or from an obscure or unknown cause

118
Q

Thrombotic thrombocytopenia purpura - TTP

A

thought to be caused by widespread endothelial damage that triggers thrombosis (clots) and platelet destruction due to a lack of activity in the ADAMTS13 enzyme ( a type of protein in the blood)

The ADAMTS13 gene controls the enzyme, which is involved in blood clotting not having enough enzyme activity causes overactive blood clotting

119
Q

S/S of thrombotic thrombocytopenia

A

Fever, hemolytic anemia renal failure neurological decline

120
Q

Drug induced thrombocytopenia

A

a hypersensitivity reaction causes platelet destruction. Heparin can induce a type 3 hypersensitivity reaction that can quickly be resolved after eliminating the drug

121
Q

S/S of thrombocytopenia

A

EPISTAXIS
MENORRHAGIA
PURPURA
BLEEDING GUMS
GI BLEEDS
PETECHIAE

122
Q

Treatment for thrombocytopenia

A

Immunosuppression treatments
plasmapheresis
ELIMINATE THE CAUSATIVE DRUG
PLATELET INFUSION

123
Q

Thrombosis caused by

A

High bp
Low bp
Injured vessel walls
altered blood constituents

124
Q

High blood pressure (thrombosis)

A

blood flow leads to clots developing in arteries due to increased turbulence caused by high blood pressure

this turbulent flow of blood causes damage to vessel walls or blood cells. the resulting inflammation then triggers the clotting

125
Q

Low pressure (thrombosis)

A

leads to cots in the veins due to lower blood pressure and slower flow of blood in veins as compared in arteries - slow blood clots

126
Q

Injured vessel walls (thrombosis)

A

interior of blood vessels can be damaged bu the development of atherosclerotic plaque. DEEP VEIN THROMBI in legs break off to create pulmonary EMBOLI

127
Q

Altered Blood constituents (thrombosis)

A

increased viscosity of blood
Thrombocytosis leads to increased abnormal production of platelets (40% of people with unexplained high platelet count have cancer)

128
Q

Treatment of thrombosis

A

Anti-coagulant drugs

Thrombolytic drugs

acetaminophen

129
Q

Anti-coagulant drugs treating thrombosis

A

reduce the blood cell’s ability to clot. These drugs prevent future clots but have no effect on existing clots

Heparin- injected fast acting and too high of levels causes bleeding problems

Coumadin- oral med- long acting too high of levels causes bleeding tendencies

Aspirin- oral - small does everyday prophylaxis to prevent clotting causes GI bleeding

130
Q

Thrombolytic drugs (treating thrombosis)

A

So-called clot busters these drugs break up or dissolve existing blood clots, which are the main cause of both heart attacks and stroke but do not prevent future clots (EX: TPA, streptokinase)

131
Q

Acetaminophen (treatment thrombosis)

A

Tylenol - Very damaging to the liver

Overdose accidental or intentional are lethal because the liver dies quickly

without a functioning liver, clotting factors are not available to combine with platelets and blood cannot clot.

132
Q

Pertinent lab tests for bleeding problems

A

Bleeding time tests

Blood clot test

133
Q

Bleeding time tests

A

PT AND INR (intentional normalized ratio) are used to test patients on coumadin blood thinning medication PTT test patients on heparin blood thinning medication

134
Q

Blood clot test

A

D-DIMER. Done to determine the extent of clotting in the body and is done for DVT (deep vein thrombosis) P.E. (pulmonary embolism) and DIC (disseminated intravascular coagulopathy)

135
Q

Disseminated Intravascular Coagulopathy

A

DIC is a coagulation disorder that results in both
BLOOD CLOTTING and HEMORRHAGING.

136
Q

DIC is what

A

Not a specific illness, rather it is a complication. It is always secondary to an underlying disorder

137
Q

Definition of DIC

A

DIC is a serious disruption in the body’s clotting mechanism

OVERPRODUCES MANY SMALL BLOOD CLOTS THROUGHOUT THE BODY DEPLETING THE BODY OF CLOTTING FACTORS AND PLATELETS.

THESE SMALL CLOTS ARE DANGEROUS AND CAN INTERFERE WITH THE BLOOD SUPPLY TO ORAGANS, CAUSING DYSFUNCTION AND FAILURE.

THEN MASSIVE BLEEDING CAN OCCUR DUE TO THE BODY’S LACK OF CLOTTING FACTOR AND PLATELETS. DIC IS LIFE-THREATENING AND NEEDS TO BE TREATED PROMPTLY.

138
Q

Inflammatory process activation

A

Coagulation and inflammatory pathways interact in substantial ways. Inflammation gives rise to activation of the clotting cascade and the resultant coagulation stimulates more vigorous inflammatory activity.

139
Q

triggers of inflammatory process activation

A

the chemical mediator CYTOKINE is released when the inflammatory response is triggered. CYTOKINE IS IMPLICATED AS A CAUSATIVE AGENT IN DIC.

140
Q

Triggers to organ failure (DIC)

A

sepsis and septic shock
obstetrics complication
trauma (especially burns and head injury)
Blood transfusions
some cancers
hematologic disease

141
Q

DIC basic definition

A

Increase use of platelets leads to decrease amount of platelets

142
Q

DIC S/s

A

related to either the blood clotting or the hemorrhage phase
Note: BLEEDING FROM AT LEAST 3 UNRELATED SITES IS PARTICULARLY SUGGESTIVE OF DIC

143
Q

Clotting phase of DIC

A

DVT deep vein thrombosis
Renal Failure clots in the kidneys
Difficulty breathing clots in the lungs
Neurologic changes clots in the brain
numbness clots in the spinal cord
Liver dysfunction clots in the liver

144
Q

Hemorrhage phase

A

Blood oozing from an existing IV site
Bleeding gums
GI bleeds
Petechiae/ purpura/ Ecchymosis

145
Q

Treatment of DIC

A

Life support (oxygen n, give fluids/IV meds to maintain blood pressure: probably drug-induced coma)

Treat the underlying cause (i.e. give antibiotics if caused by an infection)

Give heparin (to stop the clotting process)

Platelet transfusions (restore lost platelets)

146
Q

Pertinent Lab tests for DIC

A

Decreased platelet count (less than 100,000) and abnormal D-DImer

pathophysiology (14 decks)

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