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Flashcards in 302 EXAM 2 STUDY GUIDE Deck (100):
1

Primary headaches

migraine
cluster
tension

2

caused by genetic and environmental factors. Triggers include: variations in estrogen level, chemicals in food, and stress. Affect 20 million people in the USA. Result in considerable time lost from work. Occur in 18% of women, 6% of men. Occurs in children also & is evenly distributed between the sexes before puberty. Manifestations include:: pulsatile, throbbing, unilateral headache lasting 1-2 days, pain worsens with activity, moderate or severe pain intensity, N/V, photophobia (sensitive to light), phono-phobia (sensitive to sound).

Migraine Headache:

3

Two types of Migraine Headaches:

Migraine with aura and migraine without aura.

4

Visual sensory phenomenon that precedes migraine. Lasts from 5 minutes to 1 hour.

Aura:

5

Primarily men. Etiology is mostly unknown. Manifestations include unilateral. Clusters or bouts of headaches for days followed by long period of spontaneous remission. Extreme pain with short duration, localized around the eye. Redness and tearing of eyes. Pupil constriction, Ptosis. Nasal congestion, runny nose. Often mistaken for sinus infections or dental problems

Cluster headache

6

Most common type of headache. Exact etiology is unknown. May be caused by sustained tension of muscles of scalp and neck. Stress, anxiety, or depression. Exact mechanisms are not known. May be a form of migraine headache that transforms gradually into a chronic tension headache. Manifestations include bilateral, dull, aching, diffuse(spread throughout), mild to moderate bilateral headache, sensation of tight band around head, not associated with N/V, not worsened by activity, and may be infrequent, episodic, or chronic. Dx: pain history, responsive to OTC drugs, & responsive to non-drug techniques.

tension headache

7

Headaches that occur 15 days o more a month.

Chronic Daily Headache (CDH):

8

how to distinguish headaches

-history/physical to exclude secondary causes
-medication history
-headache diary
-laboratory and imaging studies to rule out secondary causes

9

What is the normal ICP range?

Should be 0 to 15 mmHg.

10

What finding would alarm you in a patient to suspect neuro changes?

LOC,
pattern of breathing,
pupillary changes,
oculomotor responses
motor responses.

11

The most common scoring system used to describe the level of consciousness in a person following a traumatic brain injury.

The glasgow coma scale

12

What does this scale measure?

Basically, it is used to help gauge the severity of an acute brain injury.

13

What are the two kinds of posturing that may occur when someone has severe neuro damage?

decorticate and decerebrate.

14

flexor posturing to the cord

Decoriticate:

15

extensor posturing.

Decerebrate:

16

“the long goodbye” Most common type of dementia. Progressive disorder. Imagine of brain reveals atrophy of cerebral cortex with enlargement of ventricles. Microscopic features include Neurofibrillary tangles (protein in neurons become distorted and twisted) and senile plaques (areas of degeneration in groups of nerve cells have a plaque-like material. Manifestations: forgetfullness, emotional upset, disorientation, confusion, lack of concentration, decline in abstraction, problem solving, and judgement, and loss of ability to respond to environment. Dx of exclusion and is based on clinical findings.

alzhiemer dx

17

progressive degenerative disorder of basal ganglia function. causes dopamine depletion which causes abnormal movement. Manifestations: tremors at rest, rigidity, bradykinesia, and postural disturbances.

Parkinson's

18

Acquired inflammatory disease-demyelination of peripheral nerves. Rapidly progressive limb weakness and loss of tendon reflexes. Acute onset, ascending motor paralysis. Usually a medical emergency (life-threatening). May progress to respiratory arrest. Manifestations: ascending muscle weakness and paresis of legs to quadriplegia. Treatment: support of vital function, may use plasmapheresis or IV immunoglobin. most fully recover spontaneously within 6-12 months.

Guillain-Barre

19

Temporary decreases in brain blood flow. Brief episode of neurologic dysfunction with symptoms lasting no more than 1 hour. Complete recovery.

