NCMB Midterm 312 Lec

NCMB 312 LEC Midterm
Superficial Partial Full thickness Deep - Patient would die because of dysrhythmia
thickness burn thickness burn burn thickness - Entry wound =big
burn - Exit wounds = bigger
epidermis epidermis Epidermis Muscles &
- More movement more electricity enter the body
&portion of dermis bones
dermis Subcutaneous  Ice burn phenomenon
1st degree burn 2nddegree burn 3rd degree burn 4thdegree - Under neat the skin with the =minor injury
burn involving the nerves more damage
-Least damage -epidermis is -requires Spontaneous4. Radiation burn
because destroyed or removal of healing will - Exposure to ultraviolet light , x-rays or
epidermis is injured & Eschar & split not occur radioactive source
the affected or full
part . - portion of thickness skin Note :
-skin grafting
dermis is may grafting required
o Burn on face
be injured
S/S: S/S: - leave a deep -Injured are -
- Pink to red - Tingling red , black & is black - o Burn on perinium
- no blisters - Pain white yellow or no/little pain- Treated as a Major burn
- skin blanches - Hyperesthesia brown area or - Thin
with pressure - Blistered - lather edema - Close to infection
- Mottled is present . o Burn on eye
- Blindness
-painful but -Painful
can lead be Sensitive to
eased with cold air
cooling
week
-3-7 days -2-4 weeks week - months -months
 Palm method
- Sized ng palm ng patient

- 1 palm is = 1 % the same size of the patient
BURN DEPTH
BURN
Types of burn
1. Thermal burn
- Most type of burn
- Caused by exposure to flames , hot liquids
,steam or hot objects .
2. Chemical burn
- Caused by tissue contact with strong acids ,
alkalis or organic compounds .
- Harder to treat alkaline
3. Electrical burns
- Out side burn
- Affect the muscle ex, heart
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(Occures ocasionally in this phase)
- Beginning on the fourth / fifth postburn day , K
shifts from extracellular fluid into cells .
 Metabolic acidosis loss of sodium depletes fixed
based ; relative carbon dioxide content increases
PHASE OF BURN INJURY
Emergent phase / resuscitative phase _______ Rehabilitative phase _____________________
- more on ABCD - Begins with major wound closure & ends w/ the
- Onset of injury highest possible level of functioning.
- Continues 48 hrs/ completion of fluid - Emphasis on psychological adjustment
resuscitation prevention of scars & contractures prevention of
- completion of fluid resucitation scars & contractures resumption of pre burn
- Trying to wrap the patinet to evphorative fluid activity
loss Local effects of burn
- Evaluate immediate problems - Dilation of the capillaries ( increase the
- Fluid loss edema formations , potential for permeability- Plasma with albumin )& small
peripheral circulatory impairment vessels in the arear of burn
- Immidiate can focuses on maintaning open  capillary permeability
airway adequate breathing & circulation ,  plasma seeps out in the tissues
limiting extend of injury & maintaining functions  edema & blisters injury to cell & allows K to
or vital organs escape in the extracellular compartment
Edema &  cardiac output
Acute phase/ intermediate________________
SYSTEMIC EFFECTS
- Begin 48-72 hrs
 Fluid balance & blood needs = blister
- To correct the fluid shifting  1kg = 1 L
- After injury or beginning of diuries until near - Evaporative fluid loss may 3-5 L or more /24 hr
wound closure in complete period
- Colaborative approach to care is directed toward  Shift of plasma proteins from capillaries may result
continued assessment & maintenance of the the hypothermia
cardio , respi , G.i , nutritional status , wound  Blood is shunted from the kidneys to compensate
care , pain control & phychological interventions for the fluid deficit and the urine output falls if noy
& prevention of infections corrected
 Fluid remobilization phase ( state of diuresis) tissue perfusion
- Intertitial fluid  plasma cardiac output
 Hemodilution (decreased hematorict) hypovolemic shock
 R-blood cell consentration is diluted as fluid enters  Weight loss should not exceed 1kg/day
the intravascular compartment , loss of red blood  RBC are destroyed & causing = hemoglobinuria
cells destroyed at burn site  Hemoconcentration will result because the
 Increased urinary output liquid blood component is lost in extravascular
- Fluid shift into intravascular compartment space .
increase renal blood flow & causes increased  Potassium excess massive cellular trauma
urine formation causes release of K into ECF
 Sodium (Na) deficit w/ diuresis  Sodium deficit
- Sodium is loss w/ water , existing serum sodium - Na is lots in trapped edema fluid & exudate & by
is diluted by water influx shift into cells
 Potassium (K) deficit
 Metabolic acidosis - Paralytic ileus = vomiting ( di gumagalaw ang
- Cause by loss of bicarbonate ions accompanies chan) = les perfusion = acid stays 
the sodium loss  Curling Ulcer  burn patient only experience
 Respiratory system this ( because of the
- Carbon moxide poisoning leading cause of the  Correct fluid & electrolyte balance
deaths , - Fisrt 24-48 hrs
- It displaces displace oxygen on hemoglobin - IV fluid balance solution (LR)
blood is unable to transport O2 to the - Insertion of indwelling catheter to monitor
tissues output
- Smoke inhalation injury causes loss of ciliary - Check for signs of fluid overload cersus
action & severe mucosal edema dehydration
- Surfactant activity is reduced  atecelactasis - Monitor bp
caused by hydrochoric acid , plastic , acids - Temp
- Weight
- Electrocytes
- PRBC – 2-5 days afters burn
FLUID RESUSCITATION INTERVENTION
- Correct fluid & electrolyte Imbalance
Parkland/ Baxter Formula - Emergent phase – acute phase
= 4ml LR x weight in kg x TBSA - Computation start at the time of the injury not
the patient came to the emergency room or
- Weight could be round off = kg( of pound hospital .
convert to kg ( divide by 2.2 ) ( time of the injury )
Ex. 150 pnd divide by 2.2 Ex. 8 am start of the burn
!!!!!DO NOT GIVE DEXTROSE SOLUTIONS !!!
-it may cause Osmotic Diuresis

