Exam IV

pH normal range

7.35-7.45

what is it called when pH is less than 7.35

acidosis

too much hydrogen ions

body is not getting rid of enough co2

COPD, pneumonia, post op patients, narcotics

what is it called if pH is greater than 7.45

alkolosis

too little hydrogen ions

boyd getting rid of too much co2

How do the lungs and kidneys work together to maintain acid-base

balance, and what is the primary role of each system?

lungs expel co2

CO2+H2O(lungs) —> H2CO3—> H+HCO3(kidney)

CO2 normal ranges LUNGS

35-45

less than 35 is alkalosis (pH of more than 7.45 is respiratory alkalosis)

more than 45 is acidosis (pH of lower than 7.35 will mean it is respiratory acidosis)

HCO3 normal range for bicarbonate RENAL

21-28

more than 28- alkalosis

less than 21- acidosis

bicarb of less than 21 pH much be less than 7.35 to say its metabolic acidosis

EX. pH-7.18(low), CO2- 52(high), HCO3-22(normal)

pH-acid

CO2-acid

HCOs-normal

must be repository problem

respiratory acidosis

what interferes with homeostaisi when it comes to acid blaance

high/low rr, renal problems

oxygenation

measured using arterial blood gas

PaO2- partial pressure of oxygen in arterial blood- normal is 80-100, lower than 80 is hypoxemia, less than 70 is hypoxia

SaO2- oxygen carrying capacity of hemoglobin-

repiatory buffers

regaulated by rr

retention or increase in co2

generation of carbonate

renal buffer is most effective but slowest may take 24 hours

excretes retention of hydrogen and bicarbonate

kidneys secrete and reabsorb hydrogen and HCO3-

deadly levels of pH

less than 6.8 or more than 7.8

hydrogen and potassium relationship

normal- potassium inside the cell and low hydrogen

acidosis- hydrogen moves into cell, potassium moves out= hyperkalemia (dysrhythmias)

alkalosis- hydrogen moves out of cell and potassium moves in=hypokalemia

if pH is low expect high potassium- acidosis

if pH is high expect low potassium- alkolosis

repsiratory compenstation

rr compenstation- FAST

-if pH is low (acidosis) you breathe faster so there is less co2 and higher pH

-if pH is high for alkolosis you breathe slower which leads to high co2 and low pH

ROME

R- respiratory

O- opposite (pH hihg-PCO2 low- alkolosis) (pH low-PCO2 high-acidosis)

M- metabolic

E- equal (pH high- HCO3 high-alkolosis) (pH low-HCO3 low-acidosis)

renal failure

metabolic acidosis

diabetic ketoacidosis

metabolic acidosis

respirtory filaure

resiratory acidosis

prolonged vomiting

metabolic alkolosis gettign rid of all hydrogen/acid

hyperventilation

respiratory alkolosis

hypoventilation

respiratory acidosis

sedative or opiod use

respiratory acidosis

response to anxiety/fear/pain

respiratory alkolosis

overuse of antacids

metabolic alkalosis

putting too much base in

pregnant people are at risk

asthma

respiratory alkolosis for early stage, late stage is repsuroayr acidosis

EX. pH- 7.49(high, alkalosis), CO2-29(low, alkalosis), HCO3-20(low, acidosis)

kidneys trying to compensate for the respiratory system, only partially compensated since the pH is not normal yet

fasting/starvation

metabolic acidosis

posioning

metabolic acidosis

COPD

respiratory acidosis

bacterial pneumonia

respiratory acidosis

acute hypoxia early stage

respiratory alkalosis

excessive gastric suctioning

metabolic alkolosis

acute hypoxia late stage

repsirtaory acidosis

end stage renal disease

metabolic acidosis

hypercapnia high co2 levels

respiratory acidosis

the resukt of a patients abg indicates an oxygen level of 72 mmHg. what should the nurse monitor closley absed on this finding

level of conciousness

in caring for a pateints with acid base disorders, it is imortat that the nurse understand what regarding the renal buffering system

