1c and 1d EXAM #1 patho

edema

excessive accumulation of fluid in the interstitial spaces

localized edema

due to trauma or around an organ (i.e. sprained ankle)

-negative pitting edema

generalized edema

uniform distribution of fluid (i.e. right sided congestive heart failure)

-positive pitting edema

capillary hydrostatic pressure CHP

pushes fluid out of capillary

capillary osmotic pressure COP

pulls fluid into capillary (albumin attracts water)

what happens to Capillary Hydrostatic pressure during edema?

It goes up, which increases blood volume and blood pressure as well

what happens to capillary osmotic pressure during edema?

it goes down, not absorbing enough fluid back into capillaries (hypoproteinemia)

what effect does histamine have on capillary permeability

easier to filter (more pores/exits), no change in pressure

two common causes of edema

hypertension and congestive heart failure

Left sided CHF

congestion in lungs (pulmonary edema)

Right sided CHF

congestion in the body (pitting edema, fluid congests in vena cava)

ascites

accumulation of fluid in peritoneal space

MCC: liver failure

patho of ascites

low albumin means low COP reabsorption which means edema

Anti Diuretic Hormone effect

NO PEEING, water reabsorption in kidney

Aldosterone Hormone effect

kidney reabsorbs sodium from pee, water follows sodium and excretes potassium. Less water loss

ADH and Aldosterone released because of

low BV and low BP triggers release of these hormones.

goal is to increase BV and BP and less water loss

ANP and BNP released because

high blood volume and high blood pressure

goal is to decrease blood pressure and blood volume and increase water loss

ANP and BNP effect

kidney secretes salt into urine and water will follow, more water loss

when does the kidney release renin for RAAS

low blood volume

low blood pressure

low sodium levels

effect of RAAS

increase blood volume/pressure

increase Antidiuretic hormone/ aldosterone

less urine output

SIADH (syndrome of inappropriate ADH secretion)

-too much ADH

-less urine output/ low volume

-higher concentrated urine

-lower concentrated blood

DI (Diabetes Insipidus)

-too little ADH

-high urine output

-low urine concentration

-high blood concentration (hyperglycemia)

causes and S/S of SIADH

MCC: idiopathic

brain trauma, cancer, medication SE

S/S: fatigue, confusion, lethargy

causes and S/S of DI

pituitary tumor, kidney damage, medication SE

S/S: excessive thirst and urination (polyuria/polydipsia)

dehydration S/S

Hypotension and tachycardia, decreased urine output, increased urine concentration, increased blood concentration

sodium characteristics

-major cation outside of the cell

-maintain tonicity (cell size) of ECF

-facilitate nerve conduction

Na effect in hypertonic alteration for cells

Low water levels inside cell, High sodium levels outside of cell

Water escapes cell to follow ECF Na and cell shrinks

Na effect in hypotonic alteration for cells

High water levels inside cell, low sodium levels outside cell

Water rushes inside cell to follow gradient of Na

Hyponatremia causes

low salt intake

high water intake (water intoxication)

SIADH (high ADH)

Hypernatremia causes

high salt intake

low water intake (dehydration)

Diabetes Insipidus (low ADH)

hypersecretion of Aldosterone

S/S of hyponatremia

lethargy, hyporeflexia

S/S of hypernatremia

restlessness, hyperflexia

Osmolality

concentration of stuff in the blood

Na:H20 is homeostasis

Hypertonic solution and causes

concentrated blood

(hypernatremia, decreased water intake/ increased water loss, Diabetes insipidus)

Hypotonic solution and causes

diluted blood

(hyponatremia, increased water intake or decreased water loss, SIADH)

Hypokalemia causes

Reduced intake of K+ potassium (elderly, alcoholism, anorexia)

Increased entry of K+ into cells (alkalosis, too much insulin)

Increased loss of body K+ (vomitting,diarrhea)

Hyperkalemia causes

Increased intake of K+

Increased exit of K+ from cells (acidosis, trauma,insulin deficiency)

Decreased renal excretion of K+ (renal failure, low aldosterone)

S/S hypokalemia

muscle weakness, cramps

EKG (inverted/flattened T wave, prominent U wave)

S/S hyperkalemia

muscle weakness, spasticity

EKG (wide QRS w/ Tall peaked T waves)

why do those with hypokalemia experience muscle cramps/weakness?

potassium helps move calcium out of the cell allowing muscle to relax

what are the three states extracellular calcium exists?

Ionized Ca2+ (50%) = Free and available (active form)

Protein bound calcium (41%) - mostly albumin (helps maintain homeostasis of calcium

Hypokalemia pH level relations

high pH, low H+, low K+

Hyperkalemia pH level relations

low pH, high H+, high K+

relation between hydrogen and calcium

low hydrogen = low calcium

high hydrogen = high calcium

calcitriol (active form of Vit D3)

activated in kidney

Ca2+ absorption in GI

Ca2+ reabsorption in Kidney

Enhanced bone mineralization

Vitamin D and calcium relation

Vitamin D helps absorb calcium in GI tract

kidney failure linked to hypocalcemia

Can’t activate Vit-D3, low calcium absorption in GI, low Calcium reabsorption in kidney = hypocalcemia

relation of PTH and Calcium

PTH will be secreted to increase Calcium levels

How does PTH regulate Calcium levels

@ Kidney (calcium reabsorption and Vitamin D activation)

@ Bone (break down bone/osteoclast activity)

what is released when blood calcium levels are too high?

