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Notizen

Pathophysiology Midterm

Rebecca Anderson Englisch 7 Seiten

Inhalt der Notizen (7)

Seite 1

​​​​​​ Disease: impairment of cell, tissue, organ, or organ system

Communicable: caused by infectious agent; can spread

Non-communicable: can refer to chronic diseases; doesn’t spread

causes of disease

idiopathic: cause is unknown\

iatrogenic: a treatment, procedure, or error caused the disease

Types of Prevention

Primary: prevent the disease from occuring

Secondary: early detection/ treatment via screening

Tertiary: rehab after disease is detected; to prevent complications

Pathophysiology: the study of functional changes that occur from injury, disorder, or disease

acute disease: develops quickly, marked signs, short term

chronic disease : milder, develops gradually, long term

subclinical state: pathological changes occur, but there are no obvious manifestations

latent state no symptoms or clinical signs evident

incubation period: time of exposure to microorganism and onset of signs and symptoms

prodromal period: early development of disease; signs nonspecific or absent. You know you are sick, but don't know what is wrong

manifestations : signs and symptoms of the disease

remission: manifestations of disease subside or are absent

precipitating factor: condition that triggers an acute episode

complications: new secondary or additional problems

sequelae: unwanted outcomes of primary condition

convalescence: period of recovery

prognosis: probability of recovery/ other outcome

rehabilitation: maximizing function of diseased tissues

Clinical Manifestations

things to think about

signs vs symptoms

local vs systemic

acute vs chronic

remissions vs exacerbations

Seite 2

Diagnosis

identification of specific disease through evaluation of signs and symptoms, lab tests, or other tools

more than 1 factor usually required to verify diagnosis

Etiology

causative factors in a particular disease

etiological agents:

congenital defects

inherited or genetic disorders

microorganisms like viruses or bacteria

immunologic dysfunction

metabolic derangements

degenerative changes

malignancy

burns/trauma

environmental factors

nutritional deficiencies

Seite 3

Pathogenesis

origination and development of illness/ disease

Things to consider that impact pathogenesis

age

gender

race

ethnicity

socioeconomic status

locale

Cellular Responses to Stress

atrophy : decrease in SIZE of cells; leads to reduced tissue mass

reduced use of the tissue

insufficient nutrition

decreased neurologic or hormonal stimulation

aging

hypertrophy: increase in cell SIZE; results in enlarged tissue mass

additional work by the tissue (like an enlarged heart muscle resulting from increased demands)

example: effect of consistent exercise on skeletal muscle leading to enlarged muscle mass

excessive hormonal stimulation may also stimulate cell growth

hyperplasia: increased NUMBER of cells; results in enlarged tissue mass

hypertrophy and hyperplasia can occur simultaneously (uterine enlargement during pregnancy)

can be compensatory mechanism to meet increased demands

can be pathologic when there is a hormonal imbalance

can be increased risk of cancer when hyperplasia occurs

metaplasia: mature cell type is replaced by a different mature cell type

can result from VIt A deficiency

may be an adaptive mech that provides a more resistant tissue

new cells present a stronger barrier, but result in decreased defenses because the original cells are no longer present as a defense mech

dysplasia: cells vary in size AND shape within a tissue

rate of mitosis is increased

from chronic irritation infection

can be a precancerous change

Pap smear tests for atypical cells (detection of dysplasia)

anaplasia: undifferentiated cells with variable nuclear and cell structures

characteristic of cancer and is the basis for grading the aggressiveness of a tumor

neoplasi: "new growth"; tumor

malignant neoplasm = cancer

Seite 4

Cell Damage

apoptosis: programmed cell death; normal occurrence in body

can increase when cell development is abnormal, cell numbers are excessive, or cells are injured or aged

cells self-destruct, appearing to digest themselves enzymatically and then disintegrate into fragments

ischemia: deficit of oxygen in the cells due to circulatory obstruction

always leads to hypoxia

hypoxia: reduced oxygen to tissues; can be caused by ischemia, but can also occur on its own

Necrosis: when a group of cells die

liquefaction necrosis: dead cells liquefy b/c of release of cell enzymes

when brain tissue dies or in certain bacterial infections in which a cavity or ulcer may develop in the infected area

coagulative necrosis: cell proteins are altered or denatured, and the cell retains some form for a time after death

heart attack- lack of oxygen causes cell death

fat necrosis: fatty tissue broken down into fatty acids; can increase inflammation

caseous necrosis: form of coagulation necrosis

thick, yellowish "cheesy" substance forms

infarction: area of dead cells as result of oxygen deprivation

gangrene: area of necrotic tissue that has been invaded by bacteria

Seite 5

filtration: movement of water/solutes from high P to low P (blood to ISF)

osmosis: movement of water from low P to high P (ISF to blood)

hydrostatic pressure: PUSH force of fluid against a barrier

osmotic pressure: PULL force of fluid being drawn to physical components

osmoreceptors in hypothalamus: detect fluid volume and concentration; thirst mechanism

