patho exam 4

body fluid

-body's water and particles dissolved in it
Function:
-lubricant
-metabolism- solvent for chemical reactions
-transport of oxygen, nutrients, chemical messengers and waste
-regulates body temperature

extracellular body fluids

-interstitial (fluid between cells)
-intravascular (blood vessels)
-connective tissue
-transcellular (GI, cerebrospinal, and synovial)
-rich in Na, chloride, and bicarbonate ions
-low in KCL, Mg, and phosphate ions

intracellular body fluids

-2/3 of fluids except in infancy
-high KCL ions, Mg ions, organic phosphates, and proteins
-low Na and chloride ions

diuresis

-increased production of urine by the kidneys
-diuretic drugs increase ___
-produce diuresis:
--exercise
--thirst and drinking
-four types of diuretics
1. loop
2. thiazide
3. potassium sparing
4. osmotic

osmolality

-solute concentration in the blood
-osmosis: movement of water across a semi permeable membrane from area of lower concentration to an area of higher concentration
-sodium: a solute; makes 80% of serum osmolality
-water follows salt
-COP= oncotic pressure

electrolyte movement

-
intravascular
: blood plasma; vasculature, circulation; picks up oxygen and nutrients
-
interstitial fluid/components
: movement between capillaries and the cells
-
intracellular compartments
: fluid into the cells membranes
-ICF= 65-70%
-EFC= 30-35%

fluid homeostasis

-fluid intake and absorption
-drinking and cellular metabolism
-thirst triggered by:
--osmolality of extracellular fluid
--decreased circulating blood volume(baroreceptor mediated and angiotensin II and III)
--dry mucous membranes

movement of body fluids

-
diffusion
: movement of particles down a concentration gradient
-
osmosis
: diffusion of water across a selectively permeable membrane
-
active transport
: movement of particles up a concentration gradient, requires energy

capillary/interstitial fluid exchange

1. capillary hydrostatic pressure: forces fluid out of the capillaries into the interstitial
2. colloid osmotic pressure: pulls fluid back into capillaries
3. interstitial fluid hydrostatic pressure: forces fluid out of the interstitium into capillaries
4

hydrostatic vs osmotic pressure

-on arterial side: hydrostatic is greater than osmotic-> pushes o2 rich blood to heart
-on venous side: osmotic pressure is greater than hydrostatic-> pulls o2 poor blood back to veins
-on interstitial side of arterial -> osmotic pressure is greater than

fluid homeostasis hormones

1. ANP and BNP released when the heart is stretched
-promote fluid excretion
-Na and water excretion in urine
2. aldosterone: secreted by the adrenal cortex
-stimulus for release- angiotensin II- activated by circulating blood volume and increase KCl in p

tonicity

-isotonic: a solution that has the same salt concentration as the normal cells of the body and the blood
-hypertonic: a solution with a higher salt concentration than in normal cells of the body and blood -> less particles in cell- pull out and shrink
-hy

volume deficit

-decrease in saline in the same concentration as the normal extracellular fluid
causes
:
-emesis(vomit), diarrhea, hemorrhage, third spacing
CM
:
-increased HR, postural B/P, weight loss, flat neck veins, prolonged capillary refill, lightheadedness, dizzi

volume excess

-amount of extracellular fluid abnormally increased
-addition or retention of saline
causes
-excessive infusion of isotonic solutions(NS, LR, D5W)
-renal retention of Na and water (CHF, cirrhosis, chronic renal failure)
CM
:
-weight gain, edema, bounding

hyponatremia(low sodium)

-too much water for the amount of Na ion present
-extracellular fluid reduced osmolality (too dilute)
-Na concentration below the limits of normal
causes
:
-tumors that secrete ADH (causes kidneys to retain water), excessive water intake, beer potomania
C

hypernatremia(high sodium)

-serum Na above the upper limits of normal
-extracellular fluid too little water for the amount of Na ions
causes
:
-concentrated tube feedings, IV infusion hypertonic solutions
CM
;
-confusion, lethargy, seizures, and coma, thirst, oliguria

dehydration

-too small of volume in extracellular compartment and body fluids too concentration
causes
:
-V/D
CM
-weight loss, postural hypotension; lightheadedness; rapid, thready pulse

edema(interstitial fluid volume)

