test 2 Flashcards
diabetic ketoacidosis (DKA)
deficiency of insulin
characterized by hyperglycemia (BG>250), ketosis, acidosis (pH <7.3), dehydration, polydipsia, polyuria, kussmaul breaths
usually found in type 1 diabetics
how often should you check BMP in DKA or HHS
Q4 BMP
DKA/HHS collaborative care
2-3 IV access
IV insulin
cardiac monitor for low K+
NS, D5 when BG <250
BMP, BG checks
maintain patent airway
patient education
IV insulin
start at 0.1 U/kg/hr
BG should be reduced 36-54 ml/dl/hr
check BG every hour on this
hyperosmolar hyperglycemic syndrome (HHS)
Medical emergency
Only occurs in type II diabetics
no ketones in urine
BG >600 mg/dl
enough insulin in body to prevent ketoacidosis, but the insulin isnt working properly
symptoms are stroke like- slurs, loss of feeling.
seizures possible
glucosuria and dehydration also occur
risk factors for HHS
UTI
Pneumonia
Sepsis
New onset of type 2 diabetes
Highest score for glascow coma score
15 - best
what to assess before given electrolytes like K+
urine output
if pt cant urinate, they cant excrete unneeded electrolytes
What is the least amount BG needs checked when a diabetic is sick with anorexia, nausea, vomitting
4-6 hours or sooner
Diabetes insipidus
caused by ADH deficiency
Polyuria- up to 20L/day
Polydipsia
Dehydrated
high sodium
Nocturia
Low BP
Low urine osmolarity <100
Low specific gravity <1.005
Serum osmolarity >295
tests- 24 hr. I&O, blood test, water deprivation test, ADH levels
central (neurogenic) DI
caused by head trauma, posterior pituitary
water deprivation will be a increase between 100-600 mmol/kg and decrease UO
treatment is hypotonic saline or dextrose 5%, vasopressin hormone therapy, decrease thirst (chlorpropamide, carbamazepine)
nephrogenic DI
Renal issue. Kidney fails to respond to hormone
Will eventually cause kidney failure
monitor daily weights
water deprivation test may increase but no greater then 300mmol/kg
Treatment is low salt and thiazide diuretic
primary DI
Due to excess water intake. Caused by psychological disorder or lesion in thirst center- hypothalamus/pituitary
Treatment is to tell them to not drink as much water
syndrome of inappropriate antidiuretic hormone (SIADH)
high production of sustained increation of ADH
Fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine, and normal renal function, muscle cramping, polydipsia, DOE, low urine output
diagnosed by serum Na <134, , serum osmolarity <280, urine specific gravity >1.025
severe SIADH symptoms
Na <120
vomiting
abdominal cramps
twitching
seizures
cerebral edema
coma
biggest cause of SIADH
small cell lung cancer
SIADH care
low sodium
daily weights
keep HOB low
diuretics
fluid restriction
cerebral salt wasting
pt will hyponatremic and hypovolemic.
treatment is IV fluid and salt
monitor I&O
Hyperthyroidism
intolerance to heat, fine straight hair, bulging eyes, facial flushing, enlarged thyroid, tachycardia, weight loss, diarrhea, finger clubbing
most common form is graves
thyroid storm
life threatening
excessive amounts of hormones released- T3, T4
could be caused by stressor, thyroidectomy
symptoms- severe tachycardia, hyperthermia, irritability, seizures, coma, abdominal pain, delirium
thyroid storm care and diagnostics
decreased TSH <0.4
elevated T3 and T4
patients should have 4000-5000 calories and low fiber meals
normal radioactive iodine uptake (RAIU)
15-25%
what should people with radioactive iodine therapy do
avoid close contact with people for 7 days after therapy
hypothyroidism symptoms
hair loss
lethargy
dry skin
muscle aches
constipation
intolerance to cold
anorexia
facial and eyelid edema
brittle nails
weight gain
bradycardia
myxedma coma
medical emergency
skin and subcut tissue puffy, facial edema, mask like affect
hypothyroid symptoms plus impairment of consciousness
diagnosed by TSH level and free t4
treatment- IV thyroid hormone therapy, low calorie diet
if not treated could lead to organ failure
relationship of TSH for myxedema coma
elevated when in thyroid
low when pituitary or hypothalamus
what to worry about with thyroid module
airway!
