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Pathophysiology final

Terms in this set (81)

Benign tumors: can they spread?
Kill?
What do they closely resemble?
No
no
tissue
(T/F) Benign tumors are usually necrotic
T/F) Benign tumors retain normal fx
False
True
What are the borders like on a malignant tumor?
Can they infect other tissue types easily?
What normally in-place precaution is disabled here?
Irregular.
No, tissue specific, but can rapidly change and mutate.
Apoptosis disabled
What is the most common carcinogen?
Tobacco use
What allows tumors to metastatically grow?
Specialized enzymes and receptors enable them to escape their tissue of origin and spread.
Myeloid neoplasms result from transformation and proliferations of _______ in bone marrow.

Abnormal _____ cell formation

Common features?
WBC

STEM

OVerproduction of fxal bloodc ells, bone marrow hypocellularity, chromosomal abnormalities
Myeloid neoplasm manifestations:

Over 20% of what WBC in bone marrow?
Fatigue, bleeding, sweating, abdominal discomfort. Philadelphia chromosome; translocation 9 and 22.

Over 20% blasts in bone marrow
What cells are affected in lymphoid neoplasms?

Manifestations?
B/T cells. 95% malig B cell, 5% T cell

Fatigue, anorexia, infection suspetriblily, enlarged lymph nodes, painful inflamed spleen.
What two blood parts are decreased in lymphoid neoplasms? (cell type and clotter)
RBC's and platelets
Acute symptoms of ALL
Bone pain, bruising, fever, infeciton, bleeding, kids may not want to twalk, inlarged liver / spleen / lymph nodes, a lot of pain.
Who can get Hodgkin disease?

What is it primarily characterized by?

What virus is typically found?
Anyone

Reed sternberg c ells

Epstein barr
Clinical Manifestations of Hodgkin disease
Swelling of lymph nodes, weight loss, fever, pruritus, lymph node enlargement above diaphragm.
Who typically gets NON-Hodgkin disease?
What is it characterized by?
What cells are primarily affected?
Adults, 95%
No reed-sternberg cells
B/T/NK cells
symptoms of non hodgkin disease?
swollen lymph nodes
sweating
weight loss
itching (Pruritus)
SVC obstruction
spinal cord compression
Causes of Na deficiency (hyponatremia)
Gain of more water than salt
excess ADH
Salt loss more than water
Clinical manifestations of hyponatremia

Normal range for Na? (mEq/L)
N/V, headache, anorexia, confusion, lethargy, seizures, cerebral herniation

135-145 mEq/L
Causes for Hypernatremia
Too little water, more salt than water
Clinical manifestations of hypernatremia
Thirst, confusion, lethargy, seizure, coma
Normal range for K (mEq/L)
3.5-5 mEq/L
Causes of hypokalemia
decreased intake / increased secretion
Clinical manifestations of hypokalemia
Muscle problems, hyperpolzariatroin of RMP, mm weakness, alterations of cardiac conduction (changes in HR or BP) and resp paralysis
Causes of hyperkalemia
Increased intake, shift of K from cells into fluid. Decreased excretion.
Clinical manifestations of hyperkalemia
Mm dysfx
intestinal cramping
cardiac dysrhythmia
Normal range of Ca
9-11 mg/dL or 4.5-5.5 mEq/L
Hypocalcemia causes
increased excretion/ decreased intake.
increased secretion
pancreatitis
Clinical manifestations of hypocalcemia
Hyperexcitable neuromuscular cells.
positive trousseau and chvostek signs *****
mm twitch/cramping
hyperactive reflex
Hypercalcemia causes
increased Ca intake, too much vit D / Ca in general.
shift of Ca from bone to ECF; bone tumors, hyper parathyroid
decreased excretion
clinical manifestations of hypercalcemia
Mm weakness, fatigue, constipation, renal calculi, slow reflexes
Normal range for magnesium
1.5-2.5 mEq/L
Hypomagnesemia causes
decreased intake / absorption
chronic alcoholism
Hypomagnesmia Clinical Manifestations
excitability, insomnia, hyperactive reflexes, positive trousseau and chvostek signs
Hypermagnesmia causes
increased intake, laxatives or oveer use of antacids
hypermagnesemia clinical manifestations
Depression of neuromuscular fx, decreased release of acetylcholine.
lethargy
hypotension
drowsiness
mm weakness
Normal pH range:
PaCO2:
HCO3:
How many bicarb to H2CO3(carbonic acid)? (ratio)
7.35-7.45
38-42mmHg
22-28 mEq/L
20:1
What's the first line of defense for pH change?
2nd?
3rd?
Bicarb buffer system
resp
renal / metabolic
Clinical manifestations of metabolic acidosis
headache, lethargy, anorexia, deep, rapid respirations (Kussmaul), nausea, *diarrhea*
resp acidosis clinical manifestions
headache, dysrythmias, restlessness, tremors, lethargy, blurred vision.
metabolic alkalosis clinical manifestations
postural hypotension, hypokalemia, increased neuromuscular excitability, mm weakness and cramping
resp alkalosis clinical manifestations
increased neuromuscular excitability, numbness of fingers or mouth, decreased ionized Ca, increased excitability of central or peripheral membrane
Carpal/pedal spasms
Clinical manifestations of right sided HF
Peripheral edema.
Jugular venous distention.
Asdities hepatomegaly.
Fatigue, weight gain, anorexia.
Left sided HF clinical manifestations
Tachycardia, dyspnea cough, cyanosis, fatigue, confusion, restlessness, wheezes, cerebral perfusion.
Myopia:

