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Pathophysiology Taylor > Exam #3, Quiz 1 > Flashcards

Exam #3, Quiz 1 Flashcards

1
Q

What does cells primarily reply on?

A

Oxygen

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2
Q

What is the normal body pH?

A

7.35-7.45

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3
Q

What are the four primary functions of blood? x4

A
  1. Transport oxygen and nutrients to all tissues
  2. Remove wastage products of cellular metabolism?
  3. Active in the bod’s defenses/ immune system
  4. Help maintain body homeostasis
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4
Q

What are the two separate circulatory systems and what does each do?

A
  1. Pulmonary circulation: allows the exchange of oxygen and carbon dioxide in the lungs
  2. Systemic circulation provides for the exchange of nutrients and waste between the blood ad the cells throughout the body
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5
Q

What do arteries do?

A

Transport blood back to the heart.

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6
Q

Blood flows

A

Arteries -> Arterioles -> Capillaries -> Venules -> Veins _> back to the heart -> lungs

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7
Q

What is in the larger veins that help push blood towards the heart

A

Valves

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8
Q

Why does blood flow in the wrings depend on?

A

Skeletal muscle action, respiratory movements, and gravity

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9
Q

What are the three layers of walls of arteries and veins made of?

A
  1. Inner layer: tunica intima, an endothelial layer
  2. Middle layer: Tunica media, a layer of smooth muscle that controls the diameter of lumen size (diameter) of the blood vessels
  3. Outer layer: tunica adventitious, or external, connective tissue later that contains elastic and collagen fibers

Capillary walls have a single endothelial later allows for easier transport into tissues

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10
Q

What is hematocrit levels and what do they do?

A

Number of cells in the blood

Proportion of cells in blood
Viscosity, thickness, of blood
Males average 42-52%
Females averages 37-48%
Elevated HCT- Dehydration of excess cells
Decrease HCT- blood loss or anemia

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11
Q

What is plasma?

A

Yellowish fluid remaining after cells are removed

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12
Q

What is plasma protein?

A

Albumin- maintains osmotic pressure. (Keeps fluid where its suppose to be)

Globulins and antibodies- immune response

Fibrinogen- clotting

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13
Q

Where do blood cells originate?

A

Red bone marrow

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14
Q

What are myeloid stem cells?

A

Precursors for RBCs, platelets, and granulocytes (Eosinophils, Basophils, and Neutrophils)

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15
Q

What are Lymphoid stem cells?

A

Precursors for B lymphocytes, T lymphocytes, and natural killer cells

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16
Q

What is erythropoietin?

A

From the kidneys stimulates erythrocytes, rbc production. (Hematopoisesis) in response to tissue hypoxia

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17
Q

What does adequate RBC production and maturation depend on?

A

Amino acids, iron, Vitamin B12 and B6, Folic acid

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18
Q

When does hemoglobin become fully saturated?

A

With oxygen in the lungs

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19
Q

What color is oxyhemoglobin?

A

Bright red

Also is a good indicator for distinguishing the difference from arterial blood from venous blood

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20
Q

What happens as blood circulates through the body?

A

Oxygen dissociates from hemoglobin to enter tissues

Deoxygenated blood is dark blush’s red in color
Found in venous blood

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21
Q

What can oxygen easily be displaced from hemoglobin by?

A

Carbon monoxide, which binds tightly to the iron in place of oxygen, causing a fatal hypoxia, takes all four oxygen receptor sites

CO2 Poisoning can be recognized by the bright cherry red color in the lips and face

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22
Q

What is hemolysis of erythrocytes?

A

Excessive hemolysis or deconstruction of RBCs, as with hemolytic anemias, may cause elevated serum bilirubin levels&raquo_space;> jaundice

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23
Q

What is leukopoiesis?

A

The production of WBCs, it is stimulated by colony stimulating CSFs produced by cells such as macrophages and T lymphocytes

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24
Q

What are lymphocytes? (B and T cells)

A

Immune response

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25
Q

What are neutrophils?