papillary thyroid cancer
most common type. grows slow
spread to neck lymph nodes
painless nodule, palpable, hemoptysis, airway obstruction possible
risk factors- head/neck radiation, radioactive fall outs, goiter, women, whites, asian
thyroid cancer diagnostic and treatment
diagnostics- ultrasound, PET, fine needle aspiration, elevated serum calcitonin and thyroglobulin
treated with unilateral lobectomy or thyroidectomy with bilateral lobectomy, lymph node removal, RAI therapy, chemo
subtotal thyroidectomy
removes 90% of thyroid
2 diff procedures that are minimally invasive
~endoscopic- cancer has to be <3cm and benign
~robotic- best for smaller nodules on only one side
talking may be difficult for few days after surgery
have suction and trach around in case of emergency
complication of thyroid removal
if parathyroid is removed, hypoparathyroidism and hypocalcemia develop
trousseau sign
curl of thumb with blood pressure cuff being inflated due to low calcium
chvostek’s sign
twitch of face with light tap due to low calcium
symptoms of addison’s disease
bronze pigment of skin
change in distribution of hair
GI distribution
weakness
hypoglycemia
postural hypotension
weight loss
acute adrenal insufficiency
*life threatening
primary is caused by addison’s -> decreased glucocorticoids and androgens.
Secondary is caused by lack of pituitary ACTH secretion
s/s- hypotension, tachycardia, dehydration, hyponatremia, hyperkalemia, hypoglycemia, fever, weakness, confusion, shock
acute adrenal insufficiency diagnostics and care
diagnostics- ACTH stimulation, electrolyte levels
treat underlying causes- (tumor, fungal infection), lifelong therapy- glucocorticoids, salt additives, frequent monitoring, *never skip doses
corticosteroid effects (what it’s used for)
anti inflammatory action
immunosuppression
maintenance of normal BP
Corticosteroid side effects and pt teaching
decreased Ca and K
increased BG and BP
moon face
delayed healing
suppressed immune system
personality change
protein depletion
increased gastric acid
thin skin
truncal obesity
Teaching- restrict sodium if edema occurs, exercise, therapies to reduce osteoporosis, notify HCP if epigastric pain occurs
pheochromocytoma
tumor of adrenal medulla
SNS effects occur
s/s- palpitation, headache, episodic sweating
do frequent checks of vitals
NEVER PALPATE ABDOMEN
main treatment is surgical removal
What med helps nephrogenic DI
Thiazide diuretic
Meds that can CAUSE nephrogenic DI
lithium, declomycin, amphotericin
Normal platelet level
150-450
what is thrombocytopenia
platelet count under 150
causes of thrombocytopenia
immune thrombocytopenia purpura (ITP)
Thrombotic thrombocytopenic purpura (TTP)
Disseminated intravascular coagulation (DIC)
Heparin-induced thrombocytopenia (HIT)
drugs
infections
hematologic malignancy
manifestations and diagnostics of thrombocytopenia
asymptomatic, bleeding
diagnosed by platelet count, bone marrow aspiration, specific assay- determines what type, coagulation
what number of platelets is the max to get a platelet transfusion
platelet count must be under 100
immune thrombocytopenic purpura (ITP)
most common acquired thrombocytopenia caused by abnormal destruction of circulating platelets.
these platelets are coated by an antibody, and once it reached the spleen, they are destroyed by macrophages.
The platelets lifespan is much shorter then normal with this disease
how long do normal platelets survive
8-10 days
immune thrombocytopenic purpura (ITP) care
Therapy doesn’t begin until platelet count is less than 30
therapy if needed: corticosteroids, splenectomy (last resort), IVIG, immunotherapy, rituximab
NO PLATELET TRANSFUSION UNLESS UNDER 10
rituximab for thrombocytopenia
Lyse the B cells which helps reduce our immune recognition and reduces destruction of platelets
thrombotic thrombocytopenic purpura (TTP)
MEDICAL EMERGENCY- bleeding and clotting simultaneously
Increased aggregation that forms micro thrombi that end up depositing in our arterioles or capillaries.