 Carbon monoxide poisoning
- Carboxy hemoglobin
(If carboxy is in the rbc = patient will die )
Modified Brooke
0.5 ml /kg /% TBSA burn
- protenate or 5% albumin in isotonic saline PROMOTE HEALING

- administer ½ in 1st 8 hrs , give remaining half in next 16
hrs. - Acute phase
- electrocytes ( lactated ringers) - Patient must be protected
= 1.5 ml x kg x TBSA burn - Reverse isolation , wound care at least once a
day
Nursing care for burn patients
G.I system _____________________________
 Debridement (Removal of non viable tissue )
- Dec. blood flow to the intestines  causing
paralytic ileus gastric & nausea  Hydrotherapy
- Used to loosen dead tissue
- Maximum of 30 mins
 Escharotomy - More hypersensitivity
- ( of leathery covering of dead tissue conductive - Rash
for bacterial growth ) - Burning
- To alleviate constriction & infection - Itching sensation
SUPPORT NUTRITION
2. Mafenide Sulfamylon
- High caloric CHO, CHON diet
- Open method
- May have TPN or tube feeding , vitamin B, C &
iron - Remove previously applied cream
3. Silver Nitrate
- H2 blockers , antacids prevent curling ulcers
- Keep dressing wet w/ solution to avoid over
- NGT for gastric decompression to prevent
concentration .
distension , paralytic ileus .
- Can leave gray or black stain
PREVENT COMPLICATION OF IMMOBILITY
- Prevent contracture by maintaining joints in
neutral position of extension SKIN GRAFTS
- Shoes to prevent foot droop , splints
- ROM at each dressing changes
- Stryker frame
- Facial exercises
SUPPORT PATIENT - Must be e mobile ( e mobilization for 2 weeks)
- Counseling regarding change of image - Should not be wet
- Demonstrate acceptance , Expression of feelings - Graft light (check the skin every shift , smell, feel
- Prepare patient for discharge it)
Cosmetic surgery , pressure garments  squeeze some blood or secretion = infected
 discoloration = rejection
- Not be expose to the sun
Habat tank o Animals skin = not permanent graft
Plain lss
- May asin
- Binabad yung os ilalagay sa burn = to soften the A. Postage stam graft __________________
skin - Earlier method of accomplishing the same goals
as a mesh cover.
CONTROL PAIN
- Donor skin is cut into small pieces & applied to
- MEPERIDINE / PORPHINE the burned area
- Given I.V at first due to impaired circulation & B. Sheet grafting______________________
absoption . analgesic 30 mins
- Large strips of skin place over the burn as close
- Before wound care . as together as possible
TYPES SKIN GRAFTS

TOPICAL ANTIBACTERIAL AGENTS
1. Xenografts______________________________
1. Silver sulfadiazine - Skin from animals , usually pigs
- Stain and inching sensation (porcine xenografts)
- Flammazine ,
- silvadene close method 2. Homografts_____________________________
- Skin from another person
3. Autografts ______________________________
- Skin form another part of the clients body
= sarili nyang balat
4. Mesh grafts_____________________________
- Machine used to mesh skin obtained from a
donor site so it can be stretched to cover a large
area of burn .
- disease
Communicable They usually involve few people during specific
periods.
4. Out break
- Greater than the anticipated increase in the
number of endemic cases
- If not quickly controlled epidemic
Communicable disease
- An illness due to an infections agent or its toxic
product which is trassmitted to a person or
animal directly or indirectly via of an
intermidiate animal host ( vector) , vehicle
( water , food , blood) or inanimate environment.
 Contagious
The infection process

- easily transmitted from person to person
 Infectious
- not transmitted by ordniary conact but require a
disrect inoculation , througg a break in the
previously intact skin or mucous membrane .
1. Agent
- Any microbe capable or producing disease
a. Bacteria
Spherical – cocci
Nod-bacilli
Spiral – spirilli
b. Viruses – RNA/DNA
c. Rickettsiae- Gm(-) bacteria like
organism, like viruses they require host
cell for replication .
d. Chlamidia – like viruses , thery are
intracellular obligate bacteria
e. Fungi ( mycoses) – mold or yeast
Why do infection occurs
f. Protozoa
- Low
g. Helminthis – round , tape, flukes
immunization
Insidance of disease  Pathogenicity ______________________