bicarb9natre is excreted if the body is in alkalosis

EX. PaCO2- 33, paO2-94,HCO3-19, SaO2-98

fully compemnstated metabolic acidosis

pH is normal

Co2- alkolosis

bicarb- acidic

sicne the pH is less than 7.40 we know that metabolic was the problem since that kind of matches up with bicarb

rr compenstation happened ot fix the problem by breathing fast

Ex. pH- 7.31;PaCo2-48 and HCO 24

respiratory acidosis

the nurse provides care for a patient admitee ot the unit with respiratory failure and respiratory acidosis. thenurse correlates which data from the patient history as the probable cuase for the current diganosis

recent sevrere pulmonary infection

which intervention is used for respiratory acidosis

perform chest physiotherapy (clears the lungs and airway)all

allen test

compress both arties until the skin on the palm appers blanched, the ulnar artery is releases which results in returing of color to the hand

this si important to test becuase it shows circulation to se if its a good spot to get accurate abg

unchecked ng tube suction can lead to what

metabolic alkalosis

removing too much acid from the stomach, just like vomiting can lead to more base than acid

a patient not excerting hydrogen due to renal failure may also not be able to reabsobr

bicarb

a patient with metabolic alkalosis is at risk for which condition

seizures

low calcium=increased excitibaility

high potassium=increased excitability

metabolic alkalosis is commonly asssociated with

hypokalemia- weakness, arrythmias, muscle cramps

potassium goes into the cell

loss of chloride is commonly seen in

vomitting\

stomach contains hydrochloric acid so its leaving when you vomit

pateints presnets with lethargy, hypotension, dysrhytmias, decreased loc

acidosis

no oxygenation

a patient with diabetic ketoacidosis will most likely have

metabolic acidosis

a diabetes patient presents with deep, rapid breathing (Kussmaul), fruity breath odor, weakness, and confusion

metabolic acidosis

which finding indicates compenstaion for metabolic acidosis

deep rapid breathing

your patient is in renal failure, they may have difficulty excreting this blank causing blank

hydrogen, acidosis

you get rid of hydrogen when you pee

a pateint with diahrea for 3 days has a blood gas of ph-7.25 co2-34, hco3-10 which is

metabolic acidosis

if ph is low what will happen to potassium

potassium will be high

what will vomiting do to potassium

decrease potassium, alkolosis

what will diuertics do to potassium

lower it, alkolosis

kidney failure will do what to potassium

higher it, acidosis

what would ahppen to potassium with dka

higher potassium, but total low, acidosis

pump can deleievr what kind of insulinn

rapid acting and short acting

best for type 1 diabetes

insulin pump

change the needle every 2-3 days

goes into sub q tissue in stomach

does not replace finger stick

rapid and short acting insulin

set pump to deliver a dose in a basil/long acting rate based on metabolism

not recommended for

insulin pen

casn put mixed insulin in it

only by 1 unit

have to prime it

change needle every time

defien glucose regulation and why it is vital

all of our cells need glucose, negative feedback loop that is regulating the glucose level to keep the body in homeostasis and provide energy to the brain

hyper/hypoglycemia can cause organ dysfunction, cellular injury, or death

differentiate between glycogenolysis and gluconeogenesis

glycogenolysis- liver breaks down stored glucose

gluconeogensis- body makes new glucose from fats and proteins

what are the normal fasting and postprandial blood glucose ranges for euglycemia

70-99 fasting

<140 1-2 hours after meals

descrieb the role of insulin and counterregulatory hormones

insulin lowers blood sugar and counterregulatory hormones increases it

explain how insulin facilitates glucose uptake by body cells

insulin carries glucose to the cells and changes the cells permeability to let glucose eneter the cell for energy and storage

glucose regulation

glucose regulation is the body ability to maintain normal blood glucose levels through a balance of insulin and couterregualtormy hormones

hypoglycemia- BG<70 mg/dL (severe <54)