ADH: promotes resorption of water into blood from kidney tubules

secreted in response to dehydration

if you take water out of the tubules, get more concentrated urine

increases water resorption = less water excreted in urine

aldosterone: determines resorption of sodium and water

reduces sodium excretion from body

increases sodium reabsorption and increases potassium secretion

ANP: regulates fluid, sodium, anpotassium levels

reduces workload of heart by regulating these

in the kidney- increases GFR by altering pressure in glomerular capillaries

reduces reabsorption of sodium in DCT by inhibiting ADH

also reduces renin secretion, so renin-angiotensin system is inhibited

result of ANP = fluid loss from extracellular compartment and lowered BP

reduces aldosterone secretion = potassium retention

Edema

excessive fluid in the interstitial compartment

swelling/enlargement of tissues

can be localized or throughout the body

can impair tissue perfusion

can trap drugs in IF

causes of edema:

increased capillary hydrostatic pressure

more of the force pushing fluid out of the vessels

caused by higher BP or increased BV

forces the increased fluid out of the capillaries into tissues

cause of pulmonary edema

loss of plasma proteins

more fluid in interstitial space

low blood albumin = decreased capillary osmotic P "pull"

loss of the force pulling fluid into vessels = decreased plasma osmotic P

less albumin= less water being pulled in = fluid stays in interstitial space = edema

obstruction of lymphatic circulation

can be caused by a tumor

causes localized edema

excessive fluid and proteins are not returned to the general circulation

increased capillary permeability

normally causes localized edema

can be due to an inflammatory response or infection

histamines (chemical mediators) increase capillary permeability

this is why an inflammatory response or infection can cause edema

can also result from bacterial toxins or large burn wounds and result in widespread edema

Seite 6

Effects of Edema

swelling (pale/red in color)

pitting edema (excess IF)

generalized edema causes increase in body weight

impairs function: restricts range of joint movement, reduces vital capacity, impairs diastole

pain: edema exerts pressure on local nerves; cerebral edema can cause headaches; stretching of capsule in organs

organ capsules are normally more fibrous and not very elastic

impaired arterial circulation = ischemia, leading to tissue breakdown

edema in skin : susceptible to tissue breakdown from pressure

Dehydration

causes

inadequate intake

excessive loss

or both

vomiting and diarrhea

excessive sweating- loss of sodium and water

diabetic ketoacidosis- loss of fluid, electrolytes, and glucose in urine

insufficient water intake

use of concentrated formula in infants

infants and elderly people are more seriously affected by dehydration because they lack significant fluid reserves and the ability to conserve fluid quickly

infants:

greater insensible water losses through their proportionately larger body surface area

increased need for water due to higher metabolic rate

with dehydration, the vascular compartment is rapidly depleted (hypovolemia), affecting heart, brain, and kidneys

effects of dehydration:

dry mucous membranes in mouth

decreased skin turgor/elasticity

lower BP

weak pulse

fatigue

decreased mental fxn

confusion

loss of consciousness

signs and symptoms of dehydration

decreased skin turgor and dry mucous membranes

sunken eyes

infants have sunken fontanelles

decreased BP, rapid and weak pulse

increased hematocrit

increased temp

decreased level of consciousness

urine- low V and high specific gravity

body compensates for dehydration by:

increasing thirst

increasing HR

constricting cutaneous bv's, leading to cool and pale skin

produce less urine

concentration of urine

Seite 7

Third-Spacing

fluid shifts out of the blood into a body cavity or tissue where it is no longer available as circulating fluid

ex: peritonitis, inflammation/ infection of peritoneal membranes, burns

result = fluid deficit in vascular compartment (hypovolemia) and a fluid excess in interstitial space

fluid remains in third space until basic cause is removed

weighing the pt will not reflect this shift in fluid distribution

hematocrit and electrolyte concentrations will indicate it

burns-- third spacing is evident as edema in the area of the wounds

Hyponatremia

causes:

excessive sweating, vomiting, diarrhea

diuretics combined with low sodium diet

hormonal imbalances

insufficient aldosterone

adrenal insufficiency

excess ADH secretion

diuresis

excessive water intake

effects:

fatigue, muscle cramps, abdominal discomfort/ cramps, nausea, vomiting

decreased osmotic P in ECF

fluid shift into cells= hypovolemia and decreased BP

cerebral edema = confusion, headache, weakness, seizures

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Beschreibung
Notiz am Pathophysiology Midterm, erstellt von Rebecca Anderson am 03/10/2017.
Erstellt von
Rebecca Anderson
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