1. Epidemic disease - Ability to cause disease
- Occur in greater number than what is expected a. Virulence severity or harmfulness
in a specific arear or region over a specific time b. Invasiveness
2. Pandemic disease (ability to enter &move through tissue)
- It is an endemic that spreads over multiple - Tendency to spread
countries or continents c. Elaboration of toxin
3. Endemic disease d. Viability - Ability to survive outside the host
- Present in a population or community at times 2. Reservior
- An animal or plant in which an infections agents
lives & reproduces in such a manner that it can
be transmitted to man ( principal habitat )
a. Human
b. Animal
c. Non-animal -street dust , garden soil ,
lint from bedding .
3. Portal of entry
- Path or way in which the organisms leaves the
reservior this is where the organisms grow
a. respiratory tract- most common in man
b. gastrointestinal tract
c. genito-urinary tract
d. open lesions
e. mechanical escape – includes bites of insects
f. blood
- Time a case is infectious to others .
4. Mode of transmission
- Horizontal transmission
A. By close contact ______________________
1. Direct contact
- Person to person
- Sexually transmitted (STI)
2. Indirect contact
- Inanimate
- Families object
3. Droplet spread
- Close range spray of contaminated object
- Coughing , sneezing or talking by an infected
person
B. Airborne transmission_________________
- Result from inhalation of evaporated droplets
suspend in airborne dust particles or vapors
C. Vector borne transmission
- When arthropods such as flies , mosquitos , ticks
transfer an organism
D. By vehicle route______________________
- Through contaminated items
1. Food – salmonellosis
2. Water – shigellosis , cholera
3. Drugs – bacteremia resulting from infusion of a
contaminated infusion product .
4. Blood – hepatitis B , AIDS
VERTICAL TRANSMISSION – mother to child

