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Adult health 2 > test 2 > Flashcards

test 2 Flashcards

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
Q

myxedma coma

A

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

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26
Q

relationship of TSH for myxedema coma

A

elevated when in thyroid
low when pituitary or hypothalamus

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27
Q

what to worry about with thyroid module

A

airway!

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28
Q

papillary thyroid cancer

A

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

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29
Q

thyroid cancer diagnostic and treatment

A

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

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30
Q

subtotal thyroidectomy

A

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

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31
Q

complication of thyroid removal

A

if parathyroid is removed, hypoparathyroidism and hypocalcemia develop

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32
Q

trousseau sign

A

curl of thumb with blood pressure cuff being inflated due to low calcium

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33
Q

chvostek’s sign

A

twitch of face with light tap due to low calcium

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34
Q

symptoms of addison’s disease

A

bronze pigment of skin
change in distribution of hair
GI distribution
weakness
hypoglycemia
postural hypotension
weight loss

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35
Q

acute adrenal insufficiency

A

*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

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36
Q

acute adrenal insufficiency diagnostics and care

A

diagnostics- ACTH stimulation, electrolyte levels

treat underlying causes- (tumor, fungal infection), lifelong therapy- glucocorticoids, salt additives, frequent monitoring, *never skip doses

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37
Q

corticosteroid effects (what it’s used for)

A

anti inflammatory action
immunosuppression
maintenance of normal BP

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38
Q

Corticosteroid side effects and pt teaching

A

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

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39
Q

pheochromocytoma

A

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

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40
Q

What med helps nephrogenic DI

A

Thiazide diuretic

41
Q

Meds that can CAUSE nephrogenic DI

A

lithium, declomycin, amphotericin

42
Q

Normal platelet level

A

150-450

43
Q

what is thrombocytopenia

A

platelet count under 150

44
Q

causes of thrombocytopenia

A

immune thrombocytopenia purpura (ITP)
Thrombotic thrombocytopenic purpura (TTP)
Disseminated intravascular coagulation (DIC)
Heparin-induced thrombocytopenia (HIT)
drugs
infections
hematologic malignancy

45
Q

manifestations and diagnostics of thrombocytopenia

A

asymptomatic, bleeding

diagnosed by platelet count, bone marrow aspiration, specific assay- determines what type, coagulation

46
Q

what number of platelets is the max to get a platelet transfusion

A

platelet count must be under 100

47
Q

immune thrombocytopenic purpura (ITP)

A

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
Q

how long do normal platelets survive

A

8-10 days

49
Q

immune thrombocytopenic purpura (ITP) care

A

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
Q

rituximab for thrombocytopenia

A

Lyse the B cells which helps reduce our immune recognition and reduces destruction of platelets

51
Q

thrombotic thrombocytopenic purpura (TTP)

A

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
Q

thrombotic thrombocytopenic purpura (TTP) care

A

treat underlying cause- could lead to death if not treated

plasmapheresis, corticosteroids, rituximab, cyclosporine, splenectomy

NO PLATELET TRANSFUSIONS!!!! - could lead to increased clotting

53
Q

what is plasmapheresis

A

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
Q

Heparin-induced thrombocytopenia (HIT)

A

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
Q

Heparin-induced thrombocytopenia (HIT) care

A

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
Q

what thrombocytopenia is platelet transfusion not contraindicated in

A

ITP, but levels must be under 10,000

57
Q

normal cell proliferation vs abnormal

A

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
Q

normal vs abnormal cell differentiation

A

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
Q

what is leukemia

A

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
Q

carcinogens

A

chemicals- benzene, arsenic
radiation- UV, atomic bomb
Virus- Hep B, HPV, HIV

61
Q

where does lymphocytic leukemia start

A

lymphoid cells

a primary WBC in immune response

62
Q

where does myelogenous leukemia start

A

myeloid cells- granulocytes, monocytes

63
Q

acute lymphocytic leukemia (ALL)

A

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
Q

acute lymphocytic leukemia (ALL) diagnostics

A

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
Q

chronic lymphocytic leukemia (CLL)

A

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
Q

what leukemia is philadelphia chromosome not seen in

A

chronic lymphocytic leukemia (CLL)

67
Q

Acute myelogenous leukemia (AML)

A

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
Q

Acute myelogenous leukemia (AML) diagnostics

A

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
Q

chronic myelogenous leukemia (CML)

A

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
Q

2 phases of chronic myelogenous leukemia (CML)

A

chronic stable- usually asymptomatic for many years

acute aggressive- must be treated asap

71
Q

chronic myelogenous leukemia (CML) diagnostics

A

PHILADELPHIA CHROMOSOME! (98% cases)
low RBC, Hgb, Hct
increased banded neutrophils, myeloblast, basophils

72
Q

Leukemia treatment and care

A

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
Q

what leukemia can rituximab be used in

A

chronic lymphocytic leukemia

74
Q

3 stages of chemo

A

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
Q

lymphoma

A

malignant neoplasms of the bone marrow or lymphatic structures that cause proliferation of lymphocytes

2 types
hodgkins
non-hodgkins- most common

76
Q

hodkin’s lymphoma

A

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
Q

hodkin’s lymphoma diagnostics

A

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
Q

hodgkin’s lymphoma staging

A

Stage 2- above the diaphragm or localized
Stage 3- crossed the diaphragm, above and below
Stage 4 - organ involvement

79
Q

non-hodkins lymphoma

A

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
Q

B cell lymphoma

A

non hodgkin lymphoma- aggressive

Originates in the lymph nodes usually in neck or abdomen

81
Q

Burkitt’s lymphoma

A

non hodgkin’s lymphoma- highly aggressive

originates in the B cell blasts in the lymph nodes

82
Q

Non-hodgkin lymphoma stages

A

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
Q

Non-hodgkin lymphoma diagnostics and treatment

A

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
Q

rituximab for lymphomas

A

Attacks CD20 antigen on cancer cells causing cell death

85
Q

multiple myeloma

A

neoplastic cells proliferate in the bone marrow and destroy bone

86
Q

CRAB symptoms multiple myeloma

A

Calcium high
Renal failure
Anemia
Bone pain

87
Q

multiple myeloma diagnostics and care

A

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
Q

Bodies ability to initiate a immune response

A

immunocompetence

89
Q

Decreased immunity- body cant fight how immunity as it should

A

incompetent immune system

90
Q

Undesirable reaction produced by normal immune system, just hypersensitized

A

hypersensitivity

91
Q

type I hypersensitivity reaction

A

IgE mediated reaction

allergic response. happens within 5-30 mins.
mediators are released from mast cells

92
Q

type II hypersensitivity reaction

A

cytotoxic and cytolytic reaction

blood transfusion reaction. mediated by IgG or IgM,

STOP THE BLOOD. send it to lab for testing

93
Q

type III hypersensitivity reaction

A

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
Q

type IV hypersensitivity reaction

A

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
Q

intervention for allergy

A

Epinephrine, o2 thru non-rebreather, patent airway- possible intubation, IV access, correct hypotension, remove allergen

96
Q

how to correct hypotension

A

fluids, volume expander, vasopressor
elevate legs
recumbent position

97
Q

latex allergy

A

could be type I or type IV

98
Q

what foods to be tested for with latex allergy

A

Nuts, avocados, peaches, kiwis, bananas, tomatoes, grapes

99
Q

difference between scratch test vs patch test for allergies

A

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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