A

First responders to tissue damage

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26
Q

What are immature neutrophils called?

A

Band, immature

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27
Q

What does bands do? Also what is the phrase we use when we indicate this?

A

Often increase in number in response to bacterial infection

Shift to the left (shift as in bands)

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28
Q

What are basophils?

A

Become mast cells that release histamine

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29
Q

What are eosinophils?

A

Active in allergic reactions and parasitic infections: asthmatics

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30
Q

What are monocytes?

A

Become macrophages active in phagocytosis

Also known as pac man cells

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31
Q

What are the three steps in hemostasis?

(Thrombocytes, platelets, essential part of the blood clotting process)

A
  1. Immediate response of a blood vessel to injury is vasoconstriction or vascular spasm
  2. Thrombocytes, platelets, adhere to the underlying tissue at the site of injury and can form a platelet plug in the vessel if its small
  3. It its a larger vessel, platelets can trigger the clotting, coagulation cascade.
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32
Q

Where are clotting factors produced primarily?

A

Liver

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33
Q

What is Vitamin K required for?

A

Synthesis of most clotting factors, especially prothrombin

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34
Q

Calcium

A

Also essential in the clotting factor

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35
Q

What helps with the clotting cascade?

A

Applying pressure, cold application, or thrombin solution can help speed up clotting

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36
Q

What happens if you have liver issues with the clotting cascade?

A

No clotting, increase bruising

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37
Q

Human Blood Clotting: Chart

A

Starts:
Damage blood vessel: injury to vessel lining triggers the release of clotting factors
->
Clotting Factors
->
Prothrombin ->Thrombin. -> Fibrinogen (soluble). -> Fibrin. (Insoluble) ->
1. Activated platelet: Formation of platelet plug, vasoconstriction limits blood flow and platelets form a sticky blue
2. Fibrin Strand - Blood Clot: Development of Clot: Fibrin strands adhere to the lug to form an insoluble clot

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38
Q

What are blood types determined by potencies of?

A

Specific antigens on surface of RBCs

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39
Q

What blood type is the universal donor?

A

Type O-

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40
Q

What blood type is the universal recipient?

A

AB

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41
Q

What is important about an RH factor?

A

May cause blood incompatibility in the mother if RH negative and the fetus us RH positive

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42
Q

Why can plasma be administered without risk of a reaction?

A

Because it does not have antigens or antibodies?

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43
Q

What are transfusion reactions, clinical manifestations?

A

Base line vitals, always needed

Feeling of warmth in that involved vein, flushed face, headache, fever and chills, pain in the chest and abdomen, decrease blood pressure, rapid pulse

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44
Q

What is a CBC?

A

Overall cell count

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45
Q

What is a CBC with differential?

A

Closed look at percentages f the different EBCs; can help identify diagnosis— separate all cells out

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46
Q

What is a blood smear?

A

Looks at cell structures (anemias), cell shape, size, and color

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47
Q

What is hemoglobin and hematocrit anemias?

A

Low hemoglobin enemia

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48
Q

What is reticulocyte?

A

Immature RBC Production, sickle cell

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49
Q

What is bone marrow aspiration and biopsy?

A

Bone marrow function, cancer test

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50
Q

What are serum levels?

A

Iron, Vitamin B12, folic acid, glucose

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51
Q

What is a PTT, INR?

A

Coagulation indicators, coagulation - warfarin/cumiden

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52
Q

What are the four treatments for low cell count?

A
  1. Whole blood, Packed RBCS, Platelets- replace cells or platelets
  2. Plasma products or colloid infusions-expand volume and balance osmotic pressure
  3. Epoetin (made in kidneys) - simulates production of red bloodcells: sympathetic eurothropostein
  4. Bone marrow or stem cell transplants treatment of some cancers and immunodeficiencies specialties
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53
Q

What is reduced oxygen supple due to decreased hemoglobin?

