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Thrombocytopenia
Too little platelets <100,000
spontaneous bleeding and bruising
Acute (hemorrhage)
Eti:
Rapid loss of blood loss as in hemorrhage caused by trauma, childbirth, or rupture of a major blood vessel or organ
Severe GI bleeding can occur in disorders such as esophageal varices or penetrating peptic ulcer
Patho:
Large numbers of RBCs and plasma volume are lost
Lack of RBCs to carry oxygen causes tissue hypoxia
Fluid lost from bloodstream stimulates sympathetic nervous system, systemic arterial vasoconstriction, fluid shift from tissues into capillaries, stimulation of RAAS, and antidiuretic hormone (ADH) release
all act to increase fluid volume in bloodstream
CM:
Hypotension, tachycardia, tachypnea
Hemoglobinopathy (Sickle Cell)
Etiologies:
Inherited disorder of the structure of the HGB that can lead to destruction of RBC and can’t carry oxygen
Patho:
Under hypoxia, severe stress, infection, or dehydration, the SCA Hgb becomes distorted in shape changing into sickle-cell shape
These abnormal cells have a shortened life span of 10-20 days
Due to being broken down faster by the spleen than the bone marrow can replenish, it leads to hemolytic anemia
Distorted RBCs cannot pass easily through capillaries → become trapped → block blood flow and create obstructions to tissues and organs → cause ischemia and tissue hypoxia → can lead to organ damage and possible infarction
CM:
Fatigue, exercise intolerance
Frequent hemolysis of RBCs → increased heme breakdown in circulation → causes high levels of bilirubin in the bloodstream (hyperbilirubinemia) → jaundice and bile concentration in the gallbladder which can lead to gallstones
Microcytic hypochromic anemia (Iron deficiency anemia)
Low MCV indicates small size of RBCs and low MCHC indicate pale color of RBCs
Increased risk:
women of childbearing age- due to pregnancy, delivery, and breastfeeding use a lot of iron
Infants and children- infants may need more iron because not enough in cows milk & children need extra iron during growth spurts
Vegetarians- Not eating meat so they need to supplement with other iron-rich foods
Elderly adults- poor diet and lack of stomach acid can cause iron deficiency
Individuals with GI bleeding- person with peptic ulcer, esophageal varices, or cancer of GI tract can lose blood in the stool
Patho:
Iron is needed in the diet to synthesize Hgb
Heme portion of Hgb contains iron that carries oxygen atoms
Lack of sufficient iron leads to poor oxygen transport by iron-deficient Hgb molecules
Due to this, the body must used stored iron from ferritin complexes in the reticuloendothelial cells, bone marrow, liver, and spleen
Once circulation transferrin becomes depleted of iron, Hgb synthesis is impaired and iron-deficient erythropoiesis starts to occur
As Hgb synthesis decreases, RBC numbers diminish
RBCs that are synthesized are abnormally small and pale
CM:
Fatigue, weakness, exercise intolerance
Melena
Women may have menorrhagia
Hair loss, cheilitis, glossitis, koilonychias (spoon-shaped nails), and pica (craving for nonfood substances such as ice, clay, starch, chalk, dirt, or other materials)
Cold intolerance and feeling of tingling or numbness in fingers occur
Acute Lymphocytic Leukemia (children, abrupt onset)
T and B cells
T and B cells in the bone marrow do not fx so they don’t mature beyond Blast stage
T and B cells Increase in number leaving no room for healthy WBC, RBC, and platelets in bone marrow
Lack of WBC → neutropenia
Lack of RBC -> anemia
Lack of Platelets → thrombocytopenia
Chronic Lymphocytic Leukemia (adults, slow onset w/ reduced fx (insidious)
B-cells
B cells can’t differentiate from precursor B cells into mature B cells in bone marrow
Release low levels of immunoglobulin, mutated immunoglobulin, or none at all
B cells accumulate in bone marrow results in decreased healthy RBC, WBC, platelets
Risk Factors:
Older Age
White
Herbicides and insecticides (Agent Orange used during Vietnam war)
Males
Family history of Cancer
Eti: Genetic changes like a chromosomal abnormality
CM: No symptoms early
Enlarged, painless lymph nodes
Fatigue, fever, pain in Upper Left Abdomen from enlarged spleen
Night sweats, weight loss
Acute Myelogenous Leukemia
Blast cells
Proliferation of undifferentiated WBCs (excluding lymphocytes) in the myeloblast stage within the bone marrow
Bone marrow will have more than 20% myeloblasts (blast cells) = high → proliferation of Blast cells → decrease in RBC → Anemia (bleeding/bruising)
Proliferation of Blast cells affect spleen → abdominal pain, liver, lungs → pneumonia
Risk factors
Male
Smoking
Childhood ALL or MDS
CM:
Infection, chills, night sweats, fatigue, easy bruising, nosebleeds, low appetite, abdominal pain, pneumonia, swollen lymph nodes, enlarged spleen, loss of appetite, abdominal pain
Eti: Radiation therapy/chemo
Chronic Myelogenous Leukemia
Non-functioning mature cells
Overproduction of “mature” myeloid cells in the bone marrow
Myeloid cells look mature, but they do not function. Affects adults.