Hyperopia:

Presbyopia
Nearsightedness; concave lenses

Farsightedness: convex lenses

Cannot read right in front; old age
astigmatism:
irregularity in curvature of lens / cornea
Strabismus:
squint / cross eyed condition. misaligned
amblyopia:
lazy eye; poor vision of both eyes or one eye even with glasses. unexplained
What makes retinopathy different than the other eye disorders?
Symptoms/causes?
Medical emergency.
Seepage of vitreous humor. leaks behind and causes further detachment
What eye disorder is the leading cause of blindness in those 55+?
Macular degeneration
Normal intracranial pressure (ICP) is:
0-15mmHg
Clinical manifestations of ischemic stroke:
hemisensory loss, contralateral hemiplegia, contralateral visual field blindness
clinical manifestations of hemorrhagic stroke:
motor and sensory deficits, language deficits, cog deficits. FAST: face arm speech time
Major diff between CVA and TIA
CVA is a rupture of artery with permanent effects.
TIA is if things are temporary and without perm brain damage.
Pathophysiology of MS
inflammation, demyelination, axonal loss, neurodegeneration, tissue damage
Clinical manifestations of MS
Weakness/paralysis of limbs
Diplopia
slurred speech
spasticity of muscles
Numbness/tingling
patchy blindness
Vertigo
Tinnitus
Impaired hearing
nystagmus
Dysarthria, dysphagia
Constipation, spastic bladder
Flaccid bladder
Sexual dysfunction
Anger
Euphoria
Depression
Patho and clinical manifestations of ALS
Atrophy of muscle fibers.
Mm twitches (fasciculations). muscle cramps. tight and stuff muscles. slurred and nsal speech.
Patho and clinical manifestations of guillain barre syndrome:
Body attacks the nerves. Weakness and tingling in extremities. Medical emergency, fatigue, paralyzes body but most make a recovery
Primary level of prevention:

2ndary:

Tertiary:
Reduce exposure/lower susceptibility. (seatbelts, vaccines)

Early detection/screening, stop smoking programs

rehab, supportive care, reduce disability to get fx back
Hypertrophy:
increase in cell size
hyperplasia
increase in number of cells
atrophy
decreased cell size, waste away.
metaplasia:
cell type changes, cell that are different appearing in places where the should be.
Type 1 hypersensitivity reaction: reaction how soon?
what is the mediating antibody?
Main effector cells?
Immediate; 15-30min
IgE
Mast cells and basophiles
Type 2 hypersensitivity reaction: aka what?
immediate or long?
What kind of reaction?
example:
tissue- specific/cytotoxic/cytolytic.
usually immediate
transfusion reaction
RhoGAM b/c mom rh neg fetus rh pos. myasthenia gravis and graves.
Type 3 hypersensitivity RXN:

Type 4:
immune complex rxn, may result from infection / environmental antigen.

delayed, no primary antibody involvement
Obstructive vs. Restrictive Lung Disease
Obstructive: wall of lumen causes impingement.
Restrictive: reduced expansion of lung tissue
obstructive pulmonary disorders
Asthma, chronic bronchitis, emphysema.
restrictive pulmonary disorders
pneumonia, neuro, pneumothorax
B12/folate deficiency patho and clinical manifestations
path: lack of intrinsic factor. autoimmunity. disruption in DNA synth.

Clinical manifestations: dementia, cog dysfx, delusions, irritability, mem impaired.
Folate def: blunt affect, depression, insomnia.
both include pallor, pedal edema, tachypnea, dyspnea, nocturia
3 mains risks of thrombus formation:
Vessel injury
abnormal blood flow
hypercoagulability (inflammatory state)
Risk factors for hypertension and treatment
smoking, obesity, sedentary lifestyle, genetics, age, poor diet

treatment is to ensure healthy heating, smoking cessation, get moving
Patho and treatment of a MI
Caused by thrombotic occlusion of coronary vessel. Interrupts blood flow. Cell injury irreversible after 30-40min.

treatment includes reducing demand; decrease HR, PR, and AL. stop clot, open back up, increase O2
Symptoms of MI
Elevated troponin. Severe, crushing chest paid radiating to arm, shoulder, jaw, back. N/V, diaphoresis, SOB.
Acute Coronary Syndrome qualified by:
Unstable angina and MI
Types of acute coronary syndrome:
unstable angina, NSTEMI, STEMI
Primary Adrenocortical insufficiency aka:
What kind of disease?
destruction of what?
hormone in excess?
Addisons disease
autoimmune
all layers of adrenal cortex.
ACTH
Secondary adrenocortical insufficiency: affects what part of brain:
Main lack of what hormone?
hypothalamic - pituitary dysfx
ACTH
What hormones are low in adrenocortical insuffiency:
cortisol and aldosterone
Red flags of adrenal crisis:
Nausea vomiting diarrhea.
Hypotensive and tachycardic
hypoglycemia
poor peripheral perfusion
Causes of a primary immunodeficiency:
Direct effects:
What genetic component is important to note?
Primary s/s:
congenital, genetic, or acquired defects.
affect immune cell fx.
sex-linked (rare).
severe, recurrent, unmanageable infections.
Endemic
constant to a location, stays within its general area
Epidemic:
spread to many people at same time; high rate of transmission
pandemic:
spread to large amount of people across many different locations
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