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Test 4 Blueprint / Content Summary
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40 questions in same format as other tests.
Neurologic Disorders (10-14 questions)
general terms (be sure you understand mydriasis, miosis, nystagmus, papilledema)
o mydriasis?pupil dilation?sympathetic (adrenergic) response that occurs upon
exposure to darkness: a sympathetic branch of the cranial nerve that innervates the
muscles around the pupils releases norepinephrine attaches to adrenergic receptor
sites on those muscles & cause them to contract, which dilates the pupil.
o miosis?pupil constriction?parasympathetic (cholinergic) response that occurs upon
exposure to light: a parasympathetic branch of the cranial nerve that innervates the
muscles around the pupils releases acetylcholine attaches to cholinergic receptor
sites on those muscles & cause them to relax, which constricts the pupil.
o cataracts: usually age-related, slow development of protein on the lenses so that
o glaucoma?narrowing of the angles of the eyes so that aqueous humor cannot be
properly absorbed intraocular pressure increases and impedes peripheral vision;
open-angle usually slow and painless, closed-angle more acute and painful from the
o AMD?age-related macular degeneration?the macula coordinates central vision, so
that is what is affected in this disease; often a dark spot is seen in the middle of the
central visual field.
CNS disorders: general concepts:
concepts of ICP (intracranial pressure) vs CPP (cerebral perfusion pressure)?body keeps
these two in balance
o ICP very reliant on CPP & vice versa
o abnormal CPP often results in increased ICP:
CPP can be too low in states like hypotension, hypovolemia, atherosclerosis of
carotid arteries, etc?this can cause ischemia & hypoxemia of the
braincerebral edema increased ICP
or CPP can be too high (ex?high BP) and cause intracerebral bleeding, etc
edema increased ICP.
o increased ICP (IICP)
causes of increased ICP (IICP): often caused by cerebral edema secondary to:
CPP abnormalities ischemia & hypoxia;
irritants like hemorrhage, infection, acidosis
? almost any kind of brain problem has potential to generate cerebral
edema & therefore increased ICP.
body cannot tolerate much of an increase in ICP; if ICP is increased:
? prevents oxygenated blood from being able to easily get into brain
arteries (ie, decreased CPP)
? causes malfunction of various parts of brain, with varied sequela
general sequela / S&S of IICP
o change in level of consciousness (spectrum of changes, depending on degree of IICP)
o pressure on respiratory centers Cheyne Stokes (altered breathing pattern in
comatose state; pressure other parts brain stem decerebrate & decorticate
posturing (also only found in coma states)
certain reflexes can be affected, such as Babinski?s (plantar reflex)?in someone over
2 years old, positive Babinski?s usually indicates cerebral lesion of some sort (such as
edema, tumor, etc); also loss of primitive but essential reflexes like cough & gag &
o if IICP gets bad enough can cause brain herniation
specific sequela / S&S of IICP as categorized according to whether there is a diffuse problem
or a focal one in the brain
o diffuse problems usually associated with:
generalized S&S such confusion & other signs of decreased LOC (spectrum of
changes, depending on degree of IICP)
usually fairly symmetric changes in the body bilaterally, including reflex
o focal problems:
usually associated with asymmetric, unilateral findings-- focal S&S in the
body, depending on where in the brain the lesion is
if there is focal pressure (lesion, edema, etc) on motor tracts in brain there
would likely be paresis (and maybe reflex changes) on contralateral side of
the body below the neck (opposite to where the brain lesion is)
if there is focal pressure on CNs there would likely be dysfunctions of face,
eye movement, etc, on contralateral side
treatment for brain disorders: most interventions for brain-related problems are geared
towards lowering ICP by:
o keeping head of bed up at ~ 30 degrees
o keeping BP not too high & not too low
o sometimes giving diuretics.
specific CNS disorders
vascular disorders: stroke (AKA cerebrovascular accident [CVA], AKA brain attack)
o causes: list on pg 7 of notes (generally same risk factors as CV disease & HTN)
o 2 types?ischemic & hemorrhagic
o ischemic?thrombotic, embolic [& TIA]
thrombotic-- thrombus forms in arteries going to brain or within brain itself &
causes ischemia to distal tissue
embolic?clot breaks off from a thrombus (ex?clots in left atrium that develop
in left atrium during atrial fibrillation can become emboli) & lodges elsewhere
in a cerebral artery & causes ischemia
TIA?transient ischemic attack?NOT a true stroke
o hemorrhagic?intracerebral bleeding from head injury, burst aneurysm, HTN, coagulation
S&S of stroke depend on area of brain it happens?right or left hemisphere, cerebellum,
hemispheric stroke: S&S usually manifest as some combination of the following:
o paresis on contralateral side below neck & shoulders because of decussation
of corticospinal tract (AKA pyramidal tract).