euglycemia (normal, pre and post prandial)- BG 70-140

hyperglycemia- post pradial BG- >140 (severe >180)

pathophysiology- food is stomach that is transported to the blood, insulin gives signal to go to bloodstream to et sugar and carry to cells where they are energized. if not enough carbs glucagon is released (<70) to help breakdown stored glucose (glyconeogenesis). insulin normally allows glucose to eneter cells —> used for energy (ATP)

in fed state- blood glucose rises —> insulin rlewased by beta cells —> liver takes up glucose and stores as glycogen —> cells take in glucose for energy—> blood glucose stable

if insulin is absent or ineffective: glucose stays in the blood—> hyperglycemia —>

blood becomes hyperosmolar —> pulls fluid from the cells —> dehydration —> kdineys try to remove glucsoe —> polyuria(too much urination)

counterregulitaory hormones (glucagon , cortisol) increases glucose further—> cells become starved despite high blood sugar —> body breaks fat—> ketones—> ketoacidosis(DKA)

-chronic hyperglycemia damages the blood vessels and organs

in fasted state- glucose call —> glycogen released by alpha cells —> liver breaks down glycogen, releases glucose—> cell take in glucose for energy —>bloo gluose stable

what is the process called for liver storing glucose

glucogenesis

polyfacsia

too much hunger

carbohydrate

provide 4 kcal/g and are the primary energy source

general population- 45-65% of carbs in the diet

diabetes patient- 33-40%

simple carbs- rapdily absorped- glucose, fructose, galactose (use for diabetes patients)

complex carbs- provide sustained energya and fiber

glycogen stored in lievr and muscle- muscleself use energy, liver share with the body energy

if inadequate carb intake - fat breakdown—> ketone production (ketogenesis)

glycogenesis

glucose —> glycogen

glycogenolysis

glycogen —> glucose

is hyperglycemia or hypoglycemia easier to manage

hypo- insulin (very deadly)

hyper- glucogen, epinephrine, cortisol, GH, ACTH, thyroxine (tiem to fix this)

metabolic syndrome

simultaneous presence of metabolic factors that increase risk for type 2 diabetes

three of the following traits present-

• abdominal or central obesity

• increased serum triglycerides greater than or equal to 150 mg/ dL

• decreased high density lipoprotein less than or equal to 40 mg/dL in male individuals, less than 50 mg/dL in female individuals

• hypertension greater than or equal to 130/85 mmHg

• fasting blood glucose greater than 100 mg/dL

hyperglycemia signs and symptoms

thirst- sugar pulls water from cells and wants to get rid of it

urinate often-

dry skin- dehydrated

hungry- cells are not getting aything, starving

blurry vision- increased sugar makes vessels in eyes damaged(diabetic retinalopothy)

drowsy-

slow healing wounds- the blood is not circulating properly and the immune system is down sicne the blood isn’t regulating

sugar is high in the blood, but not being utilized

treatement- check sugar, call provider

hypoglycemia signs and symptoms

shaky

fast heartbeat

sweating

dizzy

anxious

hungry

blurry vision

fatigue

headache

irritable

treatment that is easily absorbs- juice, cracker, candy. check sugar, give 15g of carbs, then check again, if still less than 70 then do 15 more grams if that doesn’t work call the doctor

patients that take insulin but aren’t diabetic

when cortisol is increased

those who take steroids (can increase glucose)

type 1 diabetes mellitus

type 1- autoimmune dysfunction involving the destruction of beta cells in the pancreas. not preventable

• can happen at any age, usually less than 30

• cause is unknown (maybe viral infection, no vaccines, family history, etc)

• fatigue, excessive thirst, frequent urination, weight loss, blurred vision

• symptoms and treatment is the same as type 2

• wont survive without insulin, only meducation they take is insulin

type 2 diabetes mellitus

progressive condition due to the increasing inability of cells to respond to insulin and a decreased production of insulin. could be reversible and preventable

