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MEPN Patho

MEPN Pathophysiology Study Outline

QuestionAnswer
Cheyne-Stokes respirations characteristics- alternating periods of shallow breathing with apnea
seen in dying process and CHF Cheyne-Stokes respirations
hypercapnia increase of PaCO2 in blood; >45-50 mmHg
Partial Seizure begins locally; superficial focus
simple partial seizure without impairment of consciousness
complex partial seizure with impairment of consciousness
generalized seizure bilaterally symmetric and without local onset; consciousness always impaired or lost
status epilepticus subsequent seizures before the regain of consciousness from preceding seizure
aura mini seizure or "feeling" of impending doom
prodromal phase malaise or headache hours to days before seizure onset
tonic phase state of muscle contraction with excessive muscle tone
clonic phase state of alternating contraction and relaxation of muscles
postictal phase time period immediately following the cessation of seizure activity
Alzheimer disease cortical nerve cell looks like a tangled mess
Alzheimer's damage plaques, tangles, transmitter defects, abnormal amyloid deposition; neurofibrillary tangle/senile plaque; may be genetically abnormal prions
Parkinson disease manifestsations forward, perpetual gait, tremors, pill-rolling, rigidity, akinesia (poverty of mvt.), postural abnormalities
degeneration of basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway Parkinson's Disease
Epilepsy causes disease marked by recurrent seizures; repetitive abnormal electrical discharges within the brain
Idiopathic Seizures spontaneously without known cause; possibly genetic
Symptomatic Seizures identifiable cause
Cryptogenic Seizures symptomatic without abnormalities
Epilepsy triggers hypoglycemia, fatigue, lack of sleep, emotional or physical stress, febrile illness, large amounts of water ingestion, constipation, stimulant use, hyperventilation, etc.
cor pulmonale (old term) pulmonary heart disease; R ventricular enlargement (hypertrophy, dilation, or both); secondary to pulmonary HTN cause by disorders of lungs or chest wall; edema
cor pulmonale manifestations obscure at rest; decreased cardiac output with exercise; chest pain; peripheral edema, hepatic congestion, and jugular venous distention; underlying lung disease
PND paroxysmal nocturnal dyspnea
noc SOB in laying position PND
PND R/t obesity, COPD, chronic bronchitis
sit up to relieve PND s/s
PND reason/cause obstructive apnea; wake up unaware, anxiety, LOC
PND D/t L ventricular failure; results from the fluid in the lungs caused by redistribution of body water while the individual is recumbent
Orthopnea laying generalized SOB
dyspnea from pulmonary congestion when lying down; horizontal position redistributes body water, causes abdominal contents exert pressure on diaphragm, decreases efficiency of respiratory muscles orthopnea
Pulmonary edema fluid in lungs; most common in L-sided heart failure;hear rales/crackles;type of V/Q shunting
Asthma symptoms inspiration/expiration wheezing, non-productive cough, tachycardia
Chronic bronchitis inspiratory/expiratory wheezing, 'slightly' productive cough, tachycardia
causes of chronic bronchitis smoking, occupational chemical exposure
chronic mucous production stimulation without expectoration chronic bronchitis
Emphysema abnormal permanent or gas exchange pathways and fibrosis/scarring; no return, permanent back-up
emphysema causes smoking
s/s of emphysema barrel-chest (overusing accessory muscles) expiration is prolonged because hypercapnic- trying to push off/exhale CO2; air trapped in overinflated alveoli; no or decreased cilia 2ndary to smoking
Pul. Fibrosis people exposed to inhaled toxins; TB, AIDs, ARDS: disease/chem. irritant; no cough, cilia
Black lung coal miners
"dusting" chemical inhalation kids; permanent lung damage; can't inflate
layers of scar tissue for alveoli fibrosis
Atelectasis alveoli collapse lung/ compression- put on ventilator
possible cause ot atelectasis OD of O2 during surgery
Bronchiectasis persistent abnormal bronchi dilation; foreign body infection; CF kids;mucous plugs
Aspiration foreign material into lungs; people with altered consciousness/vomiting uncontrollably and trying to get a breath; esophageal varices