transmission through placenta
5. Portal entry of organism into human

- Venue through which the organism gain
entrance into the susceptible host
a. Respiratory tract
b. Gastrointestinal tract
c. Genitourinary tract
d. Direct infections of mucous membrane/skin
6. Susceptible
- Age , nutritional status , host immune response
 Intubation period
- Time from infection until onset of symptoms
- No sign symptoms
 Period of communicability
o
Antiserum – serum that contains
immunoglobulins from blood of humans or
animals that recovered from a certain disease
when they developed certain antibodies against
IMMUNIZATION
 Immunity particular antigens .
- The condition of being protected against any 3. Subclinical immunity____________________
particular disease - Due to constant exposure to a certain disease .
1. thus Ab are produce to encounter act infection
- Actual participation of an individual body tissue/
fluids in producing immunity . longer acting
GENERAL CNTRAINDICATIONS TO RECEIVING
2. Passive immunity AN IMMUNIZATION INCLUDE :
- Transfer of antibodies , antibodies not coming 1. Severe febrile illness
from individual self . short acting / temporary 2. an allergic reaction to previously administered
TYPES OF IMMUNITY immunization
3. live vaccines are not administered to anyone w/
1. Natural _____________________________
an altered immune system .
a. Active immunity (NAI)
- Acquired through recovery from certain disease CONTROL & MANAGEMENT OF INFECTION
- By nature ex. Person is infected w/ a disease like - Consideration before taking care of an infected person
chicken pox :
b. Passive
- Acquired through placental transfer maternal 1. Know the causitive agent
transfer of anti bodies 2. Know the body secretion that harbors
the microoganism
- Children below 6 moths enjoys antibodies from
3. Know the mode of transmissio
mother
2. Artificial_____________________________ A. Control aspect_____________________
a. Active immunity (AAI) - To limit spread of infection
- Acquired through administration of vaccines & a. Quarantine – limitation of freedom of
toxoids movement of a well person during the longest
a) Vaccines incubation
- attenuated / weakened microorganism given to b. Isolation – seperation of infected person
stimulate body to produce antibodies & provide during the period of communicability
immunity against disease. 1. Strict isolation - protection of other
b) Toxoids people
2. Reverse isolation – protection of the
- Attenuated toxins
patient
(poisonous substances produces by
microorganism ) - Protect other and protect you
b. Passive Guidelines for isolation precautions in hospitals developed
- Acquired through an administration of an by the center for disease control & prevention (CDC)
antitoxin , antiserum , convalescent serum & 1. Standard precaution
gamma globulins - Are those designated for the care all facility
patients regardless of their diagnosis or
o Antitoxin – antibody capable of neutralizing presumed infection
specific toxins that are causative organism of - The precaution applies to blood , all body fluids ,
disease secretion & excretion except sweat: mucous
membranes , skin that is intact
2. Transmission based precautions o Terminal disinfection
- Instituted for patients who are known to be or - The disinfection & sterilization of patients
suspected of being infected w/ a highly supplies & equipment after the patient is
transmissible infection discharge from the unit or hospital .
o Prophylactic disinfection
- Preventive measure to prevent spread of
A. Airborne precaution infection
- Reduce the risk of airborne transmission of o Disinfectant
infectious agent . - Usually a chemical; agent that destroy disease
- Use special air handling & use of respiratory causing pathogens or other harmful
protection such as mask microorganism , but not kill bacterial spores
a. Droplet precaution - Refers to substance applied to inanimate objects
- Reduce the risk of transmitting infectious agents o Antiseptic
through large particle droplets - Substance that prevents or arrest the growth of
- Large particles droplets don’t remain in the air & microorganism .
generally travel short distance (3ft) - Preperations
- Used of mask -
b. Contact precautions o Sterilization
- Decreased the risk of transmission by direct - Process of complete destruction of all
contact or indirect contact . microorganism & their bacterial spores /
c) Indirect contact endospores on a substance by exposure to
- occur through patient care activities that physical or chemical agents .
required direct contact o Preventive
d) Indirect contact - Preventive the recurrence of infections
- involves coming on contact w/ a contaminated a. Health teaching / education
inanimate object .
- Use of gloves , a mask & a gown
B. Preventive
- Prevent recurrence of infection
a. Health teaching /education - There will
be a change in knowledge / skills /
attitude
b. Immunization - 3 laws implemented : o CDT vaccine ( cholera/dysentery
1. PD 996 expanded program on /typhoid)
immunization ( EPI) - 6 months immunity – given only on
2. UN goal (UCI) universal child outbreaks.
immunization – proclamation #6 o Anti rabies vaccine
3. National Immunization day ( NID) - Animals are the targets
DISINFECTION C. environment sanitation_____________
e) Destruction of pathogenic microorganism - Control of arthropods & rodents
outside the body through direct physical or - Also includes the submission od sex workers to
chemical means . examination versus
o Concurrent disinfection GC – 2x / month
- Concurrent cleaning & sterilization of patient Syphilis – once a month
supplies & equipment during hospitalization . HOST
1. Patient – person who is infected & manifest EXPANDED PROGRAM ON IMMUNIZATION ( EPI)
signs & symptoms of disease
 Launch in July 1976 by doh in cooperation with the
2. Carrier - person who is healthy but harbors the
WHO & UNICEF to ensure the infants / children &
organism & is capable of transmitting the
mothers have access to routinely recommended
disease but does not have signs & symptoms
infant / childhood vaccines
3. Suspect – person who has medical history ,  Vaccination among infants & newborns (0-12
signs & symptoms that suggest that person is months ) against seven vaccine , preventable
suffering that particular disease disease , tuberculosis , poliomyelitis , diptheria
4. Contact – person who is in close association ,tetanus , pertussis , hepatitis & measles .
with an infected person , animal or object .  Presidential degree No. 996 (September 16 , 1976)
IMMUNIZATION – EPI - updates
Providing for compulsory basic immunization for
o General objectives infants & children below eight yrs .
- To further understand & gain knowledge about
Philippine national immunization program
o Specific objectives
- Understand what is immunization EM &
- understand the different vaccines included in epi
& its characteristic .
- describe some new vaccines / program updates
- determine the describe immunization schedule
()
- describe vaccine – preventable disease
- learn the general principle in vaccination
- Learn about contraindicasion to immunization &
EPI …
o Immunization
- Is the process by which vaccines are introduced
into the body before the infection sets in.
- It promotes health & protects children from
disease – causing agents
o
o Vaccines
- The causative agent of a disease so modified as
to be incapable of producing the disease yet at
the same time so little changed that is able when
introduced into the body , to elicit production of
specific antibodies against the disease
- These are always antigen , therefore they always
induce active immunity when administered
thereby causing the recipients immune system to
react to the vaccine that produces antibodies to
fight infection , & are the most useful the
prevention of disease .
VACCINE Minimum age at fisrt Number of doses Minimum interval Reason

dose between doses
Varicella vaccine 12 moths 2 3 months Protection against

(Children 13 yo& above chicken pox
– 4wks)
Hepatitis A vaccine 12 moths 2 5 months Protection against
(HAV) Hepatitis A virus
Human papiloma 9 years old 9-14 y/o – 2 >6 months
virus ( HPV) vaccine 15 above – 3 >0.2 & 6 months
Fluid imbalance
PROGLEM:
1. Fluid volume excess (FVE)

- Clinical manifestation of disease
ETIOLOGY :
Memorize uu \
a.  intake of fluid
b.  excretion ( di muna mailabas(baka sira 2.  excretion
yung kidney ) ) =kidney impairment  Diuresis
 Kidney impairment  Diarrhea
  ADH  Vomiting ( excretion )
  Aldosterone  Diaphoresis
c. Fluid shifting from intravascular to interstial  Bleeding
space 3. Fluid shifting
- From intravascular to interstitial
PATHOPYSIO:
- BURN ( burn edema)
CLINICAL MANIFESTION :
Risk for injury
Shock ( hypovolemic )
DIAGNOSTIC TEST :
a. Central Venous Pressure (CVP)

b. Osmolality
c. Hematocrit
- Inc. fluid vol dec. hematocrit
d. Serum specific gravity
- 02  no change but if ..
e. Urine specific gravity
- Urine becomes more consenntrated
- USG .
MANAGEMENT :
a. Restrict fluid
b. Restrict sodium
- Sodium attracts water
c. Monitor VS
d. Monitor I & O
e. Weight patient daily
f. Manage the cause = the cause will be treated
g. Diuretics ( as ordered )
h. Dialysis( pag sira yung kidney )
2. Fluid volume deficit
- Clinical manifestation of disease
ETIOLOGY:
1. intake
 those patients altered mechanism
MANAGEMENT:
1.  fluid IVF/ ORS