TIA

20

Vascular disorder that injures brain tissue. Leading cause of mortality and morbidity. High risk: Hypertension and diabetes. More common in men.

stroke

21

both limbs on one side.

hemiplegia/hemiparesis

22

both upper or lower limbs

paraplegia

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all 4 limbs

quadriplegia

24

is an abnormal, overreaction of the involuntary (autonomic) nervous system to stimulation. This reaction may include:

Change in heart rate
Excessive sweating
High blood pressure
Muscle spasms
Skin color changes (paleness, redness, blue-grey skin color)

common cause is spinal cord injury



Autonomic hyperreflfexia

25

what to do with a patient with autonomic hyperrreflexia

Sit up and raise their head
Remove tight clothing

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abrupt and temporary alteration in cerebral activity resulting in changes in electrical discharge from neurons

Causes brief disruption in brain’s electrical functions

will have a temporary alteration in level of arousal

seizure

27

2 classifications of seizures

focal seizures & generalized seizures

28

most common type.

Involve one hemisphere of brain (begins in specific or focal area)

focal seizure

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involve whole brain; begin simultaneously in both hemispheres

generalized seizures

30

2 types of generalized seizures

Absence (typical & atypical)

Tonic-clonic

31

simple (petit-mal)--lasts only a few seconds.

blank stare, motionless, unresponsiveness; motion does occur in many cases

Typical (petit-mal)

32

similar to typical; greater alterations in muscle tone and less-abrupt onset and cessation

atypical

33

most common major seizure (lasts 60-90 seconds)

tonic-clonic

34

Epileptogenic focus

Group of hypersensitive neurons

Easily activated by:
hyperthermia
hypoxia
hypoglycemia
hyponatremia
repeated sensory stimulation
certain sleep phases

seizures

35

early manifestations (malaise, headache, depression) that may occur hours or days before seizure

prodrome

36

immediately precedes onset of generalized seizure; “funny feeling,” dizziness, numbness, peculiar sensation

aura

37

sharp contraction of muscles with extension of extremities and immediate loss of consciousness

tonic phase

38

rhythmic contraction and relaxation of extremities

clonic phase

39

lasts 30-90 min

immediately following seizure (confusion)

postictal phase

40

Continuing or repetitive seizure activity (seizures that do not stop spontaneously or occur in succession without recovery.

Medical emergency that requires immediate intervention

Status epilepticus

41

Abnormally low hemaglobin level

Etiology: R/T bleeding, hemolysis, deficient production

Manifestations: tissue hypoxia. not enough oxygen getting to cells

anemia

42

How your body responds to anemia....

tachycardia
pallor
tachypnea
dyspnea
erythropoietin release

43

S/sx depend: rate of hemorrhage & if bleeding internal or external

Rapid loss—circulatory shock/collapse

Slower—amount of loss may reach 50% without S/Sx

Blood loss anemia

44

initially RBCs normochromic, nomocytic. (normal iron & normal shape)

Erythropoietin stimulated d/t hypoxia

Bleeding controlled? enough iron stores? RBC concentration returns to normal in 3-4 weeks

acute blood loss

45

premature destruction of RBCs
Retentition of iron and hemoglobin destruction
Erythropoietin increase
RBCs normocytic & normochromic
Bone marrow hyperactive

S/Sx: Easily fatigued, dyspnea, hypoxia

hemolytic anemias

46

Loss of cell membrane surface

Cell becomes tight sphere—not disc.

Can still carry O2: susceptible to destruction as passes thru spleen

Inherited disorders of cell membrane

47

Abnormal hemoglobin—Hemoglobin S

Chronic hemolytic anemia:
-pain & organ failure
-RBCs become rigid, distorted, damaged
-Reoxygenation in lungs—Sickled cell returns to normal shape


Problems
-Repeated deoxygenation—sickled cells permanently sickled
-Infants—normally asymptomatic until 8-10 weeks—HbF replaced by HbS
-Consequences of RBC sickling: Chronic hemolytic anemia—RBCs destroyed. Blood vessel occlusion.

Sickle Cell Dx- HbS

48

how long do sickled RBCs live?

