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 body’s 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
o 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.

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 (kussmaul’s)
- 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 difficulties with speech
o 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