2. Monitor VS
3. Monitor I & O
4. Weight patient daily
5. Manage the cause
6. Maintain fluid volume
Yung sodium na pumasok lalabas uli

Yung potassium na lumabas ay papasok ulit =
ELECTROLYTES active transport = sodium & potassium pump
- Impulse transmission
 Electrical (focus) Sodium
 Chemical - 135- 145 meq/L
NERVES - Major cation outside the cell
o Neurons – functional unit PROBLEM

o Action potential – rapid change in the a. Hypernatremia
membrane potential -  serum sodium more than 145 meq/L
( mabilis na pag babago ng membrane potential)
- Clinical manifestation of the disease
ETIOLOGY
Membrane potential:
o Resting membrane potential
- Electrical charge at rest
Stimulus will open up for sodium = sodium

enters the cell
1.  sodium &  water
When the membrane becomes more +
= hypernatremic hypervolemia
= depolarization  Sea drowning
  aldosterone (  sodium & water
Membrane more – back to resting retention)
= repolarization 2. Inc Na& dec. water
= hypernatremic hypovolemia
 Dehydration – water loss 2.  Na rich food
- MOST COMMON 3. monitor vitals signs
3.  Na & normal water 4. monitor I&O
= hypernatremic Euvolemia 5. weigh patient daily
6. promote safety measures
DIAGNOSTIC TEST :
7.
1. Serum sodium 8. manage the cause
2. Osmolality (since this is only clinical manifestation )
9. diuretics depends on the cause
MANAGEMENT : hypernatremia
1. Restrict sodium rich food

2.  water  Osmolality
3. Monitor VS - Concentration of all soluts
4. Monitor I&O -  sodium =  osmolality
5. Weight the patient -  sodium =  osmolality
6. Promote safety measures
7. Manage the cause
b. Hyponatremia
-  serum sodium less than 135 ,eq/L
- Clinical manifestation
ETIOLOGY : Potassium
1.  Na & water - 3.5 – 5.5 meq/L

= hyponatremic hypovolemia - Regulate the kidney( potassium regulate
kidney )
2.  Na & inc . water - Clinical manifestation of disease
= hyponatremic hypervolemia A. Hyperkalemia
3. Dec. Na & normal water - Inc. K >5.5 meq/L
- Most sensitive muscle = cardiac muscle
= hyponatremic euvolemia
CLINICAL MANIFESTATION :
MANAGEMENT : hyponatremia ETIOLOGY :hyperkalemia

1.  water intake 1. Inc. K intake
 Inc Iv administration
 Lethal injection
Can cause cardiac arrest
2. Dec. K excretion
 Renal impairment
( sira yung kidney hindi nya nailabas )
 aldosterone
 K sparing diuretic
3. K shifting from ICF to ECF
 Massive tissue damage burn , prolonged
surgery ,
 Metabolic acidosis
(sa outside of the cell inc. concentration

hydrogen ion concentration sa labas from
higher to loew concentration papasok sya sa cell
= hydrogen imbalance cell ilalabas nya ang
potassium sa cell = K = hyperkalemia =
potassium shifting
o Muscle cells B. Hypokalemia

- Most sensitive cells to potassium changes - < 3.5 meq/L
- Most sensitive cell = Muscle cells
- It can be idiopathic
MANAGEMENT :hyperkalemia ETIOLOGY: hypokalemia
1. Restrict K rich food 1. K intake
2. Dialysis – immediate indication for dialysis is 2.  K loss
hyperkalemia  Diarrhea(most common)
(kidney injury / renal impairment )  Diuresis
3. Insulin IV = regular insulin 3. K shifting from ECF to ICF
4. Glucose glucose IV (baliktad naman pumasok naman sya )
- Push K into the cell  Alkalosis
5. Calcium gluconate Mababa yung hydrogen ion ( lalabas
- antagonize the effect of the K on cardiac cells yung hydrogen ion ) kasi konti yung
6. treat metabolic acidosis nasal abas ( kokonti yng cation sa loob
- sodium bicarbonate the K + inside the cell increases =
- monitor ECG ( disrythmia) alkalosis  K shifting
7. promote safety measures
8. promote safety measures = dec. K serum <3.5 3.5 meq/L
9. fluid & high fiber food for constipation
10. Manage the cause = hyperkalemia
CLINICAL MANIFESTATION : - Major regulatory hormone
- Regulates vitamin D metabolism
2. Calcitonin – ¯ Ca
Vitamin D
Vitamin D in the
skin 7 hydroxy vitamin D / 7
hydroxycholesterol
MANAGEMENT: hypokalemia
1.  K rich food (When it expose to UV sunlight =cholecalciferol (vit

2. K supplement – kalium durule D3) absorb to the blood
3. KCI IV replacement –
 liver = 25 hydroxycholecalciferol (25hydroxy
!!BUT DO NOT GIVE IV BOLUS
VD3)
( prior to giving K chloride monitor urine output .
monitor for the earliest adverse effect phlebitis = in kidney =1,25 dihydroxy Vit D3
can cause inflammation ,)

