patho module 1

atrophy

decrease in cell size

physiologic atrophy

decrease in cell size as a result of development

pathologic atrophy

decrease in cell size as a result of decreased workload, pressure, use, blood supply, nutrition, hormones, nerves

example of physiologic atrophy

thymus involution in children

example of pathologic atrophy

limb in a cast causing muscle atrophy, pressure injury, chronic ischemia

cachexia

whole body muscle wasting

2 main reasons for decrease in cell size with atrophy

loss of nerve/hormonal supply, ubliquin proteasone pathway

Hypertrophy

increase in cell size

what causes hypertrophy

response to a mechanical load/stress (increases afffected organ size

physiologic hypertrophy

results from increased demand, hormone supply, hormone stimulation, or growth factors

ex of physiologic hypertrophy

enlargement of heart or skeletal muscle from exercise

Ex of pathologic hypertrophy

chronic HTN leading to heart overload and HF (cell dies and loses function)

hyperplasia

increase in the number of cells from an increased rate in cellular division

where can hyperplasia occur

organs with stem cells (skin, bone marrow, intestinal lining, liver)

compensatory hyperplasia

adaptive mechanism that enables organs to regenerate

ex of compensatory hyperplasia

callus, liver regenerating after mass removed

hormonal hyperplasia

increase number of cells in organs that are regulated by hormones

ex of hormonal hyperplasia

puberty

physiologic hyperoplasia

enlarged breasts in pregnancy

pathologic hyperplasia

abnormal proliferation of cells in response to excessive hormonal stimulation

how is cancer related to hyperplasia

cells start dividing without control

ex of pathologic hyperplasia

menstrual cycle

normally endometrium grows when exposed to estrogen but if there is increased production of estrogen then there can be endometrial growth

dyplasia

abnormal changes in shape, size or organization of cells

metaplasia

reversible replacement of one mature cell type by another less mature cell type that can survive in the environment

metaplasia example

smokers lungs changing cell types to adapt to the smoking

how to reverse metaplasia

remove the source of stress/irritation

aplasia

congenital lack of organ or tissue, absent precursor cells

hypoplasia

congenital lack of cells in organ or tissue, some precursor cells but not plenty

ischemia

reduced blood flow or oxygen to organ and tissue that can cause cell death

what causes ischemia

blockage from the inside or injury from the outside

what is ICF

all fluid within cells, is 2/3

what is ECF

all fluid outside of cells, is 1/3

what does ECF include

interstitial fluid and plasma, intravascular fluid, transcellular fluid

ex of transcellular fluid

fluid in epithelial lined cavities

what contributes to less TBW

more fat

what is filtration

fluid moving out of capillaries

what is reabsorption

fluid moving into capilarries

what can an increased membrane permeability cause in term of water movement between plasma and ISF

escape of plasam proteins to ISS causing edema

edema

excess fluid in ISS

what are some causes of edema

Increased permeability of capillary walls; Increased capillary pressure due to heart failure; Inflammatory conditions; and Venous or lymphatic obstruction, na/water retention

types of edema

localizaed, generalized, dependent

tx of generalized edema

diuretics, elevate, compress

effusion

fluid accumulation in space or cavity

what can edema cause

decreased intravascular volume because fluid moved out to ISS

what regulates amount of sodium in ECF

increased GFR, aldosterone and natriuretic peptides

what does aldosterone look at to regulate sodium balance

circulating blood volume, BP, and plasma concentration of NA and K

how does aldosterone regulate sodium

when blood volume, BP decreases,or Na in renal tubule is low, renin is released. Renin stimulated formation of angiotensin I. ACE converts angiotensin I to angiotensin II which is a vasodilator and increases BP. Angiotensin II stimulates secretion of aldosterone and ADH. Aldosterone promotes Na and water reabsorption.