o paresis on contralateral side above neck & shoulders
o hemisphere-specific problems like aphasia & inability to do math (would mean
a lesion in left hemisphere) or decrease in spatial understanding, insight into
condition, & left-sided neglect (would mean a lesion in right hemisphere).
cerebellar stroke: vertigo, nystagmus, loss of balance
brain stem: depends on where?respiratory problems, CV problems, CN problems
tx: clot-busting drugs sometimes can be used in ischemic stroke, also anticoagulants
like heparin to prevent further clots; for hemorrhagic stroke usually need to treat cause
like performing surgery to fix aneurysm; also, for all types strokes-- any interventions
that help decrease hypoxia & IICP HOB up, give O2, BP management.
degenerative disease of brain
o Alzheimer?s?type of dementia caused by abnormal accumulation of amyloid in
brain tissue & the presence of neurofibrillary tangles inside cell bodies of neurons
of brain both situations interrupt nerve signals & cause S&S such as severe
memory, behavioral, and motor changes
o Parkinson?s?caused by decrease in dopamine in the basal ganglion of the brain,
which are part of the extrapyramidal system
without inhibitory effect of dopamine, acetylcholine is ?free? to bombard
receptor cells with excitatory impulses
this cholinergic over-activity causes a ?circuit-overload? effect on muscles
that is manifested as rigidity (ex??cog-wheel rigidity?), slow movement
(hypokinesia), tremors such as pill-rolling tremor (dyskinesia), shuffling
gait (AKA Parkinsonian gait, or basal ganglion gait).
treatment is to give dopamine and anticholinergic medication.
o multiple sclerosis
autoimmune disorder in which our own T-cells attack myelin sheaths of
random axons in the brain.
this eventually causes scarring & sclerosing of the myelin sheath cells,
affecting the parts of the body controlled by those areas; this is called
since myelin sheaths are important in maintaining velocity of nerve
signals, damage to the myelin results in slowed or interrupted signals
S&S?asymmetric, varied areas, depending on damage sites; ex-weakness of an extremity, bladder problems, ataxia, vision problems.
other brain / meningeal disorders
intense, often one-sided headache caused by hyperreactivity of
combination of vascular and neural responses, causing pain and other S&S
often has individual triggers and stages that include prodrome (which
sometimes involves an aura of some sort), actual pain, and postdrome
tx?trigger-avoidance, NSAIDS (to counter inflammatory prostaglandin
involvement), and abortive drugs which should be taken as early into the
migraine as possible to stop the evolvement of events.
o seizures?sudden, chaotic discharge of neurons in brain
called epilepsy if a chronic, usually congenital origin
2 categories of szres?general (pt always unconscious, tonic-clonic
movement) & partial (varied degrees of consciousness & motor
involvement, usually local)
post-seizure state of re-organization of brain signals called post-ictal state
?pt groggy, confused.
if seizure continues unabated it is called status epilepticus.
o meningitis (infection /inflammation of meninges)
inflammation causes increased permeability of meningeal structure
edema this irritates nerve endings of spinal meninges plus often causes
photophobia, headache, irritability, restlessness, confusion
neck stiffness; also, positive Brudzinski?s and Kernig?s signs?these
are maneuvers that ?stretch? the inflamed meninges & cause pain
and/or stiffness in bending neck & knees.
CSF?high protein (due to presence of bacteria & exudates from
inflammatory response), high WBCs, low glucose (bacteria feed on
types of meningitis:
viral usually mild S&S?viral meningitis also called aseptic
worse type of meningitis is meningococcal?virulent endotoxin that
can cause petechiae and purpura?skin involvement
4. peripheral nervous system disorders
neuromuscular junction disorders?myasthenia gravis
o caused by autoantibodies that destroy acetylcholine receptors at the distal end of
o characterized by weakness that gets worse with activity and better with rest
o tx?cholinesterase is an enzyme that breaks down the extra acetylcholine in the
junctional synapse as part of normal ?clean up?, so by giving anti-cholinesterase
drug, less acetylcholine is broken down & more is available to compensate for less
o because T-cells are involved, sometimes thymectomy helps (T-cells mature in
Endocrine Disorders (10-14 questions)
hyperthyroidism?a state of excess T3 & T4 secreted by the thyroid.