caused by plasma enzyme deficiency (ADAMTS 13) that breaks down vWF (von williebrand clotting factor)
s/s- anemia, thrombocytopenia, neuro and renal abnormalities, fever
thrombotic thrombocytopenic purpura (TTP) care
treat underlying cause- could lead to death if not treated
plasmapheresis, corticosteroids, rituximab, cyclosporine, splenectomy
NO PLATELET TRANSFUSIONS!!!! - could lead to increased clotting
what is plasmapheresis
Plasmapheresis- reverses process of TTP by adding vWF and the enzyme ADAMTS 13 by removing blood, adding this and removing the vFW with platelet attraction, then replacing blood back to body
used on a normal basis until are normal and hemolysis has ceased. Pt receiving this will also receive corticosteroids
Heparin-induced thrombocytopenia (HIT)
Immune response to heparin causing platelet fibrin thrombi. Won’t happen immediately when starting heparin, will take 5-14 days
could cause venous thrombosis- DVT, pulm embolism
arterial thrombosis- stroke, necrosis
treatment is to stop heparin
Heparin-induced thrombocytopenia (HIT) care
stop heparin
other drug such as warfarin, argatroban
plasmapheresis
protamine sulfate
treat embolus
surgery
NO PLATELETS since we stopped heparin infusion- increase risk of thrombotic event
what thrombocytopenia is platelet transfusion not contraindicated in
ITP, but levels must be under 10,000
normal cell proliferation vs abnormal
normal: aptosis- cells know when to die, and have contact inhibition- don’t overgrow
abnormal- overgrow, don’t know when to die, don’t respect boundaries
normal vs abnormal cell differentiation
normal- orderly process where the cell has appropriate cell formation and doesn’t dedifferentiate: knows what to do and sticks to it for the rest of its life
abnormal- malformation, cells dedifferentiate, can become malignant: the cells change paths from what they should be doing which could cause malignancy
what is leukemia
malignant disorders affecting the bloodstream and blood forming tissues of the bone marrow, lymph system, and spleen
it is fatal if untreated
effects all ages
carcinogens
chemicals- benzene, arsenic
radiation- UV, atomic bomb
Virus- Hep B, HPV, HIV
where does lymphocytic leukemia start
lymphoid cells
a primary WBC in immune response
where does myelogenous leukemia start
myeloid cells- granulocytes, monocytes
acute lymphocytic leukemia (ALL)
immature small lymphocytes proliferate in the bone marrow
S/S- occurs abruptly- FEVER, bleeding, fatigue, bone and joint pain, CNS (N/V, legarthy)
most common in children
acute lymphocytic leukemia (ALL) diagnostics
low RBC, Hgb, Hct, platelet count
WBC may be elevated or normal
transverse lines of refraction on x-ray
philadelphia chromosome may be present
chronic lymphocytic leukemia (CLL)
Production and accumulation of functionally inactive but long lived, small, mature appear lymphocytes. B cells are usually involved,
more common in older adults
s/s- usually asymptomatic, may have pain, paralysis, enlarged lymph nodes, pulmonary symptoms due to mediastinal enlargement
diagnosis- anemia, thrombocytopenia
what leukemia is philadelphia chromosome not seen in
chronic lymphocytic leukemia (CLL)
Acute myelogenous leukemia (AML)
uncontrolled proliferation of myeloblasts (neutrophils, eosinophils, basophils)
occurs mostly in adults.
risk factors- men, previous chemo, smoking, age
S/S- Abrupt onset, May have serious infections, abnormal bleeding. Fever , tired, SOB, not much of appetite, bruising
Acute myelogenous leukemia (AML) diagnostics
Low RBC, Hgb, Hct, platelet count
WBC may be low to high with myeoblasts
hypercellular bone marrow with myeloblast- immature RBC
philadelphia chromosome may be seen
chronic myelogenous leukemia (CML)
Excessive neoplastic granulocytes (Neutrophils, eosinophils, basophils) in the bone marrow that move into the blood and infiltrate the spleen
S/S- asymptomatic when early, fatigue, weakness, fever, sternal tenderness from enlarged lymph nodes
has 2 phases
2 phases of chronic myelogenous leukemia (CML)
chronic stable- usually asymptomatic for many years
acute aggressive- must be treated asap
chronic myelogenous leukemia (CML) diagnostics
PHILADELPHIA CHROMOSOME! (98% cases)
low RBC, Hgb, Hct
increased banded neutrophils, myeloblast, basophils
Leukemia treatment and care
chemotherapy drugs
corticosteroids
radiation- often done before bone marrow transplant
Hematopoietic stem cell transplant
manage bleeding
symptom management
avoid invasive procedures
monitor granulocytes counts
be aware of risk of infection
what leukemia can rituximab be used in
chronic lymphocytic leukemia
3 stages of chemo
3 stages of chemo
1. Induction- remission. Pts may be neutropenic, have thrombocytopenia, and anemia, NEUTROPENIA PRECAUTIONS NEEDED- higher risk for infection
2. Post induction or post remission- we are eliminating the remaining cells, can last several months
3. Maintenance therapy- pts are getting therapy every 3-4 weeks, can last up to 3 years. Depends on type of therapy and how they react.