-excessive fluid in the interstitial compartment
can be caused by
:
1. increased capillary hydrostatic pressure(pushes into interstitial)
2. increase interstitial fluid osmotic pressure
3. blockage of lymph drainage
4. decreased capillary osmotic pressure

hydrostatic pressure increases(edema cause)

venous obstruction
:
-thrombophlebitis(inflammation of veins)
-hepatic obstruction
-tight clothing on extremities
-prolonged standing
salt or water retention
-congestive heart failure
-renal failure

edema

-interstitium is elastic and expandable
-excessive fluid in interstitium
-classic sign of fluid volume excess
-1 L fluid = 1 kg/2.2 lbs
-significant increases in ECF volume occurs before edema is visible

edema due to increased capillary hydrostatic pressure

Causes
:
-increase arterial or venous pressure
-capillary distention due to increase vascular volume
examples
-68 y.o male with heart failure, lungs with bilateral scattered crackles; 2+ pedal edema bilaterally

edema due to decreased capillary colloidal osmotic pressure

causes
:
1. decreased production/loss of albumin
2. loss of plasma proteins in burns
3. plasma proteins synthesized in liver/lost via kidney
4. edema is non dependent
examples
:
-burns
-inflammation
-immune response

edema due to obstruction of lymph flow

causes
:
-lymph system moves proteins that cannot be reabsorbed into the capillaries back into the circulation
examples
:
-cancer of lymph system
-removal of lymph nodes
-infection of lymph nodes

third spacing

-shift of intravascular fluid to a space in which the fluid can not be used
-fluid shifts to transcellular compartments- usually a serous cavity
-self perpetuating because:
1. fluid is usually protein rich
2. tends to accumulate and not reabsorb
3. becaus

electrolyte balance

-fluid intake and output, acid base balance, hormones and cell functions all influence
-because electrolytes function collaboratively, changes in one electrolyte can affect the balance of other electrolytes
-electrolytes: substances that are electrically

normal lab values

-sodium: 135-145 meq/L
-potassium: 3.5-5.0 meq/L
-chloride: 95-105 meq/L
-bicarbonate: 22-28 meq/L
-calcium: 9-11 mg/dL
-phosphat: 3.2-4.3 mg/dL
BUN: 8-18 mg/dL
creatinine: 0.6-1.2 mg/dL

sodium

-main ECF cation
-governs osmolality
-influences water distribution
-aids in acid-base balance
-activates muscle and nerve cells

hyponatermia

-dilute body fluids with H2O> Na
causes
-excess Na loss
-renal diuretics
-GI(N/V/D, NG drainage)
-skin(burns, open wounds)
-excess H20
-excess hypotonic IVF or IVF without sodium
-SIADH(syndrome of inappropriate ADH)
signs and symptoms
-anorexia
-confusio

hypernatermia

-gain of Na, without water or excess H20 loss without as much Na loss
-cant respond to normal thirst mechanism
-excessive IV Na
-overuse of enteral tube feedings
-watery diarrhea
-diabetes insipidus
signs and symptoms
-extreme thirst
-dry, sticky mucous m

potassium

-main intracellular cation
-regulates excitability of cells, determines cell electrical status
-helps to control intracellular osmolality

hypokalemia

causes
:
-K+ loss from: renal system, GI system
-decreased K+ intake
-shift of K+ from ECF to ICF
--acid base disorder
--hydrogen shift out of cells to help correct pH
--potassium from ECF shifts into cells to maintain electroneutrality
signs and symptoms

hyperkalemia

causes
-increase K+ intake
-decrease K+ output
-shift of K+ from ICF to ECF
-acid base problems: shifts H+ into cells and K+ out of cells
treatment
:
-NaHCO3, calcium gluconate, glucose
-subacute: treat underlying cause

magnesium

causes
:
-decreased intake: malnutrition, alcoholism
-decreased absorption
-increased losses: GI losses, renal losses
-drug induced hypomagnesemia; GI laxatives, renal losses

hypomagnesemia

treatment
-oral replacement
-IV magnesium sulfate

hypermagnesemia

causes
-exogenous ingestion
-impaired renal excretion
treatment
-eliminate exogenous source of Mg

crystalloid(fluid replacement)

-replace water and sodium
-maintainance and replacement of fluids or specific electrolyte replacements
-inexpensive, no risk for anaphylaxis, viral transmission or coagulation problems
most common solution
-sodium chloride(NS)
-dextrose
-lactated ringers

colloids(fluid replacement)

-increase capillary osmotic pressure
-fluid is pulled from ECF to ICF
-plasma expanders
-consists of proteins, carbohydrates, collagen
-more expensive than crystalloid
-can affect coagulation
-no oxygen carrying ability
most common solutions
-albumin
-dex

blood products(fluid replacement)