o most common cause is autoimmune disease called Graves? disease, in which
autoantibodies mimic TSH by fitting into TSH receptors on the thyroid & causing it to
over-secrete T3 & T4
o manifests as state of metabolism overdrive?pt is often nervous, irritable, can even
have psychosis & hallucinations; CV ? tachycardia; GI?increased appetite but pt
stays very thin & fatigued from hypermetabolism; exophthalmus?tissue build-up
behind eyes; sweating, warm skin; higher body temp.
o goiter from increased activity of thyroid cells hyperplasia & hypertrophy
o lab?T4 high, TSH low due to negative feedback
o extreme version ? thyroid storm (AKA thyrotoxicosis)?extreme tachycardia, HF,
shock, temp of 103-105, agitation, delirium, seizures
o tx?anti-thyroid meds and/or thyroidectomy
hypothyroidism--low thyroid hormone secretion
o one of most common causes is Hashimoto?s thyroiditis?autoimmune disease in
which autoantibodies directly destroy tissue scarring, nonfunctional tissue
o another cause, uncommon these days because we add iodide to our salt?endemic
iodide deficiency (since iodide is a key ingredient in molecular structure of T3 & T4);
if mother is iodine-deficient, her fetus won?t develop properly child is born with
stunted mental & physical growth called cretinism
o S&S?opposite of hyperthyroidism; also, face takes on a bloated appearance called
o lab?T4 low, TSH high
o extreme version of hypothyroidism?myxedema crisis, or coma?when
hypothyroidism leads to unconsciousness, hypotension, hypoventilation.
o goiter from thyroid tissue trying to compensate for undersecretion
problemshyperplasia & hypertrophy
o tx for hypothyroidism?synthetic thyroid medication
if hyperthyroidism caused by pituitary hypersecretion of TSH TSH & T4 both high; if
hypothyroidism caused by pituitary hyposecretion of TSH (ie, a pituitary problem, not a
PTH (parathyroid hormone) largely responsible for calcium movement; calcitonin from
thyroid is second influence; they counterbalance each other.
PTH secreted when there is need for calcium to be used in other parts of body, or when
there is a state of hypocalcemia, because PTH increases movement of Ca from bone to blood
(resorption) by stimulating increase in osteoclastic activity
any situation that pathologically increases PTH results in hypercalcemia increase
chance for kidney stones, also hyperpolarization of RMP of muscle cells, so weakness,
lethargy; also, less calcium in bone, so osteoporosis
any situation that pathologically decreases PTH results in hypocalcemia?all the
opposite problems, including tetany, muscle spasms, positive Chvostek?s (from
hypopolarization of RMP?remember that hypocalcemia causes increase in
permeability of cells to Na+ more Na+ in cell = increased positivity =
calcitonin does all the opposite (ie?calcium goes into bone, etc).
o variety of causes:
long-term hypocalcemia problems (like in CRF)
age-related change in which the balance of osteocyte vs osteoclast is tipped
toward too much osteoclastic activity calcium resorption increases & bone is
menopausal changes: significantly less estrogen (atrophied ovaries) ultimately
means less stimulation of bone-building by osteocytes and more activity by
osteoclasts, so more bone resorption.
o spectrum of amount of weakening includes osteopenia?loss of bone, but not as bad
o tx?drugs that decrease osteoclastic activity and/or or build up calcium, like calcium
resorption means bringing something
back into blood; most often refers to
calcium coming into blood from bone?.
sometimes called ?bone resorption.?