GI bleeds- blood aspiration most toxic thing to have in lungs
most commonly aspirated side R side of lung because of early branching
Bronchiolitis inflammation destruction of small airways; if had as kid, becomes chronic as adult; viral infection of already diseased airway
DM I no working beta cells
DM II some working beta cells/ alpha cells stimulate gluconeogenesis in liver to increase serum glucose; noc wake up with high BS
DM II macrovascular manifestations CAD
DM II microvascular manifestations nephropathy, retinopathy, neuropathy
Complications of urinary obstruction above/below; back-up/ pooling; hypertrophy/dysfunction
Renal stones diet restriction based on make-up of stones/predisposition
calcium oxalate most common type renal stone
restrict calcium tx for calcium oxalate renal stones
renal stones often recurrences/clusters bacteria/ bladder infection leads to cystitis
Pyelonephritis kidney infection; high fever, flank pain (hammer test)
Nephrotic syndrome excreting >3.5 g/day of protein in urine; destroying glomerular cell matrix filter; kids- glom. neph. channels
strep. A bacteria can cause pyelonephritis
manifestations of pyelonephritis edema; also excrete fat, lipids, sloughing in tubules; liver pulls more proteins/lipis out in bloodstream; vicious cycle
tx for pyelonephritis kidney transplant
Prerenal vascular constriction, HTN, above kidney
Intrarenal glomerular nephritis; tubular necrosis, etc. within functional units of kidney
Postrenal obstruct urinary system; stones, etc.
Chronic gastritis elderly disease; aging, thinning, degeneration
What kind of anemia does a gastrectomy pt. experience? pernicious anemia
Abd. Visceral pain dull, vague; lots of testing/exam time
GERD- functional cause sphincter issue (secondary- H. pylori)
Duodenal ulcers H. Pylori- cause
Portal HTN and esophageal varicies vomit- aspirate; esophageal bleeding/ back-up pressure
LDL bad cholesterol goal < 100
HTN and pathologic changes in kidney RAS upreglulation or Renin; JG cells manufacture Renin; toxic at certain level; activate to Ang. II
Pulmonary emboli source DVTs from vascular tree below lung
thrombi travel from legs to lungs
thrombi travel from arms to above (CVA)
Stages of progression of CAD 1 inflammation, 2 ischemia, 3 infarction, 4 necrosis
Risk of CAD as it relates to HTN and DM smoking, family history, age, heart structural issues, past MI, diet, exercise, HTN, diabetes, wt. loss, cholesterol
HDL good cholesterol goal >60
Prinzmetal angina- when usually noc vasospasm
Shift to the left in CBC differential- what does it mean? ***band shift; elevation; left- out of control/ acute infection; right- under control/ correct antibiotics used
kidney stones cause obstruction and stasis of urine contributing to bacteriuria and hydronephrosis; irritation of epithelial lining with entrapment of bacteria
neurogenic bladder neurologic impairment interfering with normal bladder contraction with residual urine and ascending infection
macrocytic-normochromic anemia large, abnormally shaped erythrocytes but normal hemoglobin concentrations
microcytic-hypochromic anemia small, abnormally shaped erythrocytes and reduced hemoglobin concentration
normocytic-normochromic anemia destruction or depletion of normal erythroblasts or mature erythrocytes
pernicious anemia; folate deficiency anemia macrocytic-normochromic anemia
iron deficiency anemia; thalassemia; sideroblastic anemia microcytic-hypochromic anemia
posthemorrhagic anemia; hemolytic, sickle cell, and aplastic anemia; anemia of chronic disease normocytic-normochromic anemia
lack of vitamin B12, folate, or premature cell death pernicious anemia; folate deficiency anemia
lack of iron, dysfunctional iron uptake, or impaired synthesis of alpha or beta chain of hemoglobin A iron deficiency anemia; thalassemia; sideroblastic anemia
blood loss, abnormal shape, lysis, increased demand or premature destruction of erythrocytes posthemorrhagic anemia; hemolytic, sickle cell, and aplastic anemia; anemia of chronic disease
Hep A transmission fecal-oral (contaminated food or water)
found in feces, bile, and sera of infected individuals Hep A
Hep B transmission STD; contact with infected blod, body fluids, or contaminated needles
Hep C virus IV drug use
Hep D only occurs in individuals with Hep B