4. monitor ECG
most active for of Vit D
5. correct alkalosis
6. manage the cause - Inc. absorption of Ca in the GI tract
( w/ help of PTH)
Calcium - (Pag Kulang Vit D kulang din calcium natin)
FUNCTIONS:
Calcium blood ( unionized )
1. impulse transmission
- 8.5 – 10.5 mg/dl
2. bone formation
3. teeth formation Bone  blood ( resorption )
4. cloth formation GIT blood ( absorption )
- bones
Kidneys blood ( reabsorption)
- muscles
- blood
a. ionized calcium a. Hypercalcemia

- free calcium in the blood - Tumor ( inc. production of PTH can cause
- un bound tumor )hyperparathyroidism
b. unionized calcium  serum Ca. >10.5 mg/dl Ca precipitate to
- calcium binded w/ other substances form stones in the urinary tract ( urolithiasis)
a. Kidneys ( nephrolithiasis )
o calcium is regulated by hormone b. Urinary bladders ( cystolithiasis )
1. PTH Ca level ( pag mababa yung calcium Irritability of nerves
(Pag mababa yung calcium ¯ irritability of nerves )  Calcium & phosphate
– make crystals to make the bone strong bone
- Can cause CNS depression altered level of
consciousness
- PNS  ¯ impulse transmission from the
nerve to the muscles = muscle weakness
b. Hypocalcemia
-
-
- Most common problem
DIAGNOSTIC TEST :hypercalcemia

1. Serum calcium
2. MRI
3.
Hypokalemia
- Prominent U wave
Hyperkalemia Hypocalcemia
ETIOLOGY:
- Peak T wave / tall T wave 1. ¯ intake calcium & Vit D
Hypercalcemia 2. losses
Ex. Patient w/ acute panc.titis they cannot
- Shortening of the QT interval absorb calcoium nilalabaslang nila
Hypocalcemia 3. Calcium binds w/ other
subtancesunionized calcium\
- Prolonged QT interval Ca bind gluconate =
Ca bind Citrate
Ca bind Protein
MANAGEMENT: Ex. – citrated blood for blood transfusion
1. Restrict calcium rich food - Blood transfuse to us citrated blood yon para
2. Monitor ECG di mag cloth yung blood pag nag transfuse sa
3. Increase Fluid intake patient pag na transfer na mag babind sya
4. Promote safety measures sya protein
5. Manage the cause . - Alkalosis – ph high  ca bind to protient
baba yung ionized sa calcium magiging
Note: unionized may hyper
Note : all of this condition will lead to dec. calcium 02 sat – 98 – 100%
in the blood less than 8.5 mg/dl =hypocalcemia
Base excess : - 3 to +3
ND:
1. Altered electrolyt imbalance
DIAGNOSTIC TEST
1. serum calcium level

2. ecg
MANGAMENT:
1. inc. calcium rish food

Pag dumadami ang carbon dioxide dumadami
2. promote safety measure
ang acid
3. ca supplements
- PCO2 acidosis
4. Vitamin D supplements
- ¯ pCO2  alkalosis
5. Manage the cause .
 HCO3 – alkalinity
 Pospate, chloride, magnesium ( self study ) - HCO3  alkalosis
- ¯HCO3  Acidosis
Acid base imbalances - Low ph  acidosis

 Acids – extra H+ give off H+ - High pH  alkalosis
- solution contain extra hydrogen ion
4 acid imbalances
( kaya nya mag bigay ng hydrogen kasi may
extra sya sana oll ) 1. Metabolic acidosis =  HCO3
 Bases – OH accept H ion 2. Metabolic alkalosis =  HCO3
OH  they can accept hydrogen ion (H ion) 3. Respiratory acidosis =  pCO2
4. Respiratory alkalosis =  pCO2
Acid nag babase sa dami ng H ion
Pag tumataas yung H ion bumababa Ph

Metabolic acidosis
 PH 7.35-7.45 – normal -  H+
6.1 below = can cause death a. Metabolic acidosis w/ normal anion
8.0 above = not normal =Cl/HCO3
b. Metabolic acidosis w/ high anion gap = acids
ABG
Etiology : high anion gap
pH – 5.35 – 7.45
1.  HCO3 ( bi carbonate) = acidosis
po2 – 80 – 100mmHg 2.  Acids
pCO2 – 35 – 45 mmHg
HCO3 – 22 – 26 meq/L Ecf – major of anion
 chloride / normal amount = 96-106 meq/L lungs compensate  remove O2 hyperventilate
HCO3 – 22- 26 meq/L ( kussmaul’s respiration)
= this 2 are measured anion ( dapat balance sila ) Dec. CO2  normalized pH
Metabolic alkalosis
Example:
ETIOLOGY:
Other anions = UNMEASURED ANIONS
(we can see the anion gap) a.  HCO3
1. Sulfates  chloride
2. Phosphates   use of antacids( ex. Na HCO3 )
3. Lactates b. acid
 Vomiting HCI acid
Pag normal anion dap problem  nasa CL/HCO3

ang problem Metabolic alkalosis
  HCO3 / acid
CAUSES   H+ --.K shiftinghypokalemia
 pHCa bind w/ protienthypocalcemia
1. Kidney failure – cannot excrete acid  lungs compensate retain pCO2  CO2
= ( metabolic acidosis) normalized ph hypoventelation
2. Diarrhea – loss of HCO3
3. Diabetic ketoacidosis   ketone bodies
( can lead ketone acidosis)
4. Diuresis- loss of HCO3
5.  lactic acid
Etiology  dec. HCO3 / acid pH -  = acidosis

pH  = alkalosis
 Dec. pH
HCO3 -  = acidosis
Etiology  dec. HCO3 / acid HCO3 - = alkalosis
 H+ ------> K shifting hyperkalemia
¯ pH
Respiratory acidosis Regulation of acid / base

