EXAM 2

Fluid distribution at the capillary level

- Movement of the fluid in the body takes place at the level of the capillary
- Fluid is important for movement of nutrients and O2 into the interstitial and removal of wastes and
CO2 into the vessels for elimination
- Osmosis and diffusion promote movement of fluid across the semi-permeable membranes
-

Osmosis is the movement of fluid from an area of low solute concentration to an area of higher
concentration until the areas are equal concentration
Diffusion is the movement of solutes from an area of greater concentration to an area of lesser
concentration leading to an equal concentration of solutes
Hydrostatic pressure
Pushing out of intravascular space
Osmotic pressure
pulling into intravascular space
from increased osmolarity caused by
colloids (plasma protein): proteins exert osmotic pressure known as
colloid osmotic pressure (COP)
dissolved solutes: dissolved particles in blood exert osmotic pressure

Tonicity/Osmolarity
- Hypotonic/hypo-osmolar: less osmolarity than plasma (less concentrated)
Water moves out of the intravascular compartment, causing the cells to swell and burst
(decrease osmotic pressure)
Decrease production of ADH pee a lot of it out
- Isotonic/iso-osmolar: same osmolarity as plasma
Fluid remains in the intravascular compartment
- Hypertonic/hyper-osmolar: greater osmolarity than plasma (more concentrated)
Water moves out of the cell into the intravascular compartment, causing the cells to
shrink
If you have an increase in concentration of blood, more solute osmoreceptors will
increase ADH to hold onto more H20, and make thirsty to take more water in
Causes of edema
- Increase in capillary hydrostatic pressure
Increase BP from
Hypervolemia (fluid volume excess)
Vasoconstriction
- Decrease in osmotic pressure
Decreased plasma proteins
malnourished
- Increased capillary permeability
inflammation
- Lymph vessel obstruction or removal
Venous obstruction
Electrolytes
- Sodium
135-145 mEq/L, major ECF cation (this includes inside the blood vessel and the
interstitial)

Primary determinant of ECF volume and osmolality, activates nerve & muscle cells:
necessary for muscle contraction and transmission of nerve impulses, essential
electrolyte in the sodium-potassium pump
Potassium
3.5-5.0 mEq/L, Major cation of ICF, 98% of K+ is in the cell
80% of K+ excreted daily leaves the body through the kidneys
Necessary for transmission of electric impulses, particularly in nerve, heart, skeletal,
intestinal, & lung tissue
Assists in regulation of acid-base balance by cellular exchange with H+
Calcium
8.5-10.4 mg/L
Varies for different ages
Most abundant electrolyte in the body, more than 99% of bodys calcium is located in the
skeletal system
Necessary for nerve impulse transmission; muscle contraction, including cardiac muscle
Necessary for blood clotting and for strong bones & teeth
Vitamin D assists with absorption of Ca++ in GI tract

Acid-Base balance
- Concentration of H+ (hydrogen ions) in the blood
larger # of H+ ions = low pH = acid
small # of H+ ions = high pH = alkaline (base)
Acid-Base imbalance
- Metabolic Acidosis
HCO3 loss, acid retention
Possible causes: diarrhea>>lose HCO3, DKA, renal disease
Clinical manifestations: rapid deep breathing, fruity breath, HA, lethargy, N.V
- Metabolic Alkalosis
HCO3 retention, acid loss
Possible causes: vomiting>>lose HCL, gastric secretion, excess anti-acid intake
Clinical manifestations: slow, shallow respirations, restless, confused
- Respiratory Acidosis
Excess CO2 retention
Possible causes: airway obstruction, slow shallow respirations
Clinical manifestations: hypoventilation, headache, weakness, confusion, lethargy
- Respiratory Alkalosis
Excess excretion of CO2
Possible causes: hyperventilation (anxiety, pain, fear)
Clinical manifestations: hyperventilation, lightheaded, paresthesia, anxiety
Diabetes Mellitus:
- Basic problem is inadequate insulin effects in receptor tissue
o Deficit of insulin secretion
o Production of insulin antagonists
- Diabetes results from abnormal carbohydrate, protein, and fat metabolism
- Cells are unable to utilize glucose for energy so instead use fats resulting in production of
ketones (waste product)