A

ANEMIAS

54
Q

General caused of anemia X4

A

Blood loss
Decreased Erythrocyte RBC production
Increased erythrocyte destruction
Deficiency of necessary components

55
Q

What are some etiologies and risk factors of anemia? X6

A

Blood Loss: Trauma, heavy periods, gi bleeds, surgical
Rapid Metabolic Activity: pregnancy, adolescence, infection
Increased hemolysis: Sickle cell, autoimmune disorders
Inadequate dietary intake or metabolism: iron, vitamin B12, folic acid, crohns, vegans, vegetarians
Bone Marrow Suppression: radiation, chemo
Age: hugger occurrence nutrient deficits, misdiagnosis, GI bleed

56
Q

What are signs and symptoms/ clinical manifestations of anemia?

A

Decreased ph, pallor, fatigue, somnolence, headache, irritability, dyspnea on excretion, cold intolerance, dizziness, syncope fainting, tachycardia, palpitations, nail bed deformities, smooth, sore, bright red tongues, numbness/ tingling in extremities, Vitamin B 12 deficiency, Pain and hypoxia

57
Q

What are the four anemia specific labs, and what does each do?

A
  1. Mean Corpuscular Volume (MCV): Size of RBCs normcytic, micro cystic, Micocytic
  2. Mean Corpuscular Hemoglobin MCH: Amount of Hbg in RBCs: Normochromic RBC vs. Hypochromic RBS Pale
  3. Mean Corpuscular Hbg Concentration MCHC: Hbg amount relative to size of cell
  4. Iron Studies: Total iron binding TIBC- Indirect measurement of transferrin- binds with iron and transports it for storage. Ferritin- total iron stores in body
58
Q

4 different type of non specific anemia labs

A
  1. Hemoglobin electrophoresis: separates normal Hbg from abnormal, used in diagnosis in of sickle cell thalassemia
  2. Sickle cell test: Evaluates suckling of RBCs when decreased oxygen present
  3. Schilling Test: Measures vitamin B12 absorption with and without intrinsic factor (used to differentiate between malabsorption and pernicious anemia)
  4. Bone marrow aspiration: Diagnosis of aplastic anemia
59
Q

What is iron deficiency anemia?

A

Not enough iron in to make Hbg&raquo_space; less O2 transported in blood

Usually an underlying problem accompanies

Microlytic, hypochromic RBCs = pregnancy/. Breast feeding

60
Q

Etiology of iron deficiency anemia

A

Low dietary intake: especially during growth spurts and pregnancy

Chronic blood lose (ulcer hemorrhoids, cancer, excessive menses)

Malabsorption EAT Lagoons, meats, leafy greens

Liver disease, storage of iron

61
Q

Labs off Iron Deficiency Anemia

A

Low H/H
Serum ferritin, serum iron

62
Q

Signs and Symptoms or Iron deficiency Anemia

A

Pallor, fatigue, lethargy, cold intolerance, irritability, brittle hair, spoon shaped/ ridged nails, stomatitis/ glossitis, tachycardia, dyspnea, syncope

63
Q

Management of iron deficiency anemia

A

Treat cause, supplement oral or iV
EDUCATION: Oral stains teeth, Constipation and darker stools are commonly seen, take the food, take with vitamin C, helps absorption juice

64
Q

What is pernicious anemia?

A

Vitamin B12 Deficiency
Megaloblastic anemia- very large, immature, nucleated RBCs

65
Q

What is the etiology of pernicious anemia?