Etiology :  pCO2 1. Lungs
2. Kidneys
a. Respiratory center depression
3. Blood – buffer system
b. Traumatic brain injury
c. Respiratory muscle paralysis
d. Lung disease ( COPD)
Intepretation of a AB imbalance
Etiology :  pCO2  pH 7.35 – 7.45
pCO2 35- 45 
HCO3 22-26 
pO2 80-100
O2 sat 98 – 100 %
BE – 3 to +3
Respiratory Alkalosis pH 7.31  pCO2 49  HCO3 24 (N)

respiratory acidosis , uncompensated
ETIOLOGY:dec. pCO2 pH 7.48 pCO2 46  HcO3 29 (HCO3 is the prob)
= hypeventilation
metabolic alkalosis in partial compensation
(partialy compensated)
( nag uumpisa na mag compensate ang lungs )
Ex.(N) pH 7.39 pCO2 49  HCO3 27 
(Ph is normal )= fully/ compensated
(PCO2 ) respiratory acidosis compensated
Urinary tract 4. Urge incontinence
- Common in elderly
2 parts ; - Not normal
1. Upper urinary tract - They having  bladder capacity
- Kidneys o Health teaching
- ureter bladder training . scheduled urination
2. Lowe Ut 5. stress incontinence
- U. bladder - due to inc. intra abdominal pressure = (naiihi
- Urethra ka ) ( ex. Tawa ka ng tawa naiihi ka
 Urethra - most common pregnant women
- Passageway of urine from the urinary
bladder outside
 Women = shorter (most common) o health teaching
- & in close proximity w/ the anus  bladder training
 Men= longer
 U. bladder  URETER
- Passageway storage of urine . - Passage way of urine from the kidneys to the
- It can store a lot of urine – 150 ml ( stretch urinary bladder .
 send signal  brain  urge to urinate ) - Lind by smooth muscle – pag may dumadaan na
- Inervated by ANS urine nag
- SNS – urinary retention - Some times develop stones in the kidneys pwede
- PNS – bladder emptying bumagsak sa ureter urine di makakababa 
ureter Contract = severe pain
MOST PROBLEM :
KIDNEYS
1. Urinary retention
- Most important risk factor for the - major organ of excretion posterior
development of UTI abdomen .
2. Honeymoon cystitis - Along the costovertebral angle ( CVA)
- Related to sexual intercourse - right Kidney is lower than a left
- Orgasm – SNS ( because of the presence of the liver on the
- Ejaculation – SNS right side )
o Health teaching  void first prior to sexual - cm long =?
intercourse wad masyado exited - Cm wide = ?
- Thickness = ? read book daw
3. Incontinence
- Involuntary urination ( di mo mapigilan ang
pag ihi mo )
RENAL DISORDER
11/2/21
Kidney
Lengt - 10 -12 Cm
Wide – 6 cm
Thickness – 3 – 2.5 cm thick
Note: pag nag kaka chronic kidney D. nag shrishrink

yung size . ( recduce yung size )
Problem :
Upper back /plank area ang masakit –> upper urinary

tract disease
Low back / hypogastrict area – >lower urinary tract

areae
Urinary bladder / uretra  problem is on hypogastric /

Costovertebral angle lowback
 Kidney punch test Kidneys / urether  costovertibral angle / plank area
-
functions of the neprons
1. Filtrations
2. Reabsorption
3. Secretion
Note: in filtration
- By BP Hydrostatic pressure ( exerting hy
- Oncotic pressue ( attract ) ( exerted by
albumin )
- Sa glumerolus  tubular pressure ( )
Effective filtration presure ( EEFP)
EFP = hp – (op + tp)
Efp ( ex. Kunwari lamng )
Efp = 80 – ( 30 + 10 )
Efp = 40 ( the pressure will go where )tubules
( pag may stones jaan tataas ang tubular pressure
Note :
- Fluid na lumabas ( na filtrate ) = Ultrafiltrate

of blood ( ano yung lubas ? water ,
electrolytes , glucose , amino acids, urea ,
creatinine
- = 125 ml/min
- Hr = 125 ml/min x 60min/hr
- Day = = 125 ml/min x 24 hrs/day
Normal urine output