Risk factors
Old Age
Biological gender
Radiation
CM:
Fatigue, weakness – anemia
Infection, night sweats – leukopenia
Bleeding & bruising – thrombocytopenia
Full abdomen/pain in upper left quadrant – hepatomegaly/splenomegaly
Intrinsic (contact/damaged surface)
aPTT
Extrinsic (tissue factor/trauma)
PT
coagulation cascade
Coagulation factors → synthesized by the liver = form a clot
Two different pathways can activate the coagulation cascade: the intrinsic and extrinsic pathways → both end in a final common pathway → stimulates prothrombin to form thrombin and fibrinogen to form fibrin.
The intrinsic pathway is stimulated by any damage to the endothelial surface of a blood vessel, as in arteriosclerosis, or any turbulence in blood flow, as in atrial fibrillation.
The extrinsic pathway is stimulated by external trauma to a blood vessel, as happens in a laceration.
aPTT
30-40 seconds
Measures time to clot; evaluates intrinsic pathway of coagulation cascade
Prolonged aPTT suggests need for further tests. May indicate
coagulation factor deficiency
inhibitor of factor VIII
Nonspecific inhibitor, such as lupus anticoagulant
patient on heparin
PT
10-14 seconds
Measure time to clot, evaluates extrinsic pathway of coagulation cascade
Most common use is monitoring warfarin anticoagulant therapy
INR
1 second
Time for patients blood to clot compared to normal time for blood to clot
Any result >1 indicates prolonged time of clotting of blood
Breast Cancer
Eti:
Prolonged reproductive life (late menopause)
50 or older
Obesity
Increased estrogen in fat deposits
History and having no children
Patho:
EPITHELIAL cell tumors develop from cells lining the ducts or lobules of the breast → invade tissue of breasts
Estrogen receptors promote DNA replication & cell division → ER positive = breast cancer)
CM:
Single tumor- nontender, firm with irregular borders.
Most common place is the upper, outer quadrant.
Nipple discharge, swelling
Peau d’orange (thickening of skin that resembles an orange peel)
Paget’s disease- redness, crusting, pruritus, and tenderness in breast
Prevention:
Healthy weight, physical activity, no alcohol
Colon Cancer
Eti:
Genetic
Familial adenomatous polyposis (FAP) = predisposed to polyps
IBD-Ulceratice colitis and Crohn’s disease
Patho:
Begins as a polyp → becomes cancerous
Genetic changes result in defective tumor suppressor genes → activated oncogenes or mismatched gene repair
Normal colonic cells → benign adenoma → adenomatous polyp → adenocarcinoma (cancerous)
CM: Affects bowels
Fatigue, weakness, abdominal cramping, weight loss, changes in bowel habits, diarrhea, and constipation,
Iron deficiency anemia a sign of slow GI blood loss that occurs in colon cancer
Melena
Prostate Cancer
Eti:
Father or bro who had it increases your risk
Consumption of fat, red meat, fried foods, and dairy
High calcium intake → increase proliferation of cells
Alc & smoking
Prevention:
Eat lots of veggies
Moderate exercise
Increase Vitamin D → vitamin D regulates growth of tumor cells
Patho:
Adenocarcinoma mutations
Tumor suppressor genetic defect → uncontrolled cell growth in the gland → metastasis (spread of cancer throughout body)
CM:
Prostate gland can obstruct urine flow
Decrease urine in the stream
Incomplete bladder emptying
Back pain
How are Malignant tumors graded?