A

Deficit of folic acid, B9, OR vitamin B12
- Poor dietary intake, vegans and vegetarians
- Malabsorption disorders
- Folic acid deficiency increases risk for spina bifocals and other neural tube problems

** B12 Injecetions for life

** B9 think Crohns, lack of absorption, folic acid

66
Q

Patho of pernicious anemia

A

Lack of INTRINSIC FACTOR, IF, produced in gastric mucosa which is necessary for absorption

Achlorhydria: atrophy gastric mucosa - less acid production - decrease protein and iron absorption

67
Q

Diagnosis of Pernicious Anemia

A

Schilling test

68
Q

Signs and Symptoms of pernicious Anemia

A

Large, red, sore, or burning tongue BEEFY
GI Upset, nausea and diarrhea
Neurological effects from demyelination of peripheral nerves and spinal cord
Parasthesia: Burning, tingling, numbness
Ataxia: Abnormal gait

69
Q

Management of pernicious anemia

A

Oral supplements to prevent, preg females and vegetarians
Vitamin B12 injections for LIFE to treat

If problem is not absorption, oral, but can stain teeth

70
Q

What is Aplastic Anemia?

A

Impairment of bone marrow&raquo_space; loss of stem cells&raquo_space; pancutopenia ,, Not making stem cells

Unknown cause: idiopathic
TOXINS: radiation, chemicals, chemo
VIRUSES: Hep c
AUTOIMMUNE DISORDERS: lupus

Everything is low: PANCYTOPENTA
RBC&raquo_space; anemia
WBC» recurrent or multiple infections
Platelets» pet hair, bleeding tendencies, hemorrhage

71
Q

What is diagnosis and management of Aplastic Anemia?

A

Diagnosis: CBC, Bone Marrow Biopsy
Management: Treat cause, blood transfusion, bone marrow transplant

72
Q

What is sickle cell anemia?

A

GENETIC
Autosomal Recessive: genetic mutation results in abnormal hemoglobin, Hbg S formation

HOMOZYGOUS: mom and dad both have. Sickle cell disease , HBG is replaced by HBG S
HETEROZYGOUS: sickle cell trait, only occurs with severe hypoxia, got from mom OR dad

HEMOLYTIC Anemia

73
Q

What individuals usually inherit sickle cell?

A

African and middle eastern individuals

74
Q

PATHO OF SICKLE CELL ANEMIA

A

HBG is deprived from O2&raquo_space; Cell Crystallizes ad changes to sickle shape&raquo_space; Damages cell membrane&raquo_space; Hemolysis&raquo_space; short life span

Sickle cell&raquo_space; Occlude blood vessels&raquo_space; increase thrombus formation and infractions in tissue throughout thee body deprived from O2&raquo_space; blood clots, strokes

Increase breakdown of RBC&raquo_space; Jaundice, hyperbilirubinemia, gallstones

Seen in teens and young adults 20s

75
Q

Triggers of sickle cell

A

Dehydration, strenuous activity, high altitudes, illness, infection, exposure to cold

Crisis: Pain, SOB

Keep volume up, ampule space

76
Q

Symptoms of sickle cell and onset in 1 yr old, fetal Hbg fully replaced by HbG

A

ANEMIA - pallor, weakness, tachycardia, SOB
JAUNDICE- gallstones from high bile levels
SPLENOMEGALY- then infarction, resivior infection response
PAINFUL CRISES, ACUTE CHEST SYNDROME
DELATED GROWTH AND DEVELOPMENT
Heart failure
Frequent infections
STROKES AND HEART ATTACKS POSSIBLE

77
Q

Sickle cell diagnosis: trait or disease

A

Hemoglobin electrophoresis, determines trait

78
Q

Management of sickle cell

A

HYDRATION, HIGH VOLUMES KEEP PASSAGES OPEN
HYPOXYUREA
PAIN MANAGEMENT
BLOOD TRANSFUSIONS
BONE MARROW TRANSPLANT
IMMUNIZATIONS UP TO DATE
AVOID TRIGGERS

PCA pumps

79
Q

What is thalassemia?

