Flashcards in 302 EXAM 2 STUDY GUIDE Deck (100):
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).
Two types of Migraine Headaches:
Migraine with aura and migraine without aura.
Visual sensory phenomenon that precedes migraine. Lasts from 5 minutes to 1 hour.
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
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.
Headaches that occur 15 days o more a month.
Chronic Daily Headache (CDH):
how to distinguish headaches
-history/physical to exclude secondary causes
-laboratory and imaging studies to rule out secondary causes
What is the normal ICP range?
Should be 0 to 15 mmHg.
What finding would alarm you in a patient to suspect neuro changes?
pattern of breathing,
The most common scoring system used to describe the level of consciousness in a person following a traumatic brain injury.
The glasgow coma scale
What does this scale measure?
Basically, it is used to help gauge the severity of an acute brain injury.
What are the two kinds of posturing that may occur when someone has severe neuro damage?
decorticate and decerebrate.
flexor posturing to the cord
“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.
progressive degenerative disorder of basal ganglia function. causes dopamine depletion which causes abnormal movement. Manifestations: tremors at rest, rigidity, bradykinesia, and postural disturbances.
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.
Temporary decreases in brain blood flow. Brief episode of neurologic dysfunction with symptoms lasting no more than 1 hour. Complete recovery.
Vascular disorder that injures brain tissue. Leading cause of mortality and morbidity. High risk: Hypertension and diabetes. More common in men.
both limbs on one side.
both upper or lower limbs
all 4 limbs
is an abnormal, overreaction of the involuntary (autonomic) nervous system to stimulation. This reaction may include:
Change in heart rate
High blood pressure
Skin color changes (paleness, redness, blue-grey skin color)
common cause is spinal cord injury
what to do with a patient with autonomic hyperrreflexia
Sit up and raise their head
Remove tight clothing
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
2 classifications of seizures
focal seizures & generalized seizures
most common type.
Involve one hemisphere of brain (begins in specific or focal area)
involve whole brain; begin simultaneously in both hemispheres
2 types of generalized seizures
Absence (typical & atypical)
simple (petit-mal)--lasts only a few seconds.
blank stare, motionless, unresponsiveness; motion does occur in many cases
similar to typical; greater alterations in muscle tone and less-abrupt onset and cessation
most common major seizure (lasts 60-90 seconds)
Group of hypersensitive neurons
Easily activated by:
repeated sensory stimulation
certain sleep phases
early manifestations (malaise, headache, depression) that may occur hours or days before seizure
immediately precedes onset of generalized seizure; “funny feeling,” dizziness, numbness, peculiar sensation
sharp contraction of muscles with extension of extremities and immediate loss of consciousness
rhythmic contraction and relaxation of extremities
lasts 30-90 min
immediately following seizure (confusion)
Continuing or repetitive seizure activity (seizures that do not stop spontaneously or occur in succession without recovery.
Medical emergency that requires immediate intervention
Abnormally low hemaglobin level
Etiology: R/T bleeding, hemolysis, deficient production
Manifestations: tissue hypoxia. not enough oxygen getting to cells
How your body responds to anemia....
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
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
premature destruction of RBCs
Retentition of iron and hemoglobin destruction
RBCs normocytic & normochromic
Bone marrow hyperactive
S/Sx: Easily fatigued, dyspnea, hypoxia
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
Abnormal hemoglobin—Hemoglobin S
Chronic hemolytic anemia:
-pain & organ failure
-RBCs become rigid, distorted, damaged
-Reoxygenation in lungs—Sickled cell returns to normal shape
-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
how long do sickled RBCs live?