Cushing?s syndrome or disease?a state of hypercortisolism &
exogenous steroids, or
an endogenous problem such as excess ACTH from pituitary
sequelae of hypercortisolism
increased glycogenolysis & gluconeogenesis (these are
metabolic activities that cortisol increases normally, but with
Cushing?s are pathologically increased
hyperglycemiaglucosuria & polyuria & insulin resistance
ie, S&S of Type II diabetes
abnormal breakdown of adipose tissue (lipolysis) truncal
obesity, moon face, ?buffalo hump??ie, ?cushinoid appearance;?
also, increased LDLs & risk for atherosclerosis; general
abnormally catabolized protein:
muscle weakness & wasting, especially in arms &
bone cell breakdown hypercalcemia, hypercalcinuria higher
risk of kidney stones, osteoporosis, pathological fractures.
weakened collagen fibers skin fragility bruising,
interruption of arachidonic pathway so that the protective,
positive effects of prostaglandins are inhibited:
stomach lining more at risk for peptic ulcers (usually
stomach lining protected by prostaglandins)
easier bleeding (from blocking of thromboxane, a
clotting product that has prostaglandin as precursor)
peripheral vasoconstriction (prostaglandins act as
vasodilators, so when suppressed, vasoconstriction
immunocyte function easier to get infections
sequelae of hyperaldosteronism:
increased water retention
other: if there is also hypersecretion of androgens, sometimes
hirsutism is present
dx?draw cortisol levels at different times of the day
tx?withdraw or decrease exogenous steroids; fix pituitary or
that is the problem; give drugs that block aldosterone if
Addison?s disease (hypoadrenalism)?a state of hypocortisolism &
cause: most frequent one is autoimmune attack on adrenal gland
resultant destruction of tissue; other possible causes includes
sequelae of hypocortisolism: hypoglycemia, which results in
weakness, apathy, confusion; also anorexia, N, V, D,
sequelae of hypoaldosteronism: increased excretion of Na and H20
tubule into urine low blood volume, dehydration; if bad
enough, can have
severe hypotension, called Addisonian crisis.
tx?steroids, aldosterone, high-salt diet (within reason!)
DM--diabetes mellitus (disorder of endocrine pancreas)
DM is characterized by:
hyperglycemia & glucosuria, and also (most of the time) long-term
that are system-wide
usually also polyuria & polydipsia, so DM is a DRY disease.
3rd ?P? is polyphagia, excess hunger, seen in DM Type I.
diagnosis / monitoring
FBS (fasting blood sugar) > 126 on two occasions (norm = 70 to 99)
Hgb A1C: the percentage of glucose-carrying Hgb molecules over
lifespan of an RBC; norm around 4%; aim for diabetics?keep
it < 7%; high
A1C = high average daily blood glucose
Type I DM
cause: autoantibodies destroy pancreatic tissue NO INSULIN
2 categories of acute sequelae of no insulin:
hyperglycemia & its untoward effects, including dehydration.
no cellular energy source
hyperglycemia & its untoward effects
BS?s (blood sugars) of untreated type I diabetic usually run
200 to 300
high BS exceeds renal threshold & glucose ?spills? into
urine high urine osmolality H2O drawn into urine from
tubular cells polyuria & dehydration polydipsia, dry skin,
dry mucus membranes, etc.
no cellular energy source
after all glycogen is used up, gluconeogenesis begins fat
breaks down first, then muscles (protein) ketonemia &
patient stays thin & nutritionally deprived despite polyphagia.
if not treated, side effects of gluconeogenesis can lead to DKA
(diabetic ketoacidosis); S&S:
o ABGs show metabolic acidosis
o patient might have acetone breath (ketones are being
o might have Kussmaul respirations to blow off CO2 &
bring up pH.
extreme state patient could become unconscious (from
irritating effects of acidosis on brain tissue)?this would be a
form of diabetic coma.
Type II DM
patho begins with increased fat cells in the body, which causes wide
resistance to insulin
SOME glucose is getting into the cells from the blood, but
some is NOT, so the glucose in the blood increases
pancreas reacts to this continued hyperglycemia by increasing
secretion of insulin hyperinsulinemia
no matter how much insulin gets secreted, still can only get a
small portion of glucose into cells due to their insulin
resistance eventually pancreas ?poops out?? beta cells ?run
out of steam? & there is decreased insulin production
S&S- hyperglycemia & glucosuria, like type I, but no DKA or weight
loss because there is still SOME glucose getting into cells.
since this is slow process, sometimes S&S very subtle?mild
polydipsia & polyuria, fatigue
also, BS?s can get very high ? 400-900?without patient
realizing it; this can cause extremely high serum osmolality,
polyuria, & dehydration; this acute combination known as
HHNK?hyperglycemic, hyperosmolar, nonketotic state
extreme state patient can become unconscious (usually
from brain cell dehydration)?this would be another form of
tx?diet, weight loss, various combinations of meds, including
long-term problems associated with both types DM
angiopathy, from toxic effects of glucose molecules on lining of
microangiopathy?damage to small vessels
o diabetic retinopathyblurred vision, blindness
o kidney arteriolerenal failure
o capillaries of skin easy bruising
macroangiopathy?damage to medium & large vessels?