A

Genetic disorder one or more genders for Hbg are missing or abnormal

Homozygous: mom and dad, thalassemia Major, severe life threatening anemia
Heterozygous: mom OR dad, thalassemia minor, milds of anemia

Less normal hemoglobin made , alpha or beta chains affected
Cell membranes are damaged and easily destroyed
Microcytic hypochromic ( kidney signals) RBCs, increased erythropoietin levels

80
Q

Signs and Symptoms, AND Manifestations of Thalassemia

A

S/S
Delayed Growth and development, hypoxia, decreased activity and released to fatigue
Altered skeletal development: hyperactivity n bone marrow
Heart failure: increased workload

Management:
Blood transfusions
Chelation therapy for excess iron, binds and get out of body

81
Q

Clotting Disorders

A

Bleeding of the guns, nosebleeds
Petechaie, purpura- frequent bruising
Hemarthroses: Blood/ bleeding in the joints
Hemolysis: coughing up blood and Hematemesis: Vomitting up blood
Tarry Stools: gi bleed
Anemia
Feeling faint, anxious, low BP, rapid pulse

82
Q

Potential causes of clotting disorders

A

Low platelet counts — think infection, HIV, large liver/spleen
Chemo, Radiation
Aspirin, NSIAD, Coagulants,,, Peptic ulcers
Liver disease, Vitamin K Deficiency: clotting factors
Genetic Disorders

83
Q

What is Hemophilia A and the S/S?

A

GENETIC: X linked recessive, disorder manifested in males, carried by females
Deficit in Blood factor VIII (8)
S/S
Prolonged bleeding, severe hemorrhaging
Hemarthrosis: bleeding in joint
Blood in all fluids that come out

MALES SHOW S/S

FEMALES: CARRIERS

84
Q

Management of Hemophilia A

A

Management:
Desmopressin: stimulates release of stored factor 8

Replacement factor 8 infusions: periodic before procedures that could cause bleeding

85
Q

Von Willenbrand Disease Cause, S/S, Management

A

Hereditary deficiency of von willer and factor: clotting factors&raquo_space; help platelets clump, not aggregating platelets

S/S similar to hemophilia A but MILDER
Easy bruising

Management:
Desmopressin, Replacement Therapy

Not sex linking

86
Q

What is Disseminated intravascular Coagulation DIC and the Etiologu

A

Both excessive bleeding and excessive clotting: uses up clotting factors and platelets which stimulates fibrinolytic process thereby causing bleeding and severe hemorrhage

Etiology: OB Complications, Infection, sepsis, Carcinomas, Major trauma

CAN BE LIFE THREATENING

87
Q

S/s and Management of Disseminated Intravascular Coagulation DIC

A

S/S: Clotting or hemorrhage flip flop
Petechiae, bruising, purpura
Mucosal bleeding, hematocrit, low BP, Shock, Infarcts.

Management: Acute
1. Focus on the most pressing concer at the time be it bleeding or blood clots antiiicoagulants vs blood products
2. Ultimately must treat causes to resolve

88
Q

What is Thrombophilia: S/S and management

A

Not genetic
Group of inherited or acquired (sedentary, immobility, smoking, postop, estrogen products) disorders

Increase the risk of developing abnormal clots in the veins/ arteries
Increase risk for dvt, pe, pvd, mi, stroke

S/S: Depends on clot area

Management:
Treat cause for acquired thrombophilia
Anticoagulants, Coumadin

89
Q

What is Polycythemia? Primary and Secondary

A

Increased production of erythrocytes in bone marrow

Primary: Polycythemia Vera- no idea why, cancer, neoplastic disorder involving overproduction of RBCs

Secondary Polycythemia: Compensation mechanism. > increase O2 transport Chronic lung Disease or Heart disease or from living in high altitudes
Prolonged hypoxia: COPD or Heart Disease
Increased erythropoietin secretion, renal carcinoma

90
Q

Polycythemia: Increased blood viscosity and volume

A

Blood vessels are distended and blood flow is sluggish leading to frequent thromboses and infarctions

HTN, Cardiomegaly

Spleen and liver are congested and enlarged: resivors

Bone marrow is hyper cellular

Increase hemo, thick sludgey. blood viscosity
Overload of RBC, JDV.

91
Q

What is leukemia?