-carry 02
-clotting factors
-increase COP, volume
-most expensive, least available
-require human donors
adverse effects
-incomparability with recipients immune system
-can transmit pathogens from donor to recipient cross match: HIV, HEP B/C
1. packed red

diabetes

-group of metabolic disorders
-hyperglycemia resulting from defects in insulin secretion, insulin action, or both
-long term damage, dysfunction, and organ failure associated with chronic hyperglycemia especially

carbohydrates

-various forms(simple sugars and complex chemical units)
After ingestion:
-CHO are broken down and absorbed-primarily in the duodenum and proximal jejunum
After absorption:
-the blood glucose level rises temporarily and eventually returns to baseline
-reg

pancreas

-acting in concert with the liver, controls the body's fuel supply
-exocrine: cells secrete pancreatic enzymes into duct, do not secrete into the blood stream
-endocrine: cells secretes insulin directly into the blood stream

islet of langerhans secrete

-alpha cells secrete glucagon in response to low blood sugar
-alpha: glucagon- maintain glucose levels by increase release of glucose from liver to the blood
-beta cells: insulin- lowers blood glucose by facilitating the movement of glucose into body tiss

insulin

-is a hormone that facilitates movement of glucose into body tissues to lower blood sugar levels
Actions:
-promotes glucose uptake by target cells and provides for glucose storage
-prevents fat and glycogen breakdown
-inhibits gluconeogenesis(synthesis of

physiologic balance

balance of several hormones that:
-lower blood glucose levels-> insulin
-raise blood glucose levels:
--glucagon(from the islets of langerhans)
--epinephrine(from the adrenal medulla and other chromatin tissues)
--glucocorticoids: (secreted from the adrena

glucose levels

-normal fasting plasma glucose level: 80-120 mg/dl
-hyperglycemia: fasting glucose level > 120 mg/dl
-hypoglycemia: fasting glucose level < 80 mg/dl
-glucose is filtered by the renal glomerulus an is reabsorbed by the renal tubule as long as the plasma
-w

impaired carbohydrate metabolism(effects of insulin deficit)

-CHO cannot enter insulin- dependent cells
-decrease glucose used by cells
-effects:
--rapid build up of glucose in serum-> hyperglycemia
--cells begin to use of backup sources of energy (fatty acids and proteins)

impaired fat metabolism(effects of insulin deficit)

-increased lipolysis (break down of fats)
-decreased lipogenesis(formation of fat)
-Effects:
--free fatty acids(FFA) = major alternative energy source for tissues
--serum = increased FFA and glycerol
-some excess FFA is converted to cholesterol and phosph

impaired protein metabolism(effects of insulin deficit)

-body unable to store protein
-increased protein catabolism
-cessation of protein synthesis
effects
:
-increased breakdown of protein-> increased amino acids in circulation
-increased use of amino acids as alternative energy source
clinical picture:
-musc

fluid and electrolyte balance(effects of insulin deficit)

-increase serum glucose levels
-increased plasma osmotic pressure
-fluids shift into intravascular compartment
-intracellular dehydration resulting in thirst

glycosuria(insulin deficit)

-excretion of sugar in the urine
-occurs when hyperglycemia increases beyond what kidneys can reabsorb
-positive urine dipstick
-increase acetones

the three P's(clinical picture with insulin deficit)

1. polyphagia: increased hunger
-R/T catabolism of fat and protein, and relative cellular starvation
2. polydipsia: excessive thirst
-as become dehydrated -> increased serum osmolality -> triggers thirst
3. polyuria: excessive urination
-due to osmotic di

diabetes mellitus

-complex metabolic disorder in which the person has either an absolute or relative insulin deficit
-pancreas secretes either no insulin or not enough insulin
-a disease of the endocrine pancreas
-two major forms: type 1 and type 2

risk factors for diabetes

-certain medications
-race
-hypertension
-stress
-age
-inactive
-pregnancy
-high cholesterol
-obesity
-family history

hemoglobin A1C

-a serum blood test which reflects glucose level over the preceding 2-3 months
-is a better indicator of glycemic control over time than the FBS
-indicates the amount of glucose that has been attached to hemoglobin molecules over their life span

diagnosis of diabetes

1. A1C > 6.5% on two occasions
2. fasting plasma glucose of greater than or equal to 126 mg/dl
3. oral glucose tolerance test- two hour plasma glucose of 200 mg/dl on two occasions
4. symptoms of diabetes and a casual plasma glucose of greater than or equ