stroke, CAD, aneurysms, PAD.
neuropathy due to angiopathic ischemia to nerves in various tissue
direct toxicity of glucose)
o peripheral neuropathy?burning, pain, numbness of legs & feet
that can lead to high risk of trauma
o autonomic neuropathy?autonomic nervous system affected-gastroparesis, bladder control problems, ?silent MI.?
phagocytic damage from glucose toxicity high risk of infections
infections, non-healing sores)
metabolic syndrome?a cluster of conditions that greatly increases a
person?s risk for
heart disease?type II DM, elevated LDLs & decreased HDL,
hypoglycemia (BS <70)
etiology-- decreased food intake & other nutritional factors; in case
diabetes, can occur from too much anti-diabetic medication
such as insulin
S&S?fatigue, shakiness, irritability, sweating?
occur from effect of counterregulatory hormones.
tx?orange juice / sugar; IV dextrose; glucagon.
extreme state hypoglycemic coma (called insulin shock or
if due to too much insulin); much more dangerous state
GI Disorders (10-14 questions)
Disorders of stomach & intestines
problems of esophagus & stomach
gastritis?inflammation of stomach lining
acute?usually due to ETOH, NSAIDS; heals when cause is taken
chronic?may be autoimmune etiology; important possible sequela
development of pernicious anemia due to decrease in intrinsic
S&S-- heartburn, sometimes coughing
if chronic & severe enough, can develop dysplasia of esophagus?
precancerous condition called Barrett?s esophagus.
hiatal hernia?protrusion of part of stomach into thorax
PUD?peptic ulcer dz
chronic inflammation of stomach and/or duodenum resulting in
luminal lining & ulcerations
causes?NSAIDs (inhibit prostaglandin), ETOH, smoking, chronic dz,
most common triggering cause?Helicobacter pylori (H. pylori)
bacteria ingested via oral/fecal route burrows through mucous
attaches to epithelium (one of few bacteria to thrive in
creates favorable ulcer environment
painless; OR can have pain after meals
hematemesis (coffee ground or bloody); melena from digesting
tx?antacids, H2 blockers, PPI?s, antibx
IBD?inflammatory bowel dz-- chronic inflammation of walls of intestines
different from irritable bowel syndrome (IBS), which is not an
2 types?Crohn?s, ulcerative colitis
most of time ileum & cecum involved?transmural, patchy areas
autoimmune dz, so other sites of body may have S&S of
(iritis), arthritis, vasculitis.
S&S?pattern of remissions & exacerbations of pain, bloody diarrhea
possible sequelae: intestinal obstruction, fistulas, perforation
rectal & sigmoid colon are most common places, but can involve all
-- not small intestines
inflamed areas are confluent but not transmural
S&S much like Crohn's but more inclined to get dehydrated since
where water usually absorbed.
can be partial or complete occur anywhere in intestines
direct blockage?tumor, hernia
slowed / absent peristalsis?paralytic ileus (sometimes happens
surgery?prevent by early mobility)
ischemic / strangulation type situation: intussusception?
telescoping of one
portion of bowel into another; volvulus?twisting
S&S?pain, distention, N, V, dehydration, lyte imbalance; tx?prevention
pt as mobile as possible, NG tube to relieve distention, fluid & lyte
diverticulosis?state of having diverticulum (outpouchings of muscle layer
intestines into lumen); most of time asymptomatic
diverticulitis?diverticula become inflamed, infected; LLQ pain, fever,
inflammation of appendix; S&S ? periumbilical pain, RLQ pain, N, V,
peritonitis?inflammation of peritoneum of abdomen
can occur with appendicitis or any other situation in which local in
inflammation spreads or gut contents are spilled into
S&S?pain upon movement, rebound tenderness.
Disorders of accessory organs
jaundice (icterus)--deposition of excess bilirubin under skin, mucous
membranes, sclera of eyes; types (based on the part of the bilirubin cycle that has
prehepatic? too much unconjugated bilirubin in blood
this means lab results would show high indirect bilirubin & normal
basic etiology = hemolytic problems
o RBCs are being broken down at greater than normal rate or
amount greater amount of unconjugated bilirubin in blood
because liver can only normally conjugate a certain amount
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