Causes associated with sickling and occlusion
illnesses that cause hypoxia, dehydration, & acidosis
Tissue hypoxia—can occur anywhere Abdomen, chest, bones, joints
Sluggish blood flow—>damage to liver, spleen, heart, kidneys, & retinas
Atypical pneumonia—d/t pulmonary infarction
Leading cause of death in sickle cell pts
Pulmonary infiltrates form a clot
can lead to chronic respiratory insufficiency
Acute chest syndrome
children with sickle cell also have?
growth retardation & osteomyelitis
Dx for sickle cell
diagnose during infancy
screening programs for newborns
treatment for sickle cell pts
PCN prophylactically—prevents pneumococcal infection—give to children 2 months old—5 years
Hydroxyrea—reduces pain crisis and complications. (increases HbF) 40 % don't respond
Membranes destruction or lysis of RBCs
Prosthetic heart valves
acquired hemolytic anemia
anemias of deficient RBC production are caused by:
Senescent (RBCs live for 120 days then die)
RBCs breakdown--iron is released--new RBCs formed
Iron is lost in feces
usual cause of chronic blood loss
pregnant women and iron?
need 500 mg in addition
lactation and iron
1 mg iron daily
children and iron
need more in 3-24 months of age
why do adolescents need more iron?
growth spurts, poor diet, and menstruation
sx of iron deficiency anemia
compulsive eating of dirt, ice, or abnormal substances
early symptoms of iron deficiency
Pallor of theear lobes, palms, conjuctiva
later sxs of iron deficiency
Epithelial tissue changes
Spoon shaped nails
Caused by impaired DNA—enlarged RBCs- impaired maturation and division
2 causes—deficiencies of:
B12 deficiency—caused by absence of intrinsic factor (produced by parital cells of stomach lining)
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
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)
other problems with B12 deficiency
prothesis of hands, feet
loss of vibratory and position sense
treatment for B12 defiiencey
lifetime treatment with B12 IM injections or high oral doses of Vit B12
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
S/sx of folic acid deficiency anemia
similar to B12 deficiency
no neuro abnormalities
Tx of folic acid deficiency anemia
take folic acid until levels return to normal
Bone marrow stem cells defective. RBCs, WBCs, platelets all reduced
Remember leukocytes, thrombocytes have shorter life span than RBCs
aplastic anemia S/sx
Ecchymosis. Bleeding—nose, gums, vagina, GI
Increased risk infection
Other causes of aplastic anemia
viral hepatitis, mono, AIDS
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
Therapy for aplastic anemia
treatment needed for aplastic anemia
Chronic renal failure—results in anemia
Treat underlying dx—EPO, iron supplements, blood transfusion
Anemia of Chronic Dx
Celiac dx-problems digesting certain food products
PG— increased needs 5-10x folic acids
Folate deficiency r/t neural tube defects
overproduction of RBCs
Plethora—ruddiness of lips, skin
Increased blood volume, blood thickness
Clogging of blood vessels
-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)
-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%
-B&T cells involved
-Increase in those with HIV.
-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)
S/Sxs of NHL
-isolated or widespread.
Disseminated when dx.
Bone marrow involved
-Aggressive: fever, night sweats, weight loss, infections
Dx of NHL
Lymph node biopsy, CT, MRIs, Bone marrow biopsy, PET scans
Tx of NHL
which survival rate is better?
how many have complete remission of NHL
Difference between Hodgkin and NHL?
-Reed sternberg cells (HL)
-better survival rate: HL
-Where they are found
-most common childhood CA in central Africa
-100% have previous EBV infection
-being in jaw—aggressive chemo
-cure rate up to 90%
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
Sx of mono
swollen lymph nodes
increased lymphocyte count
treatment for MONO
rest and treat fever with aspirin
Death r/t cerebral clots
Painful itching—made worse by heat, water. (AQUAGENIC PRURITIS)
Tx: phlebotomies & radioactive phosphorous. want to decrease RBCs
Drugs, cancer, autoimmune dx
Congenital-- decreased granulocytes
Begins in infancy-- last for
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
(not enough platelets)
-avoid IM, Subcut injections
-aspirin, aspirin containing products
-invasive or traumatic procedures
-rectal temps, suppositories
-platelet disorder: plugs don’t form
-thrombocytopenia- decrease in # of platelets
Skin and mucous
mouth, GI tract,
Cutaneous bleeding- purple areas of bruising (purpura), petechiae