Grade I indicates that the cells are well-differentiated (normal)
Grade II cells are moderately differentiated
Grade III indicates poorly differentiated or anaplastic (abnormal)
Grading & Staging predict?
The disease course and assist in the formulation of a treatment plan
Staging uses the TNM system
T = tumor size, N = lymph node involvement, and M = metastasis to distant organs
Staging classifies the tumor according to size, invasiveness, and spread.
Difference between staging and grading?
The stage of cancer describes the size of a tumor and how far it has spread from where it originated. The grade describes the appearance of the cancerous cells.
4 Stages of Carcinogenesis
Initiation: alteration, change, or mutation of genes arising spontaneously or induced by exposure to a carcinogenic agent.
Promotion: lengthy and reversible process in which actively proliferating pre-neoplastic cells accumulate
Progression: genetic and phenotypic changes and cell proliferation occur. This involves a rapid increase in tumor size.
Metastasis: Spreading
Benign
abnormal cells that are localized, do not travel to other sites in the body, and well differentiated.
Not invasive, do not destroy surrounding tissue, and do not break away or travel from the tumor cell mass.
No metastasis
Malignant
cancer cells are invasive, penetrative, and destructive to surrounding tissue. They penetrate through basement membranes and metastasize from a primary site to a distant site through lymph or blood
Range from well-differentiated to poorly differentiated
Invasive and destructive to surrounding tissue.
Lack adhesion to the tumor mass = easily break free to travel to distant sites in a process called metastasis.
Metastasis
Angiogenesis
Need to metastasize
forms new blood vessels to metastasize
Cancer cells secrete vascular endothilial growth factor (VEGF) resulting in new blood cells to metastasize
Neutropenia
Decrease in neutrophils
Absolute Neutrophil Count (ANC): total WBC x % of neutrophils
Neutropenia: ANC < 1500
Severe neutropenia: ANC < 500
CM:
Inflammation (redness, heat, swelling)
Low fever
Considerations:
No fresh flowers, raw veggies, fruits, visitors, bathe client daily, monitor skin breakdown, no crowds, soft toothbrush
Medications: Filgrastim-colony stimulating/WBC grow, antibiotics
Complications:
Side effect of chemo
Eosinophils
allergic rxn
Response to parasitic infections
Help basophils trigger allergy immune response
Eosinophilia: high amounts of eosinophils in blood
Hemophilia A
Deficiency of factor VIII
Hereditary passed from mother to son
Causes bleeding
Diagnostic: prolonged aPTT, Normal PT
Hemophilia B
Patho: Lack of factor IX
CM:
Mainly affects males
General: weakness, tachycardia, tachypnea, spontaneous or easy bruising
Nose/throat: epistaxis, hemoptysis, bleeding gums, excessive bleeding with dental procedures
Musculoskeletal: joint pain and stiffness (due to hemarthrosis), compartment syndrome
CNS: headache, stiff neck, spinal cord syndromes (bleeding into spinal cord), intracranial hemorrhage (subdural or epidural hematoma)
GI: abdominal pain, hematemesis (blood in vomitus), melena (blood in stool)
Genitourinary: back pain, hematuria, post-circumcision bleeding in infant
Causes bleeding
Normal platelets count
90,000-450,000
Thrombocytosis
Clotting
>750,000 Body produces too many platelets after splenectomy
Heparin Induced Thrombocytopenia: Disorder develops from development of antibody to heparin. Some develop low platelet count, majority develop clots.
Immune Thrombocytopenic purpura: Autoantibodies develop against platelets.