pre-diabetes

-glucose levels > normal but < classified as diabetes
-generally asymptomatic: it is believed that this pre-diabetes state is causing vascular damage to vital organs such as heart, kidneys, brain
-pre-diabetes- AKA: impaired glucose tolerance
-new trend:

gestational diabetes

-development of diabetes during pregnancy
-50% chance of developing diabetes mellitus later in life
-mom who deliver babies weighing over 9 pounds have increased risk to develop DM
-high risk: obesity, prior history, glycosuria, polycystic ovary syndrome,

etiology of type 1 DM

May result from combination of factors:
-genetic predisposition
-some triggering event
-immunologically mediated B cell destruction(autoimmune) cant release insulin
-childhood presentation the most common
-about 5-10% of all diabetes have type 1

type 1 diabetes

1. the stomach changes food into glucose
2. glucose enters the blood stream
3. the pancreas makes little or no insulin
4. little or no insulin enters the bloodstream
5. glucose builds up in the bloodstream

type 2 DM

-a relative insulin deficiency(less insulin secretion; rather than a total deficit)
-different underlying problems than type 1 DM
-fasting hyperglycemia that develops regardless of availability of insulin
-insulin cannot get into cells
-may not have class

three metabolic abnormalities

-
impaired insulin secretion
> cause: B cell exhaustion due to overuse
-
peripheral insulin resistance
> cause R/T increased visceral fat
-
increased hepatic glucose production
> cause: R/T impaired suppression of glucose production in liver
-altered prod

diabetic ketoacidosis(DKA)

-a type of metabolic acidosis associated with diabetes produced by excessive levels of ketones in the body
-develops when ketone production exceeds cellular use and renal excretion
-often associated with increased stress
-associated primarily with type 1

diagnosis of diabetic ketoacidosis

-hyperglycemia: blood glucose > 300 mg/dl
-low bicarbonate( <15 mEq/dl)
-low pH(<7.3)
-ketonemia: positive ketones or acetones in blood
-ketonuria: positive ketones or acetones in urine

diabetic ketoacidosis CM

-rate of onset
-rapid 1 to 24 hours
-polyuria, polydipsia, polyphagia
-dehydration:
--warm dry skin, tachycardia, weak, thready pulse, acute weight loss, hypotension
-N/V, anorexia
-ketone breath- sweet, fruity odor
-mental status change: lethargy, fatigu

hyperglycemic hyperosmolar nonketotic syndrome(HHNS- type 2)

characterized by:
-serum osmolality of 310 mOsm/L
-serum glucose of > 600 mg/dl
-absence of ketoacidosis
Two Major precipitating factors:
-infection
-inadequate fluid intake(FVD)
Pathogenesis:
-develop hyperglycemia R/T acceleration of hepatic gluconeogen

HHNS(type 2)

-pathogenesis: increase glucose levels ----- osmolality = cellular dehydration
CM:
-rate of onset: 24 hours to 2 weeks
-S & S of dehydration-> dry mucous membranes and thirst
-neurologic manifestations: decreased level of consciousness(somtimes coma); pot

hypoglycemia(complication of diabetes)

AKA: insulin reaction
Due to:
-relative excess of insulin in the blood
Characterized by:
-below normal serum glucose levels
Usually results from:
-insulin injections
-oral hypoglycemic agents
CM:
-rate of onset: sudden
-lab findings: low serum glucose
-im

microvascular disease

-seems to be related to duration of diabetes not the degree of glucose control
-associated with capillary membrane thickening
-results in microangiopathy-> small blood vessel disease
-as capillary membrane thickens, tissue become increasingly hypoperfused

retinal damage(microvascular disease)

-retinopathy
-main cause of blindness in US
-small vessels in retina become occluded, causing areas of infarction

diabetic nephopathy(microvascular disease)

- glomerular basement membrane thickens and become sclerosed- thickened and hard
-eventually destroys kidneys function resulting in ESRD -> dialysis/transplant

macrovascular disease

-more associated with type 2 DM
-atherosclerosis: thickening, hardening of large arteries
-related disorders
--coronary artery disease(CAD), peripheral vascular disease(PVD), cerebrovascular accidents(CVA), increase risk of infection

increase risk of infection(DM)

1. diminished early warning system:
-R/T impaired vision and peripheral neuropathy
-may not see/feel breaks in skin integrity
2. tissue hypoxia:
-when skin integrity is broken- may not be able to get sufficient 02 and nutrients to heal
3. rapid proliferat

diabetic foot(macrovascular disease)