• 10% of the population has it

• caused by pancreatic disease, overweight, stress, medicine

gestational diabetes

a hyperglycemic condition associated with placental hormones causing insulin resistance

• may have family history

• older than 25 years of age during pregnancy

• hormones are preparing the body for the fetus and needs more glucose in response to feeding the fetus, fetus gets the sugar, and grows more

• sugar and insulin does not cross the placenta

• insulin used to treat

• placental hormones —> insulin resistance

• prior macrocosmic baby

diabetes in general

non-modifiable risk factors- family history, age, genetics, ethnicity, pregnancy

modifiable- obesity, diet, sedentary lifestyle, low exercise, stress, medications(steroids, antipsychotics)

diagnosis- first have to have a reason you think you have diabetes- three p’s (polyuria, polyphagia (extreme hunger, protein and fat used for energy, leads to weight loss), polydipsia(excessive thirst, decrease skin turgor, hypotension, weak, dry membranes)

DKA- nausea vomiting, abdominal pain, kussmal respirations, vision changes

tests- check fasting and postprandial glucose

• fasting (>126 mg/dL) normal is 70-99, fasts for 8 hours

• random glucose (>200 and symptoms)

• a1c (>6.5%) don’t fast for this test since your testing 2-3 months of your past sugar, anemia could affect it

• oral glucose tolerance test OGTT (most sensitive especially in pregnancy). fasts for 8 hours drink 50g sugary drink then test glucose an hour later 130-140 is concerning

• c-peptide (determine type 1 vs type 2) this lab test helps determine whether a patient is producing their own insulin

• autoantibodies (type 1)

• continuous glucose monitoring

treatment-

• lifestyle changes

• medications- metformin( first line type 2), insulin (type 1 and advanced type 2)

• adjust doses based on trimester, check 24-28 weeks

• acute management- DKA- fluids, insulin, electrolytes, iv dextrose push; hypoglycemia- 15g glucose (15/15 rule)

• frequent glucose checks every 4 hours

complications-

acute-

• DKA (acidosis, dehydration)- life threatening, onset over hours/days

• HHS (severe hyperglycemia >600), onset over days/weeks, neuro

• severe hypoglycemia—> coma

chronic-

• retinopathy—> bindness

• nephropathy—> kidney failure

• neuropathy—> ulcers/amputation

• cardiovascular disease—> MI, stroke

• infections

maternal-

• preeclampsia

• infections

• c section

• hemorrhage

fetal-

• baby could have hyper insulin production from mom, then they are at risk for hypoglycemia at birth since their insulin production is cut off from the mother

nursing management - blood glucose levels, vitals, mental status, signs of hypo.hyperglycemia, hydration status, urine, skin, feet, vision, medication adherence, diet, lifestyle habits, signs of infection

DAWN

naturally- normla physicological repsonse

hormonal effect- due to release of glucogen, GH, cortisol,

wat to do- nothing, your body will release insulin to get norma; blood glucose level

SOMOGYI

man made- happen mainly in DM type 1

rebound effect- due to hypoglycemic

what to do- talk to dr, what shoud be done, either decrewase insulin dose or increase actvity

this rule is followed during illness for diabetic patients

the SICK day rule

this is the best immediate treatment for conscious hypoglycemia

15g of fast acting carbs (juice, glucose tablets)

this hormone source causes insulin resistance in GDM

placenta

increased urination cuased by substances i th urine that pull water with them causing polyuria/polydipsia

osmotic diuresis

this oevrnjgith vlaue helps distiguish somogyi effect vs dawn phenonmenon

midnight glucose check

alcoohl increases risk of this dangerous glucose codntion

hypoglycemia

these medications require increased monitioring due to hyperglucemia risk

steriods

this medications should be taken by mouth 30 min before meals

glipizide

thsi class drugs decreases glucagon secretion and delays gastic emptying

glp1 receptor agonist

this class medications improve insulin snesityivty in tissues

insulin sensitizers such as metformin

correct nail trimming method

staright across