Thrombotic Thrombocytopenic Purpura: Caused by a deficiency of a metalloprotease enzyme that acts on Von willebrand factor. Specifically, ADAMTS13 is destroyed by autoantibodies. The lack of metalloprotease leads to unmodified vwf, which causes platelet adhesion and aggregation. This leads to clot formation.
Essential Thrombocytosis: Occurs in the bone marrow. High platelet number due to unknown cause.
Secondary Thrombocytosis: Caused by another primary condition. Such as iron deficiency anemia, cancer, inflammation, infection, surgery, myeloproliferative disorders.
Integumentary
Environmental Free Radicals & sun exposure → decreased elasticity
Decrease of Epidermal cells → thin skin
Skin breakdown
Decreased subermal fat layer → wrinkled appearance & can’t conserve body heat
Decreased function of melanocytes → Discoloration
Decreased sebaceous glands → Dryness
Decrease of sweat glands, hair follicles, and sensory end organs → hard to thermoregulation
Decrease in mast cells & fibroblasts → thinner layer between dermis & epidermis → less nutrients are passed into epidermis
Small blood vessle of skin = more fragile → more likely to rupture = purpura & lesions
Increase in fragility of skin & susceptibility to pressure sores
atopic dermatitis (eczema)
Elevated immunoglobulin IgE levels, as it is associated with allergy or type I hypersensitivity reactions
Eti:
Genetics!
Allergies
Being in hot and cold temperatures
Lack of fillagrin(protecting the skin border)
CM:
Pruritis → skin tear → infection
Acute: red, thick, scaly patches
Complications:
Secondary infection
Erythroderma
Contact dermatitis (Skin rash)
Delayed hypersensitivity to materials such as metals, chemicals, drugs, and poison ivy occurs days after skin contact
Eti:
Allergens
Irritants
CM:
Erhythmic vesicles, edema with bullae, burning skin pain, and itchy skin.
Seborrheic dermatitis (Patches on scalp)
Patho: Inflammation of the skin caused by excessive secretions of the sebaceous glands.
CM: Dandruff and red lesions appear to be greasy, inflamed, and itchy
Psoriasis
Genetic, chronic thickening of the epidermis.
Silver-white scales
Red thickened plaques
T-cell mediated autoimmune response to an unknown antigen.
Lesions bleed when scales are removed (Auspitz sign)
Psoriasis does not affect the upper chest or back.
Affects: creases, scalp, knees, elbow, buttocks
Primary cause:
Autoimmune response
Urticarial (Hives)
Hives - caused by allergy, severe cases including angioedema. Lesions (wheals) appear suddenly on the skin and mucous membranes. Caused by the release of histamine by mast cells.
Wheals: Elevated, irregular shape, dermal edema, pale
Treatment: Blanch with pressure
Fungal (tinea=ringworm)
Superficial fungi, also called dermatophytes, such as tinea (ringworm), live on the keratinized tissues of the skin, hair, and nails and secrete digestive enzymes that cause skin scaling, nail disintegration, and broken hair
Pruritus, skin scaling
Tinea pedis: Interventions should include: wearing cotton socks, soaking toes in Burow’s solution, keeping toes and feet clean and dry, and to continue antifungals after symptoms have subsided.