How does ADH regulate sodium?

promotes water and sodium reabsorption

HTN drugs

ACE inhibitors and angiotensin blocking receptors

what are natriuretic peptides

can cause vasodilation and therefore increase na and water excretion

what does ADH do

Facilitates reabsorption of water in nephron of kidney

what does ADH do

causes the collecting ducts of the kidney to become permeable to water, reducing the volume of urine and concentrating the urine

when is ADH secreted

when plasma osmolality increases

isotonic

proportional changes in concentration of electrolytes in relation to fluid volume, can cause hypovolemia or hypervolemia

hypertonic

increased ECF osmolarity/concentration resulting in attraction of water out of cells -- cell SHRINKAGE

hypotonic

decreased ECF osmolarity/concentration leading to water movement into cells -- cell SWELLING

hyponatremia

a condition characterized by low sodium levels in the blood, which can lead to cellular swelling and neurological effects due to excess water retention.

hyponatremia symptoms

impaired nerve condiction and neuro changes, nausea, vomiting, lethargy, confusion, seizures

hypernatremia

high sodium levels in the blood

where is most na found

ECF

what organ is essential to sodium homeostasis

kidney

describe sodium reabsorption in the kidney

in early PCT, na-phos cotransporter (na excreted)and na-hydrogen exchanger (na reabsorbed)

RAAS creates aldosterone which increases sodium reabsorption

when is ADH secreted

low BV or increase osmolarity

what does ADH

stimulates NA-K-Cl cotransporter which stimulates Na, K, and Cl reabsorption

describe what aldosterone does

secreted in repsonse to decreased BP, induces synthesis of Enac, increases sodium reabsorption and increase Bp

atriopeptin

causes vasodilation when BP is high (causes decrease in BP and decrease in sodium reabsorption)

ex. person with high sodium diet, explain sodium homeostasis

they will have increased na, BP and BV. atriopeptin will be secreted which causes the kidneys to excrete more water and sodium toto decrease BP

ex. person with high na diet, explain sodium homeostasis

BV and BP decreases, RAAS and SNS activate to increase na and water reabsorption which increases BV and BP

where is most K found

ICF

where is the measurement of K coming from

ECF (plasma)

hyperkalemia

high potassium levels in the plasma/ECF

hypokalemia

low levels in ECF/plasma

external K balance

excretion = intake

uses na-k-cl cotransporter to reabsorb k

rehgulated by aldosterone which increases k secretion

uses Na-K ATPase pump

internal K balance

K in ECF vs. ICf

kept in check by NA ATPase pump

what increases ATPase activity therefore bringing K into cells and causing a decrease in K levels

insulin, catecholamines, met alkalosis, decreased plasma osmolarity

what decreases ATPase activity therefore moving K out of cells and increasing K

cell lysis, burns, rhadbo, chemo, met acidosis, insulin deficiency, increased plasma osmolarity, beta blockers, dig, decreased renal function

what does aldosteroe do

increases na reabsorption and increases k excretion

hypokalemia

decreased k in plasma

hypokalemia synptoms

weakness, dysrhythmias, glucose intolerance, irregular HR

hyperkalemia

increase k in plasma

hyperkalemia symptoms

dysrhythmias, arrest, tingling, weak, numbness, nausea

phos reabsorption

reabsorbed in PCT using naphos cotransporter

what is phos regulated by

PTH, increase phos excretion

what is ca regulated by

PTH, increases calcium reabsorption when low

calcitonin, decreases calcium reabsorption when high

vit D, increases reabsorption in gut

PTH and calcium

increased PTH secretion when low Ca

PTH and phos

decreases reabsorption of phos

hypocalcemia symptoms

tingling, muscle spasms, cramps, ostepetrosis, tetany, chvosteks, troussseaus

hypercalcemia symptoms

fatigure, weakenss, anorexia, kidney stones, dysrhythmias

where is phos measures

plasma

where is ca measured

plasma

mag function

maintains good nerve and muscle function in heart

low mag symtpoms

muscle spams, dysrhytmias

pco2 >45

acid

pco2 < 35

base

hco3 <22

acid

hco3 >26

base

co2 problem

resp

hco3 problem

met

metabolic acidosis

low ph, low hco3