A

Cells made in bone marrow lack of platelets suppress any other type of cell production, enmity, lack of RBC, Thrombocytopenia, lack of platelets, poor response to infection

NO TUMOR, cancer is in WBC and RBC, Increase in WBC = non functional, increase bruising and bleeding

92
Q

How do kids respond to Leukemia

A

WELL in Treatment

93
Q

Leukemia overview more in detailed

A

Neoplastic disorders involving WBCs; no solid tumor, crowd out bone marrow = bone pain

One or more of the leukocytes types are present as undifferentiated, immatured bonfunction cells that multiply uncontrollably in bone marrow
Pain
Suppress production of other normal cells leading to anemia, thrombocytopenia and a lack of normal functional leukocytes

94
Q

Acute Vs. Chronic Leukemia classification

A

Acute: high proportions of very immature nonfimcytional cells, blast cells, in the bone marrow and peripheral circulation
Onset is usually abrupt
Marked signs and complications

Chronic: higher proportions of mature cells, although they have reduced function
Insidious onset and mild signs
Better prognosis

95
Q

Cell Type and Age onset for Acute lymphocytic leukemia, ALL

A

Cell type: B lymphocytes

Age onset: young children

96
Q

Acute Myelogenous Leukemia AML Cell Type and Age onset for

A

Cell type: Granulocytic stem cells

Age onset: Adults

97
Q

Chronic lymphocytic leukemia CLL Cell Type and Age onset for

A

Cell Type: B lymphocytes

Age onset: Adults >50

98
Q

Chronic Myelogenous leukemia CML Cell Type and Age onset for

A

Cell Type: Granulocytic stem cells…. Specialized WBC

Age Onset: Adults 30-50

99
Q

Signs and Symptoms of leukemia

A

Multiple infections
Severe hemorrhage - thrombocytopenia
Anemia - fatigue
Bone Pain
Weight loss, fatigueHypermetabolism
Lymph nodes, spleen and liver are often enlarged and cause discomfort

100
Q

Diagnosis and Management of Leukemia

A

Diagnosis: Peripheral blood smears and Bone marrow Biopsy

Management: Chemo and Bone marrow transplants

Acute: more abrupt onset, kids
Chronic: gradual symptom onset

101
Q

Four main functions of the lymphatic system

A
  1. Return excess interstitial fluid and protein to the blood
  2. Filter and destroy unwanted material from the body fluids
  3. Initiate an immune response
  4. Interact with all other body systems
102
Q

Lymphatic structures X5

A

Lymphatic vessels : movement of fluids

Lymphatic Tissue: Protects, line of defense

Lymph Nodes: Immune response of B and T lymphocytes, disappears during infection

Spleen, left side: Defense, Reservoir for bloo

Thymus gland: secretes hormones

103
Q

What is lymph?

A

Clear watery isotonic fluid circulated through the lymphatic vessel

104
Q

What is lymphadenopathy?

A

Inflammation or infection of lymph nodes
Common sign of another disease, viral/ malignancies

105
Q

What is the manifestation as a swollen lymph node?

A

An increase in size and extent over time usually indicates cancer

106
Q

Diagnosis of lymphadenopathy

A

Exam, Ultrasound, Fine Needle Biopsy, PET CT:
We can not usually see or feel metabolic

107
Q

How to treat lymphadenopathy

A

Treat the cause!

108
Q

What are lymphomas?

A

Malignant neoplasms involving lymphocytes proliferation in the lymph nodes.

Cause: higher incidence in adults who received radiation treatments during childhood

109
Q

Hodgkin lymphoma pathology

A

Initially a SINGLE lymph node (often in neck) > spreads to adjacent nodes then organs via lymphatic vessels

Works its way down, orderly

Orderly contagious spread

T lymphocytes defective and the lymphocyte count is decrease - increased R/F recurrent infections
T Cells: Killer vs. helper cells

110
Q

Diagnosis of Hodgkin lymphoma?