-a diabetic foot with a previous healed transmetatarsal amputation demonstrates an ulcer in the region of the ankle

pH reviews

-if H+ is high, the solution is acidic
-if no H+ is contained but accept them from acids, the solution is alkaline
-an alteration in pH is a change in the hydrogen ion concentration
-cellular metabolism continually releases acids that must be excreted fro

H+

-acids are H+ donors
-bases are H+ acceptors, or give up OH(hydroxide ion) in solution
-acids and bases can be:
1. strong: dissociate completely in solution
2. weak: dissociate only partially in solution

buffers(control of acids)

Chemicals that aid in regulation of the pH of the fluids of the body
-take up H+ or release H+ as conditions change
-buffer pairs: weak acid and a base
-exchange a strong acid or base for a weak one
-results in a much smaller pH change
1. bicarbonate buff

respiratory mechanism(buffer)

-body produces CO2
-CO2 and H20 creates carbonic acid
-exhalation excretes carbonic acid
-doesnt affect fixed acids like lactic
-body pH can be adjusted by changing rate and depth of breathing
-correction of carbonic acid dependent on components of respir

kidney excretion(buffer)

-can eliminate large amounts of acid except carbonic acid
-can also excrete base
-can conserve and produce bicarb ions
-most effective regulator of pH
-if kidneys fail, pH balance fails
-depends on normal functioning of renal system

rates of correction

-buffers function almost instantaneously
-respiratory mechanisms take several minutes to hours
-renal mechanisms may take several hours to days

acidosis

-decrease of pH of blood below normal
-principal effect of acidosis is depression of the CNS through decrease in synaptic transmission
-CM: generalized weakness
-altered CNS function is the greatest threat
-severe acidosis causes:
1. disorientation
2. com

alkalosis

-increase of the pH of the blood above normal
-alkalosis causes over excitability of the central and peripheral nervous system
-CM: numbness, lightheadedness
-it can cause:
1. nervousness
2. muscle spasms or tetany
3. convulsions
4. loss of consciousness

respiratory acidosis

carbonic acid excess caused by blood levels of CO2 above 45 mm Hg
-hypercapnia: high levels of CO2 in blood
-caused by factors that impair excretion of carbonic acid-> impaired gas exchange, impaired respiratory control
-chronic conditions:
1. depression

signs and symptoms of respiratory acidosis

-breathlessness
-restlessness
-lethary and disoriented
-tremors, convulsions, coma
-respiratory rate rapid, than gradually depressed
-skin warm and flushed due to vasodilation caused by excess co2
-H/A(dilation of blood vessels)
-tachycardia
-dysrhythmias

respiratory acidosis

1. breathing is suppressed holding CO2 in the body= increase CO2
2. kidneys conserve bicarbonate ions and eliminate H+ ions in acidic urine
3. lactic solution used in therapy is converted to bicarbonate ions in the liver

respiratory alkalosis

-carbonic acid deficit; CO2 < 35
- pCO2 less than 35 mm Hg
-most common acid base imbalance
-primary cause is hyperventilation
-conditions that stimulate respiratory center: prolonged sobbing, acute pain, acute anxiety, pulmonary disease and congestive he

respiratory alkalosis steps

1. hyperactive breathing blows off C02
2. kidneys conserve H+ ions and eliminate bicarbonate in alkaline urine
3. bicarbonate ions are replaced with chloride ions

metabolic acidosis

-
bicarbonate deficit
: blood concentrations of bicarb drug below 22 mEq/L
-causes:
1. loss of bicarbonate:
-diarrhea, GI fistula, intestinal decompression, renal tubular acidosis
2. accumulation of acids(lactic acid or ketones)
-ketonacidosis, hyperthyro

metabolic acidosis steps

1. bicarbonate decreases because of excess prescence of ketones, chloride, or organic acid ions
2. kidneys conserve bicarb and eliminate H+ ions in acidic urine
3. lactate solution in therapy is converted to bicarb ions in the liver

metabolic alkalosis

-
Bicarbonate excess
: concentration in blood is greater than 26 mEq/L; deficit in any acid accept carbonic acid
-causes: excess vomitting=loss of stomach acid, NG to wall suction, certain diuretics, endocrine disorders, severe dehydration
-compensation:

metabolic alkalosis()

-respiration slow and shallow
-hyperactive reflexes; tetany
-often related to depletion of electrolytes
-atrial tachycardia
-dysrhyhmias

metabolic alkalosis steps

1. bicarb increases because of loss of chloride ions or excess ingestion of sodium bicarb
2. kidneys conserve H+ ions and eliminate bicarb in alkaline urine
3. bicarb ions replace by chloride ions