Acidosis of Metabolic Origin

Acidosis of Respiratory Origin

Alkalosis of Metabolic Origin

Alkalosis of Respiratory Origin

What is 'Acidosis of Metabolic Origin' and what are its signs?

condition resulting from either loss of bicarbonate or retention of nonvolatile acid.

(excess acid)

Signs: Headache, lethargy, weakness, confusion

What is Acidosis of Respiratory Origin?

What are its signs?

condition resulting from excess acid in the blood secondary to carbon dioxide retention.Poor ventilation

Signs: weakness, respiratory distress, agitation, confusion, tacchycardia

What is Alkalosis of Metabolic Origin?

What are its signs?

condition resulting from either retention of bicarbonate or loss of nonvolatile acid.

excess base

signs: restlessness, muscle twitching, tingling and numbness in the fingers, seizures, coma

What is Alkalosis of Respiratory Origin?

What are its signs?

Not Very Common, Loss of C0_2,, High Blood pH

condition resulting from excess base in the blood secondary to increased carbon dioxide expiration.

signs: hyperventalation, anxiety,

Buffers (fastest within seconds): combination of a weak acid and a strong base that work to nuetralize the blood pH and keep it stable.

Respiratory(middle within minutes): rate and depth of respiration alter pH. More CO2 exhaled, less carbonic acid.

Kidney(slowest within hours/days): urine excretes excess H+, sodium carbonate, and exchanges H+ for Na+

fxn of water

temperture regulation

supports cell structure

medium for cell metabolism

nutrient transport

1. fluids

2. foods

3. fat, carbs, protein oxidation

colloidial osmotic pressure isthe osmotic pressure attributed to proteins and other macromolecules. It is meant to equalize the concentration of solute and thus osmotic pressure on both sides of the membrane.

decreased colloid osmotic pressure causes edema because the cells around are hypotonic

decreased water intake -> increased serum osmolality

hypothalamus

posterior pituitary releases antidiuretic hormone (ADH)

Kidney

retain water and sodium

1. urine

obligatory urine: the amount of fluid necessary for the body to excrete waste products and solutes

facultative urine: excess water that is excreted through urination.

2. feces

3. skin(sweat)

insensible losses

(fluid loss that cannot be easily measured (usually refers to fluid lost via sweat and respirations).)

RSL: concentration of Na, K, Cl, Urea that the kidneys must excret

(dietary protein x 5.7) + (Na+K+Cl)

maintain body fluid osmolarity

distribute boyd fluids among compartments

rgulate acid- base balance

promote meuromuscular activity

Sodium: maintains water balance, water follows sodium.

causes an excess

hypernatemia: Water loss from the plasma without a corresponding loss of sodium, or too much sodium added to the plasma without adding water. Nuerons begin to shrink

ADH

ALDOSTERONE

ADH regulates water resorption in the collecting ducts

Aldosterone regulates sodium resorption (and thus indirectly water resorption) in the renal tubules.

136-145 mEq/L.

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HYPOnatremia - < 136 mEq/L

Muscle cramps, exhaustion, lethargy

HYPERnatremia + >145 mEq/L

Confusion behavioral change, weakness, brain damage

what is the major intracellular cation and what cation and what is it important for—what can cause an excess or deficit?

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deficency: Diuretics can do this by promoting urine formation.

excess:

Hypokalemia - : < 3.5 mEq/L

Excess glucose/insulin, Diuretics, Alkalosis, Vomiting GI suction                   

Treatment: 10% KCl post meal

muscle weakness, diminished tendon reflexes, poor lung muscle breathing

Hyperkalemia +: > 6 mEq/L

Causes:   Renal Failure, Acidosis, Major Surgery Treatment:  low K+ diet

signs: muscle weakness, paralysis, tingling fingers, cardiac arrest        

Chloride: maintains water balance  and acid/base balance.

in excess:<96 vomiting treatment: add NaCl to IV

defit: >106 dehydration, acidosis, diabetes, excess Cl intake

treatment:NaHCo3

No insulin production.

the beta cells of pancreas are destroyed

therefore glucose cannot be used for energy by the cell

required insulin injects to live

typically diagnosed by age 30

Excessive thirst( polydipsia)

Freq. urination (polyuria)bc the kidney cannot handle the glucose coming in to compensate

dehydration bc of too much peeing

polyphagia: no glucose for energy so the body demands more food.

ketoacidosis

Weight loss

what is type II diabetes and how does it occur?

polyuria

polydipsia

polyphagia

wt loss

what are the different endocrine cells of the pancreas and what do they produce?

alpha cells: glucagon production

                             beta cells:  insulin production

                             delta cells:  secrete_somatostatin                                                                  inhibits insulin and glucagon

How does insulin impact lipid metabolism?

[image]      Insulin effects on fat breakdown and fatty acid synthesis

•         Reduces lipolysis and ketogenesis

•         Promotes fatty acid synthesis in the liver

•         Promotes triglyceride storage in adipose 

What was the DCCT and why was it important?

Diabetes Control and Complications Trial (DCCT)

NIH sponsored: Long-Term Study of Type 1 Diabetes

Premise: Does tight glycemic control reduce future complications?

Experimental Design:  Intense Treatment of Diabetes vs. Conventional Treatment

Diabetes Control and Complications Trial (DCCT)

Researchers followed 1,441 people with diabetes for years

Half followed their standard treatment, half followed aggressive, tight - control plan

Results:  people with aggressive, tight - control treatment had lower blood glucose levels than those on standard treatment

What are the 3 main types of oral medications for Diabetes (who takes them, how do they act, and give 1 example of each one)

Sulfonylureas/ glimepride

stimulates beta cells to create more insulin

type 2

Biguanides/ metformin

Sensitizes body to insulin already present

obese pts, type 2

Alpha-glucosidase inhibitors/acarbose

   Slow down or block carbohydrate absorption