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test 2 Flashcards

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1
Q

diabetic ketoacidosis (DKA)

A

deficiency of insulin
characterized by hyperglycemia (BG>250), ketosis, acidosis (pH <7.3), dehydration, polydipsia, polyuria, kussmaul breaths

usually found in type 1 diabetics

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2
Q

how often should you check BMP in DKA or HHS

A

Q4 BMP

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3
Q

DKA/HHS collaborative care

A

2-3 IV access
IV insulin
cardiac monitor for low K+
NS, D5 when BG <250
BMP, BG checks
maintain patent airway
patient education

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4
Q

IV insulin

A

start at 0.1 U/kg/hr
BG should be reduced 36-54 ml/dl/hr

check BG every hour on this

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5
Q

hyperosmolar hyperglycemic syndrome (HHS)

A

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

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6
Q

risk factors for HHS

A

UTI
Pneumonia
Sepsis
New onset of type 2 diabetes

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7
Q

Highest score for glascow coma score

A

15 - best

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8
Q

what to assess before given electrolytes like K+

A

urine output

if pt cant urinate, they cant excrete unneeded electrolytes

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9
Q

What is the least amount BG needs checked when a diabetic is sick with anorexia, nausea, vomitting

A

4-6 hours or sooner

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10
Q

Diabetes insipidus

A

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

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11
Q

central (neurogenic) DI

A

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)

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12
Q

nephrogenic DI

A

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

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13
Q

primary DI

A

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

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14
Q

syndrome of inappropriate antidiuretic hormone (SIADH)

A

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

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15
Q

severe SIADH symptoms

A

Na <120
vomiting
abdominal cramps
twitching
seizures
cerebral edema
coma

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16
Q

biggest cause of SIADH

A

small cell lung cancer

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17
Q

SIADH care

A

low sodium
daily weights
keep HOB low
diuretics
fluid restriction

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18
Q

cerebral salt wasting

A

pt will hyponatremic and hypovolemic.

treatment is IV fluid and salt

monitor I&O

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19
Q

Hyperthyroidism

A

intolerance to heat, fine straight hair, bulging eyes, facial flushing, enlarged thyroid, tachycardia, weight loss, diarrhea, finger clubbing

most common form is graves

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20
Q

thyroid storm

A

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

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21
Q

thyroid storm care and diagnostics

A

decreased TSH <0.4
elevated T3 and T4

patients should have 4000-5000 calories and low fiber meals

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22
Q

normal radioactive iodine uptake (RAIU)

A

15-25%

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23
Q

what should people with radioactive iodine therapy do

A

avoid close contact with people for 7 days after therapy

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24
Q

hypothyroidism symptoms

A

hair loss
lethargy
dry skin
muscle aches
constipation
intolerance to cold
anorexia
facial and eyelid edema
brittle nails
weight gain
bradycardia

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25
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
26
relationship of TSH for myxedema coma
elevated when in thyroid low when pituitary or hypothalamus
27
what to worry about with thyroid module
airway!
28
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
29
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
30
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
31
complication of thyroid removal
if parathyroid is removed, hypoparathyroidism and hypocalcemia develop
32
trousseau sign
curl of thumb with blood pressure cuff being inflated due to low calcium
33
chvostek's sign
twitch of face with light tap due to low calcium
34
symptoms of addison's disease
bronze pigment of skin change in distribution of hair GI distribution weakness hypoglycemia postural hypotension weight loss
35
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
36
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
37
corticosteroid effects (what it’s used for)
anti inflammatory action immunosuppression maintenance of normal BP
38
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
39
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
40
What med helps nephrogenic DI
Thiazide diuretic
41
Meds that can CAUSE nephrogenic DI
lithium, declomycin, amphotericin
42
Normal platelet level
150-450
43
what is thrombocytopenia
platelet count under 150
44
causes of thrombocytopenia
immune thrombocytopenia purpura (ITP) Thrombotic thrombocytopenic purpura (TTP) Disseminated intravascular coagulation (DIC) Heparin-induced thrombocytopenia (HIT) drugs infections hematologic malignancy
45
manifestations and diagnostics of thrombocytopenia
asymptomatic, bleeding diagnosed by platelet count, bone marrow aspiration, specific assay- determines what type, coagulation
46
what number of platelets is the max to get a platelet transfusion
platelet count must be under 100
47
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
48
how long do normal platelets survive
8-10 days
49
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
50
rituximab for thrombocytopenia
Lyse the B cells which helps reduce our immune recognition and reduces destruction of platelets
51
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
52
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
53
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
54
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
55
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
56
what thrombocytopenia is platelet transfusion not contraindicated in
ITP, but levels must be under 10,000
57
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
58
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
59
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
60
carcinogens
chemicals- benzene, arsenic radiation- UV, atomic bomb Virus- Hep B, HPV, HIV
61
where does lymphocytic leukemia start
lymphoid cells a primary WBC in immune response
62
where does myelogenous leukemia start
myeloid cells- granulocytes, monocytes
63
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
64
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
65
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
66
what leukemia is philadelphia chromosome not seen in
chronic lymphocytic leukemia (CLL)
67
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
68
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
69
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
70
2 phases of chronic myelogenous leukemia (CML)
chronic stable- usually asymptomatic for many years acute aggressive- must be treated asap
71
chronic myelogenous leukemia (CML) diagnostics
PHILADELPHIA CHROMOSOME! (98% cases) low RBC, Hgb, Hct increased banded neutrophils, myeloblast, basophils
72
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
73
what leukemia can rituximab be used in
chronic lymphocytic leukemia
74
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.
75
lymphoma
malignant neoplasms of the bone marrow or lymphatic structures that cause proliferation of lymphocytes 2 types hodgkins non-hodgkins- most common
76
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
77
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
78
hodgkin's lymphoma staging
Stage 2- above the diaphragm or localized Stage 3- crossed the diaphragm, above and below Stage 4 - organ involvement
79
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
80
B cell lymphoma
non hodgkin lymphoma- aggressive Originates in the lymph nodes usually in neck or abdomen
81
Burkitt's lymphoma
non hodgkin's lymphoma- highly aggressive originates in the B cell blasts in the lymph nodes
82
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
83
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
84
rituximab for lymphomas
Attacks CD20 antigen on cancer cells causing cell death
85
multiple myeloma
neoplastic cells proliferate in the bone marrow and destroy bone
86
CRAB symptoms multiple myeloma
Calcium high Renal failure Anemia Bone pain
87
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
88
Bodies ability to initiate a immune response
immunocompetence
89
Decreased immunity- body cant fight how immunity as it should
incompetent immune system
90
Undesirable reaction produced by normal immune system, just hypersensitized
hypersensitivity
91
type I hypersensitivity reaction
IgE mediated reaction allergic response. happens within 5-30 mins. mediators are released from mast cells
92
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
93
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
94
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
95
intervention for allergy
Epinephrine, o2 thru non-rebreather, patent airway- possible intubation, IV access, correct hypotension, remove allergen
96
how to correct hypotension
fluids, volume expander, vasopressor elevate legs recumbent position
97
latex allergy
could be type I or type IV
98
what foods to be tested for with latex allergy
Nuts, avocados, peaches, kiwis, bananas, tomatoes, grapes
99
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

Adult health 2 (4 decks)

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