relies on Hep B virus for replication Hep D
Hep E transmission developing countries fecal-oral; contaminated water
Hep G new strain; sexually transmitted, unknown
parietal pain localized and intense; arises from organs themselves
visceral pain dull, poorly localized and difficult to describe; related to the corresponding skin dermatomes of the affected organ
referred pain visceral pain felt at some distance from a diseased or an affected organ
GERD gastroesophageal reflux disease
reflux of chyme from the stomach to the esophagus GERD
most common portal hypertension manifestation vomiting of blood from bleeding esophageal varices
splenomegaly enlargement of the spleen
thrombocytopenia decreased platelet count
most common manifestation of splenomegaly thrombocytopenia; secondary to portal hypertension increasing intrasplenic blood pressure
progression of atherosclerosis damaged endothelium, fatty streak, fibrous plaque, complicated lesion
chronic coronary obstruction results in recurrent predictable chest pain stable angina
abnormal vasospasm of coronary vessels results in unpredictable chest pain Prinzmetal angina
myocardial ischemia that does not cause detectable symptoms silent ischemia
angina pectoris substernal chest discomfort, ranging from a sensation of heaviness or pressure to moderately severe pain
Prinzmetal angina issues often occurs at night during REM sleep and may have a cyclic pattern of occurrence; hyperactivity of the SNS
rheumatic fever diffuse, inflammatory disease caused by a delayed immune response to infection by group A beta-hemolytic streptococcus
rheumatic heart disease untreated rheumatic fever causes scarring and deformity of cardiac structures
responsible for hypertrophy of the myocardium associated with hypertension ang. II
aneurysm localized dilation or outpouching of a vessel wall or cardiac chamber
most common cause of aneurysm atherosclerosis
reason atherosclerosis is most common cause of aneurysms plaque formation erodes the vessel wall
stimulates release of catecholamines which increase heart rate and peripheral vascular constriction; blood pressure increases along with cardiac workload and oxygen demand nicotine
stimulate release of free fatty acids; raises LDL and lowers HDL levels elevated catecholamine levels from nicotine use
R sided heart failure pressure rise in systemic venous circulation resulting in peripheral edema and hepatosplenomegaly
L sided heart failure causes pulmonary edema, myocardial hypertrophy and ischemia; dyspnea on exertion, fatigue
evidenced by rales on auscultation, pleural effusions L sided heart failure
shift to the left on CBC differential bandshift out of control; signifies acute infection; increase in leukocytes
shift to the right on CBC differential bandshift under control; correct antibiotics being used; return to normal
AML- acute myelogenous leukemia abnormal proliferation of myeloid precursos cells, decreased rate of apoptosis, and an arrest in cellular differentiation; complications of bleeding and infection
CLL- chronic lymphocytic leukemia malignant transformation and progressive accumulation of monoclonal B lymphocytes; failure of B cells to mature into plasma cells that synthesize immunoglobulins
CML- chronic myelogenous leukemia invasion of bone marrow by fibrous tissue
distinguishing and diagnostic marker for CML presence of Philadelphia chromosome
MM- multiple myeloma neoplastic proliferation of immunocytes called plasma cells
manifestations of MM cortical and medullary bone lysis and infiltrate bone marrow; pain, renal failure, recurrent bacterial infections, fatigue, wt. loss, weakness, anorexia
may cause hypercalcemia characterized by neurologic disturbances: confusion, lethargy, weakness; also other renal complications multiple myeloma- MM
HL- Hodgkin lymphoma marked by presence of Reed-Sternberg (RS) cells surrounded by a background of benign-appearing host inflammatory cells
HL clinical manifestations enlarged painless mass, found mostly in the neck, pain exacerbated with alcohol ingestion; asymptomatic mediastinal mass; leukopenia
NHL- Non-Hodgkin lymphoma progressive clonal expansion of B cells, T cells, NK cells; oncogenes activated by chromosomal translocations
Created by: jjannett
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