A

DX Marker - Reedsternberg cells
Ann Arabor staging system

111
Q

Signs and Symptoms of Hodgkin lymphoma

A

1ST Sign: enlarged lymph NODE often cervical, that is painless and no tender
Spleenomegaly
Other enlarged lymph nodes
General cancer signs
Fatigue
Weight loss
Anorexia

112
Q

Treatment for Hodgkin lymphoma

A

Radiation, Chem, Surgery

113
Q

What is non Hodgkin lymphoma

A

Tends to be more widespread that Hodgkin lymphoma

More lymph nodes involved

Unorganized widespread metastasis

Extranodal involvement common : growth outside the lymph nodes

No Reee Sternberg cells

Most cases involve B Lymphocytes

114
Q

Age affected with non Hodgkin lymphoma

A

Over 60

115
Q

What are the signs and symptoms of Hodgkin lymphoma

A

Same as Hodgkin lymphoma

Usually seen more frequently in patients with HIIV

1ST symptom enlarged painless lymph node

116
Q

Treatment of non Hodgkin lymphoma

A

Difficult to treat due to widepresad metastates and extranodal involvement

Less responsive to treatment

Radiation, Chemo, Surgery

117
Q

What is multiple myeloma

A

Malignancy involving plasma cells (mature B lymphocytes involved in production of antibodies

Increased number if malignant plasma cells replace the bone marrow and erode the bone

Blood cell and antibody production is impaired

118
Q

What does multiple myeloma do?

A

Multiple tumors with bone destruction develop in vertebrae, pelvis, and sill

Pathological or spontaneous fractures

HYPERCALCEMIA cur as bone is destroyed

119
Q

What type of onset is multiple myeloma ?

A

INSIDIOUS onset, usually well advanced by the time of discovery

120
Q

Manifestations of multiple myeloma

A

Frequent infections
Pain related to bone involvement, present at rest and with activity
Pathological fractures
Anemia and bleeding tendencies because bone marrow is impaired not making platelets, wbcs, RBcs
Protenuria and kidney failures

121
Q

Management of multiple myeloma

A

CHemo
Supportive care
Analgesics for bone pain

122
Q

What is lymphedema?

A

Tissue in the extremities sell due to obstruction of lymphatic vessel and accumulation of lymph

123
Q

Etiology of lymphedema

A

Primary lymphedema’s congenital
Secondary- due to cancer, tumor, radiation therapy, damage during surgery, remove of lymph nodes

124
Q

Manifestations of lymphedema

A

Swelling, initially soft but progresses to firm, painful, and unresponsive to treatment

Increase risk for frequent infections

125
Q

Management of lymphedema

A

Bed rest, massage, elevation

126
Q

What is elephantiasis?

A

Form of lymphedema resulting from infestation and blockage of lymph vessels by a parasitic worm (filaria)

127
Q

Why is extreme swelling so significant

A

Causes extremity to look like an elephants leg

128
Q

S/S. Of elephantiasis

A

Thickening of subcutaneous tissue, frequent infections, skin ulceration ,fever

129
Q

Management of elephantiasis

A

Skin care and elevation
Antiparasitic drugs
Surgeries for shunt

130
Q

What is castleman disease?

A

Lymphoproliferation disorder, not cancer — overgrowth of lymphoid tissue

Associated with higher risk for cancers, such as lymphoma

Unicentric — affects. ONE LYMPH NODE
S/S: Depnds on location - large lump, difficulty breathing or eating, weight losss poor appetite cough
T/x: REMOVE STHE NOSE OF POSSIBLE/ IF NOT STEROIDS OR RADIATION TO SHRINK OR DESTROY THE NODE

Multicentric. — affects multiple lymph nodes decreases immune response
S/S: more systemic, fever night sweats N/X weight loss weakness spleomegaly heaptomeaglay
T/X: more difficult, too many odes to remove meds steroids anti cancer immuomadulating

Pathophysiology Taylor (5 decks)

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