Type 1 Diabetes
Risk factors:
- Genetics
- Age (acute onset in children and adolescents)
Etiology:
- Auto immune
Pathogenesis
- Autoimmune destruction of beta cells in pancreas
- Leads to absence of insulin production
- Insulin replacement required
NOT linked to obesity
Type 2 Diabetes
Risk factors:
- Obesity
- Age (>50, with slow and insidious onset)
- Increasing in teens and young adults
Etiology:
- Increased carbohydrate consumption combined with age induced decrease in metabolism
Pathogenesis:
- Decreased production of insulin and/or increased resistance by body cells to insulin
- Non-insulin-dependent therefore oral hypoglycemic medications may be used
General clinical manifestations of Hyperglycemia
Polyuria:
- Hyperosmolar filtrate because of glucosuria
Polydipsia:
- Dehydration results from polyuria leading to decreased blood volume
- Osmoreceptors detect hyperosmolar state
Polyphagia:
- Insulin deficit results in decreased transport and use of glucose in many cells
- Body wants more fuel for energy
Diagnostic findings
Fasting blood glucose level
- Test for plasma glucose levels after food has been withheld for at least 8 hours
o Glucose levels 126mg/dL more than one time of testing confirms a diagnosis
o Normal Range Fasting Blood glucose 70-110 mg/dL
Glucose tolerance test
- Insulin response to large oral glucose dose is immediate, peaking in 30 to 60 minutes and
returns to normal within 3 hours. (70-120 mg/dL)
- Measures plasma glucose 1 and 2 hours following ingestion of 75g of concentrated glucose
solution.
- Normally glucose levels return to normal 2 to 3 hours following ingestion of glucose load.
- Elevations above normal indicate that insulin is not being released.
Glycosylated hemoglobin test (HbAc1)
- clinical and subclinical diabetes
- monitor glucose levels over several months (6-12 weeks)
- acceptable level is 7% or less
Urinalysis
- glucose

If blood glucose level exceeds the reabsorption capacity of the tubules (about 160
180 mg/dL) glucose will appear in the urine.
ketones
o Excess presence of ketones in the urine (ketonuria) associated with DM
o Check the urine for ketones if blood glucose is 300 mg/dL.
o

Acute complications for type 1 diabetes

Diabetic ketoacidosis (DKA)
Risk factors:
- type 1 diabetes (insulin dependent patients)
Etiology:
- poor management of blood glucose
- insufficient inulin in blood (dosage error/non-compliance)
- onset of acute stress/infection
Pathogenesis:
- glucose cannot enter cells
- use of lipids to meet cellular needs results in production of ketones
Clinical manifestations:
- dehydration
o thirst, dry, rough oral mucosa
o warm, dry skin
- acetone breath
- lethargy, decreased responsiveness
- metabolic acidosis
o rapid deep respirations (kussmauls)
- electrolyte imbalances
o abdominal cramps, nausea, vomiting, lethargy, weakness
Acute complications for type 2 diabetes
Hyperosmolar hyperglycemic nonketotic state (HHNK)
Risk factors:
- type 2 DM
- age-related cognitive impairment
Etiology:
- poor management of blood glucose
- insufficient insulin in blood (dosage error/non-compliance)
- onset of acute stress/infection
Pathogenesis:
- hyperglycemia leads to hyperosmolar filtrate which leads to profound polyuria and
dehydration
- insidious in onset and diagnosis may be missed
Results in severe dehydration and electrolyte imbalances
Clinical manifestations:
- insidious in onset
- hyperglycemia
- severe dehydration
o increased hematocrit
o los of skin turgor
o increased heart rate and respirations
- electrolyte imbalances result in:
o neurological changes
o muscle weakness

o
o

difficulties with speech

abnormal reflexes

Complications of chronic hyperglycemia

Microangiopathy
- increased incidence of atherosclerosis
- change may occur in large arteries
o tissue ischemia, necrosis, leading to ulcer formation
o gangrene
o peripheral vascular disease
Macroangiopathy
- obstruction or rupture of small capillaries and arteries
o tissue necrosis and loss of function
o retinopathy- leading cause of blindness
o nephropathy leading to degeneration in glomeruli of kidney causing chronic renal
failure
Neuropathy
- common complication caused by ischemia in microcirculation to peripheral nerves
o impaired sensation, numbness, tingling, weakness, muscle wasting
Risk of Infections
- delayed wound healing
- infections in feet
- fungal infections
o caused by candida in vagina or oral cavity
- urinary tract infections
- dental infections