Thermal Burn Stages
zone of coagulation: deepest point of injury, irreversible tissue necrosis
zone of stasis: decreased tissue perfusion cuz damaged with some vascular damage
outer zone: increased blood flow but has minimal tissue damage and heals quickly
cellular damage alters
normal sodium and potassium into flow –> large release of potassium into extracellular fluid (hyperkalemia and cardiac arrhythmias)
Burns triggers stress response of body
Alarm State → Stimulation of SNS releasing catecholamines & activation of adrenal glands releasing epi and cortisol
Release of catecholamines → peripheral vasoconstriction - combined with hypovolemia = inadequate CO & organ perfusion = hypotension, tachycardia
In diabetes, Hypoglycemia does what
Lower than 70
Drop in glucose → Adrenal gland, pancreas, liver stimulated → Epinephrine & Glucagon released → Activates SNS → Increase blood glucose (to compensate for low glucose)
As hypoglycemia continues:
Epinephrine and & Glucagon promote gluconeogenesis in the liver
Gets stored sources of glucose & amino acids in Liver (first) → Kidneys (last resort)
As hypoglycemia progresses:
Cortisol and growth hormone released to further stimulate liver and sustain glucose output
Can occur from excessive exogenous insulin, inadequate food intake, stress, excessive physical activity, infection, illness, alcohol abuse, drug interactions, surgery, and excess insulin or oral antidiabetic meds
In Hypoglycemia glucagon is injected to RAISE glucose levels (increases glucagon secretion)
DKA
More in Type 1 Diabetes, KETONES
Ketone formation is a result of lipolysis (breakdown of fats) caused by no insulin
Ketones accumulate in the blood → metabolic acidosis (DKA)
Acid buildup → excess CO2 → CO2 eliminated through Kussmauls respirations
Lungs try to rid the body of acid by hyperventilating to release excess CO2
Potassium Supplements Needed for DKA
(False HIGH)
Serum potassium false high bc acidosis causes potassium to move from the ICF → ECF
When acidosis is diminished the potassium will move back to the ICF reveals hypokalemia
In DKA Sodium is False LOW
Dilution of excess fluid into the bloodstream = Delusional hyponatremia
Sodium levels normalize with correct blood glucose levels
DKA diagnosis
Diagnostic Criteria:
Blood glucose greater than/equal to 250 mg/dL
pH lower than 7.3
Serum HCO3 Bicarbonate- lower than 15 mEq
Ketonuria and ketonemia
DKA CM
Rapid, deep respirations = Kussmaul’s respirations
Severe nausea, vomiting, profound dehydration
Fruity breath
severe hyperosmolarity of blood and consequent loss of intracellular fluid in brain can cause coma
Abdominal pain
NOT mental changes → HHNS
Gold Standard for diabetes test
Fasting Plasma Glucose Test
100-125 = Prediabetes
Greater than 126 on 2 separate days = Diabetes
Fast for 8 hrs → Get tested → High levels ( 126 or higher) = Diabetes
Diabetes Diagnostic tests
Oral glucose tolerance test (OGTT)
Carbohydrate-rich soda ingested
Blood glucose measured 2 hours later
140-199 mg/dL = prediabetes
Greater than or equal to 200 mg/dL = diabetes
Glycated hemoglobin (A1c): measures blood sugar over past 3 months, glucose attaches to the hemo
(Used for tracking)
5.7%-6.4% = prediabetes
Greater than 6.5% = diabetes
Urine testing- glucose in the urine (glucosuria) = diabetes
Islet cell autoantibodies- presence indicates T1DM
Islets are markers when insulin producing cells in the pancreas are damaged
Attack B cells that produce antibodies
C-Peptide Test- detect if there is insulin secretion from the pancreas since when insulin is secreted from pancreas so is C-peptide
If C-peptide is low or absent = T1DM
If C-peptide level is high = T2DM
Avascular Necrosis (AVN)
deterioration of bone caused by insufficient blood supply = bone deterioration cuz lack of blood supply commonly associated with fractures
Fat Embolism
fat globules from marrow of fractured LONG bone enter circulation → block blood flow
CM:
Mental status change → client is restless and trying to get out of bed
Difficulty breathing
Petichae rash
Jaundice, fever, vision change
Eti: (LONG BONE FRACTURES have more bone marrow = more fat cells
Pelvic fracture bc leads to fat globules being released from the bone marrow and into the bloodstream. When this occurs, it results in a fat embolism that can travel to the brain, lungs or heart and be fatal.
Femur fracture
Tibia fracture
Rhabdomyolysis
breakdown of skeletal muscle tissue that causes myoglobin to accumulate in the bloodstream (when you take statins)→ gets excreted by kidneys but damages them
CM: Dark urine
What type of renal injury does rhabdomyolysis cause?
Acute renal injury
The kidney needs to filter large amounts of myoglobin at the nephrons
Myoglobin is toxic to the nephones can cause tubular dysfunction
Compartment syndrome
tissue pressure exceeds perfusion pressure = too much blood flow
Pain/swelling
Pallor
Pulselessness