20 days

49

Causes associated with sickling and occlusion

cold
stress
physical exertion
infection
illnesses that cause hypoxia, dehydration, & acidosis

50

Tissue hypoxia—can occur anywhere Abdomen, chest, bones, joints

Sluggish blood flow—>damage to liver, spleen, heart, kidneys, & retinas

Vaso-occlusive pain

51

Atypical pneumonia—d/t pulmonary infarction

Leading cause of death in sickle cell pts

Pulmonary infiltrates form a clot

SOB
fever
cough
can lead to chronic respiratory insufficiency

Acute chest syndrome

52

children with sickle cell also have?

growth retardation & osteomyelitis

spleenic injury

53

Dx for sickle cell

diagnose during infancy

clinical findings

prenatal

screening programs for newborns

54

treatment for sickle cell pts

PCN prophylactically—prevents pneumococcal infection—give to children 2 months old—5 years

Vaccines

Hydroxyrea—reduces pain crisis and complications. (increases HbF) 40 % don't respond

55

Membranes destruction or lysis of RBCs
Causes:
Drugs
Chemicals
Toxins
Infections—malaria
Prosthetic heart valves
Severe burns
DIC

acquired hemolytic anemia

56

anemias of deficient RBC production are caused by:

dietary deficiency
bleeding
increased demands

Senescent (RBCs live for 120 days then die)

RBCs breakdown--iron is released--new RBCs formed

Iron is lost in feces

57

usual cause of chronic blood loss

GI bleeds
peptic ulcers
intestinal polyps
hemorrhoids
CA
menstruation

58

pregnant women and iron?

need 500 mg in addition

59

lactation and iron

1 mg iron daily

60

children and iron

need more in 3-24 months of age

61

why do adolescents need more iron?

growth spurts, poor diet, and menstruation

62

sx of iron deficiency anemia

compulsive eating of dirt, ice, or abnormal substances

PICA

63

early symptoms of iron deficiency

Pallor of theear lobes, palms, conjuctiva

Fatigue
Palpations
Dyspnea
Angina
Tachycardia

64

later sxs of iron deficiency

Epithelial tissue changes

Spoon shaped nails

Bald tongue

Dysphagia—difficulty
swallowing

Sore mouth

Cognitive problems

65

Caused by impaired DNA—enlarged RBCs- impaired maturation and division

2 causes—deficiencies of:
Vitamin B12
Folic Acid

Megaloblastic anemias

66

B12 deficiency—caused by absence of intrinsic factor (produced by parital cells of stomach lining)

pernicious anemia

67

Foods of animal origin

Rare—strict vegetarians (no dairy, fish, meat)

Binds to intrinsic factor (parietal cells)

Goes to ileum—binds to epithelial cells

Circulated to tissues

Alcoholics & gastric bypass surgery

vitamin b12

68

hallmark problems of vit b12

RBCs large, flimsy, oval

short life span RBCs

Moderate to severe anemia, jaundice

mucosal cells change: glositis (sore tongue) & GI (diarrhea & anorexia)

69

other problems with B12 deficiency

neuro problems

prothesis of hands, feet

loss of vibratory and position sense

dementia

70

treatment for B12 defiiencey

lifetime treatment with B12 IM injections or high oral doses of Vit B12

71

Absorbed from intestines

Cereals, green leafy veggies, meats

Much lost in cooking

Malnutrition, dietary lack—most common cause. (esp. in elderly, alcoholics)


Folic Acid Deficiency Anemia

72

S/sx of folic acid deficiency anemia

similar to B12 deficiency
no neuro abnormalities

73

Tx of folic acid deficiency anemia

take folic acid until levels return to normal

74

Bone marrow stem cells defective. RBCs, WBCs, platelets all reduced

Remember leukocytes, thrombocytes have shorter life span than RBCs

aplastic anemia

75

aplastic anemia S/sx

Weakness

Fatigue

Pallor

Petechiae

Ecchymosis. Bleeding—nose, gums, vagina, GI

Increased risk infection

76

Other causes of aplastic anemia

radiation

chemicals

toxins

chemotherapy

viral hepatitis, mono, AIDS

77

Young and severely affected?

Stem cell replacement—bone marrow transplant

No transplant—immunosuppressive therapy

Graft versus host dx- if transplanted and body recognizes it as foreign body
Rejection
Infection
75% survive

Therapy for aplastic anemia

78

treatment needed for aplastic anemia

RBC transfusion

platelets

corticosteroids

79

D/t

Chronic infection
Inflammation

CA

Chronic renal failure—results in anemia

Treat underlying dx—EPO, iron supplements, blood transfusion

Anemia of Chronic Dx

80

Celiac dx-problems digesting certain food products

Drugs—seizure

CA—therapy

PG— increased needs 5-10x folic acids

Anorexia

Nausea

Folate deficiency r/t neural tube defects

Causes

81

overproduction of RBCs

polycythemia

82

spleen enlarges.