Calcitonin (tone Ca2+ down)

What are the main roles of calcium and sodium in the body?

Calcium helps with muscle contraction and nerve function; sodium helps with nerve impulses and fluid balance.

How does calcium affect sodium movement in cells?

High calcium levels can inhibit or slow sodium entry into cells (decreased excitability)

What happens to nerve and muscle cells when calcium is low?

Low calcium allows more sodium into cells (increased excitability)

How are hypocalcemia and pseudohypernatremia linked in lab testing?

Both can result from abnormal blood protein or fat levels, causing false low calcium or false high sodium readings due to lab artifacts.

S/S of hypocalcemia

Hyperreflexia

Tetany (Paresthesias/tingling of lips, tongue, fingers, feet)

intermittent muscle spasms, convulsions/seizures

Trousseau sign (BP wrist flex)

Chvostek’s sign (tapping and twitching of face)

what does a hypocalcemia EKG look like?

Long QT interval

Hypercalcemia S/S

painful bones

kidney stones (calcium stones)

abdominal groans (pains)

thrones (polyuria, dehydration)

psychiatric overtones (acting different)

arrhythmias, hyporeflexia, muscle weakness

causes of hypocalcemia

hypoparathyroidism, Vit D deficiency, malabsorption/nutritional deficiency

what does a hypercalcemia EKG look like

short ST segment

causes of hypercalcemia

hyperparathyroidism, calcium antacid abuse (tums), bone metastasis (cancer spread to bone), PTH producing tumors

Acidosis (high H+, low pH) S/S

decreased excitability of CNS (headache, lethargy, confusion)

hyperkalemia

hypercalcemia

pseudohyponatremia

Alkalosis (low H+, high pH) S/S

over excitability of CNS (restlessness, confusion, convulsions)

Hypokalemia

Hypocalcemia

Pseudohypernatremia

acid

CO2

base

HCO3 (chemical buffer)

metabolic acidosis (uncompensated)

retention of too much H+

low pH and low HCO3

metabolic alkalosis (uncompensated)

loss of too much H+

high pH and high HCO3

hyperventilation

exhale more CO2

high pH = alkalosis

hypoventilation

exhale less CO2

low pH = acidosis

respiratory acidosis (uncompensated)

because of hypoventilation

low pH and high CO2

respiratory alkalosis (uncompensated)

because of hyperventilation

high pH and low CO2

Metabolic acidosis compensation

hyperventilation, lungs blow off more CO2

low pH, low HCO3, low CO2

Metabolic alkalosis compensation

hypoventilation, lungs blow off less CO2

high pH, high HCO3, high CO2

respiratory acidosis compensation

kidney secretes more H+ and absorbs more HCO3

low pH, high HCO3, high CO2

respiratory alkalosis compensation

Kidney reabsorbs more H+ and secretes more HCO3

high pH, low HCO3, low CO2

How is Acidosis linked with Hyperkalemia?

high H+ levels and low pH levels

excess H+ moves into cell, kicks K+ out of cell

How is Alkalosis linked with Hypokalemia?

low H+ levels and high pH levels

H+ moves from IC —>EC in exchange for K+

How does Alkalosis affect calcium

Alkalosis causes binding of Ca++ to albumin, less free Ca++ in the blood (hypocalcemia=tetany)

S/S Acidosis high H+ and low pH

Hyperkalemia, Pseudohyponatremia, Hypercalcemia (muscle weakness, hyporeflexia, psychiatric overtones), decreased excitability of CNS

S/S Alkalosis low H+ and high pH

Hypokalemia, Hypocalcemia, Tetany, Hyperreflexia, over excitability of CNS

Respiratory Alkalosis causes (low pCO2, high pH)

Hyperventilation, hypoxemia, hypermetabolism, anemia, hyperthyroidism, hysteria

Metabolic alkalosis causes (high HCO3 and high pH)

Acid loss (loss of stomach acid, vomiting, antacids), hypokalemia

Respiratory acidosis causes

Hypoventilation (decreased depth of breathing), Drugs that depress the respiratory centers, and other problems that may effect breathing

Metabolic Acidosis

Shock, Diabetic KetoAcidosis (DKA), Lactic Acidosis (anaerobic metabolism/shock)

Metabolic Acidosis High Anion Gap causes

Diabetic Ketoacidosis and Lactic Acidosis (shock)

Metabolic Acidosis Normal Anion Gap

Diarrhea

Anion Gap equation (only use for metabolic acidosis)

Anion Gap = Na - (HCO3 + Cl)

Normal 10-12

High > 12

What does the body make when fasted and metabolizing fatty acids?

Ketone bodies

(Fed state and high glucose) body’s response:

Insulin released:

Glycolysis, lowers glucose levels (energy used)

Glycogenesis, lowers glucose levels (store excess glucose not used)

(Fasted state and low glucose) body’s response:

gluconeogenesis, highers glucose levels

glycogenolysis, highers glucose levels (break down sugar to be released)

why gluconeogenesis and glycogenolysis hurt those with Type 1 Diabetes

No insulin. sugar cannot get into cells.

“fasting state”, high blood sugar already, and liver increases sugar levels even more, when the problem is just with insulin

levels in Diabetes Ketoacidosis

high Ketones, high H+, low pH, high glucose