lymphoma
malignant neoplasms of the bone marrow or lymphatic structures that cause proliferation of lymphocytes
2 types
hodgkins
non-hodgkins- most common
hodkin’s lymphoma
proliferation of reed-sternberg cells or hodgkin cells in the lymph nodes
more common in males
causes- EP BARR, toxin, HIV
s/s- enlarged lymph nodes, pruritus, cough, dyspnea, stridor, dysphagia, B symptoms (night sweats, weight loss more than 10% in last 6 months, fever)
advanced stages- hepatomegaly, splenomegaly, site symptoms
hodkin’s lymphoma diagnostics
leukopenia, anemia, thrombocytopenia, elevated sedimentation rate, lymph node biopsy, bone marrow aspiration, PET/CT, increase Ca
treated by aggressive chemo.
may cause cardiac, endocrine or pulmonary toxicity
hodgkin’s lymphoma staging
Stage 2- above the diaphragm or localized
Stage 3- crossed the diaphragm, above and below
Stage 4 - organ involvement
non-hodkins lymphoma
involves lymphocytes at all stages
s/s- usually NO B symptoms, common extranodal involvement- develops outside nodes, may mimic leukemia
pain around lymph nodes, swelling of face, enlargement of lymph node, SOB, loss of appetite, diarrhea
B cell lymphoma
non hodgkin lymphoma- aggressive
Originates in the lymph nodes usually in neck or abdomen
Burkitt’s lymphoma
non hodgkin’s lymphoma- highly aggressive
originates in the B cell blasts in the lymph nodes
Non-hodgkin lymphoma stages
1- localized. single lymph node
2. two or more lymph node on same side of diaphragm
3. two or more lymph node regions above and below the diaphragm
4. widespread. multiple organ with or without lymph node involvement
Non-hodgkin lymphoma diagnostics and treatment
lumbar puncture, MRI, bone marrow aspiration, barium enema, upper endoscopy, lymph node biopsy
indolent treatment- radiation, rituximab, HSCT, drugs
aggressive treatment- chemo, intrathecal chemo, HSCT
highly aggressive treatment- aggressive chemo, HSCT
rituximab for lymphomas
Attacks CD20 antigen on cancer cells causing cell death
multiple myeloma
neoplastic cells proliferate in the bone marrow and destroy bone
CRAB symptoms multiple myeloma
Calcium high
Renal failure
Anemia
Bone pain
multiple myeloma diagnostics and care
M protein, pancytopenia, bence jones protein, high creatine, MRI/PET/CT, bone marrow aspiration
treatment- corticosteroids, chemo, immunotherapy, targeted therapy, HSCT, kyphoplasty
care- ambulate, weight bearing exercise, hydration, prevent fractures, dialysis
Pts are at fall risk
Bodies ability to initiate a immune response
immunocompetence
Decreased immunity- body cant fight how immunity as it should
incompetent immune system
Undesirable reaction produced by normal immune system, just hypersensitized
hypersensitivity
type I hypersensitivity reaction
IgE mediated reaction
allergic response. happens within 5-30 mins.
mediators are released from mast cells
type II hypersensitivity reaction
cytotoxic and cytolytic reaction
blood transfusion reaction. mediated by IgG or IgM,
STOP THE BLOOD. send it to lab for testing
type III hypersensitivity reaction
immune complex reaction
Antigen and antibody complexes not cleared completely by out immune cells- strong inflammatory response, starts damaging tissues around it, possibly leading to necrosis. associated with autoimmune disorders
type IV hypersensitivity reaction
delayed hypersensitivity reaction
occurs when tissue damage causes cell mediated immune response with T lymphocytes causing cell and tissue injury.
can occur 24-48 hours after
ex- contact dermatitis
intervention for allergy
Epinephrine, o2 thru non-rebreather, patent airway- possible intubation, IV access, correct hypotension, remove allergen
how to correct hypotension
fluids, volume expander, vasopressor
elevate legs
recumbent position
latex allergy
could be type I or type IV
what foods to be tested for with latex allergy
Nuts, avocados, peaches, kiwis, bananas, tomatoes, grapes
difference between scratch test vs patch test for allergies
scratch is a immediate response- better for food allergies
patch response is longer, looks for contact allergies