splenomegaly

Plethora—ruddiness of lips, skin

Increased blood volume, blood thickness

Clogging of blood vessels
Ischemia

Polycythemia

83

-starts with one lymph node and spreads throughout lymph system. Spread to liver, spleen, lungs, & bone marrow.
-Bimodal— early adults 15-40 and older adults 55 and older
-Increased risk if Hx of mono
-both Dx with lymph node biopsy
-usually painless enlargement of one lymph node—usually above the diaphragm (neck, supraclavicular, axilla)
-chest discomfort
-Pruitis (itching) and intermitt fevers with night sweats —classic symptoms of HL
-Dx Reed Sternberg cells found with lymph node biopsy.
-Localized at first to single group of lymph nodes —spreads to nearby lymph tissues (contiguous)
-staging more important than with NHL(since NHL is generalized)
-Fatigue, anemia, —dx spread
-most can be cured with radiation and chemo
-survival rate for adults 5 years 85%

Hodgkin (HL)

84

-B&T cells involved
-Cause unknown
-Increase in those with HIV.
-immunosuppressive therapies
-H pylori infection (stomach ulcers)
-usually start in lymph nodes—-multi-centric—-can spread to liver, spleen, bone marrow
-can spread in unpredictable fashion

Non-Hodgkin lymphoma (NHL)

85

S/Sxs of NHL

-indolent(slow growing)
-Painless lymphadenopathy
-isolated or widespread.
Disseminated when dx.
Bone marrow involved

-Aggressive: fever, night sweats, weight loss, infections

86

Dx of NHL

Lymph node biopsy, CT, MRIs, Bone marrow biopsy, PET scans

87

Tx of NHL

radiation
chemotherapy

88

which survival rate is better?

HL

89

how many have complete remission of NHL

60-80%

90

Difference between Hodgkin and NHL?

-Reed sternberg cells (HL)
-better survival rate: HL
-Where they are found

91

-most common childhood CA in central Africa
-100% have previous EBV infection
-being in jaw—aggressive chemo
-cure rate up to 90%

Burkitt Lymphoma-

92

B-lymphocytes become infected with Epstein-Barr virus (EBV)
Heterophil antibodies--used to diagnose
Infects 90%----lasts a lifetime
rest, fluid, non-steroid anti-inflammatory
transmitted by: saliva through personal contact “kissing disease”
EBV as child -- rarely get mono (immunity)
Virus remains in few B cells
Asymptomatic --- shed EBV
fever, fatigue, sore throat, & swollen lymph glands

mononucleosis

93

Sx of mono

Sx: 
fever malaise

chills

severe pharyngitis

swollen lymph nodes

increased lymphocyte count

94

treatment for MONO

rest and treat fever with aspirin

95

Death r/t cerebral clots
Painful itching—made worse by heat, water. (AQUAGENIC PRURITIS)
Tx: phlebotomies & radioactive phosphorous. want to decrease RBCs

QUIT SMOKING

Polycythemia vera

96

Never normal

Drugs, cancer, autoimmune dx

Congenital-- decreased granulocytes 

Begins in infancy-- last for
decades

G-CSF

neutropenia (agranulocytosis)

97

neutropenic precautions

Meticulous hand hygiene

Oral hygiene after meals and at bedtime

VS every 4 hours

No fresh fruit, flowers, standing water

Change IV tubing every 24 hours.

Avoid meds that may mask fever (tylenol, advil)

Administer antibiotics, antifungals/antivirals as ordered

98

(not enough platelets)

-avoid IM, Subcut injections

-aspirin, aspirin containing products

-invasive or traumatic procedures

-rectal temps, suppositories

-venipuncture

thrombocytopenia

99

-platelet disorder: plugs don’t form
-thrombocytopenia- decrease in # of platelets
Skin and mucous
membrane (nose,
mouth, GI tract,
uterus)

Cutaneous bleeding- purple areas of bruising (purpura), petechiae

bleeding disorders

100

-antibodies destroy platelets—autoimmune

-AIDS, SLE, CLL, lymphoma, Hep C

-Heparin can cause this

-Bruising, gums bleed, epistaxis, heavy menstruation

-TX—depends—nothing or corticosteroids


Immune Thrombocytopenia purpura