- 30-50 ml / hr
- 1-1.5 L/day
( ano ng yare sa iba ? na reabsorb , bumalik
CIRCULATORY SYSTEM sya sa blood = reabsorption
- Heart aorta arteries arterioles
capillaries venules  veins  vena cava Reabsorption
heart Active transport
- kidneys Simple diffusion
heart  aorta arteries arterioles  Simple diffusion
capillaries  arterioles  capillaries  Facilitated diffusion
venules  veins  vena cava  heart
RBC in urine – hematuria CREATININE – by product of muscle
metabolism ( 0.6 – 1.2 mg/dl )
WBC – Pyuria
Protein in urine – proteinuria Pag nasira yung kidney  urea & crea =
AZOTEMIA
RBC papasok sa glomerulus – afferent arteriole 3. Water regulation

- Pag nasira ang kidney = poor water
regulation = water retention  edema
4. BP regulation
Lalabas – efferent arteriole
- Pag nasira ang kidney = Bp = hypertension
5. Regulation of acid based balance

- Pag Nasira kidney - cannot excrete the acid
= metabolic acidosis
6. Regulation of electrolytes
- Potassium = hyperkalemia
- Magnesium = hypermagnesemia
- Phosphate = hyperphosphatemia ( aralin )
7. Production eritropoeitin
0 hormone that stimulate the rbc
production xx ¯ rbc production
= anemia
Secretion
8. Activation of vit D Ca absorption in the
- Active transport
GIT xx = hypocalcemia
 Water
9. Production of prostaglandin
 Electrolytes
- renal blood flow  xx  ¯ PD production
 Urea
¯ renal blood flow
 Creatinine
10. Regulation of Calcium & phosphate
 Uric acid
- xx ¯ regulation of Ca & P in the bone
deformity
Function of the kidneys
1. Urine formation ( neprons ) DISORDERS OF THE KIDNEY
 X pag nasira nag kidney walang urine formation
1. urinary tract inflammation
Dec. urine output less than30 ml = OLIGURIA
- can cause by
2. Excretion of waste products
o infection ( focused)
Urea - by production of protein breakdown
 aminoacids ( pag amino acid yung na o trauma
breakdown ) ammonia  urea  lalabas o autoimmune disease ( SLE)
nayan ( 10 – 20 mg/dl ) 2. urinary tract obstruction
o stone – lithiasis ( focused)
o tumor- benign or malignant 6. IVP
o congenital lesions Management : Pyelonephritis
 primary obstruction – inside the urinary tract
1. Avoid recurrent UTI
 secondary obstruction – outside the urinary 2. Manage fever-Tepid Sponge Bath (warm water)
tract 3. water intake up to 2-3 L
ex. Enlargement of the prostate gland 4. Acidify the urine
( to lesser the growth of the bacteria in the urine )
5. Antipyretic ( as ordered )
URINARY TRACT INFECTION 6. Analgesic
 Upper UT 7. Anti bacterial ( as ordered)
- Kidneys 8. Monitor kidney function test regularly
- Ureter 9. Monitor I &O
10. Monitor VS ( Temp)
a. Pyelonephritis
- Inflammation of the renal pelvis b. Glomerulonephritis
- Ascending infection - Inflammation of the glomerulus
- Most common - Common in children
Etiology Etiology : glomerulonephritis
Bacteria – e coli ( most common )  ascending - Group A beta hemolytic ( strep throat )
infection - Staphyloccus aureus
Autoimmune – antibodies are formed against onw

cells
Risk factors
- Systemic inflammation
- Fever & chills
- Pain – costovertebral angle flank
- Impaired kidney function
- Repeated bouts chronic pyelonephritis
Note : hematogenous bacteria ( blood )  kidneys
Diagnostic test : Pyelonephritis
- Antigen = antibody complex ( they destroy
1. Culture & sensitivity
glomerulus  cause injury to the glomerulus
2. Urinalysis
Pyuria Note : repeted gouts ba ? can cause or lead to
Hematuria chronic
Bacteriuria
Diagnostic test : glomerulonephritis
3. Kidney function test
4. CT scan 1. culture & sensitivity
5. MRI 2. Urinalysis
3. Kidney function test Bacteria  urethrovesical reflux
4. Ultrasound
 Infection to uretra – urethritis
5. Ct scan
 Infection to .. – cystitis
6. MRI
7. Restrict fluid Local inflammation
8. Sodium
s/sx
9. Weight your patient
- Pain – low back , hypogastric
 Acute GN - Swelling  stretch wall  urinary frequency
 Chronic GN ( balisawsaw)
 Rapid progressive GN - Heat – burning sensation in urination
 Nephrotic syndrome – severe proteinuria - Dysuria – painful urination
( don’t know the cause )= 3 g/ day ( irritative symptoms )
Note: !!!!
ND :
- Nephrotic – more on proteinuria  Altered ano daw
- Nephritic – hematuria  Dikona narinig
!!!!But both of the is a destruction of glomeruli Diagnostic test
membrane !!!!
1. Culture & sensitivity
2. Urinalysis
 Lower UT Pyuria – most prominent
- Urinary bladder Bacteriuria – bacteria in urine
- Urethra Hematuria
Etiology
Management :
Bacteria Independent Intervention
1. Avoid urinary retention
- E coli 
2. Proper perineal care
- Klebsiella
3. Change patients catheter
- Serratia
4. Proper used of tampoon , feminine wash ,
Risk factor 5. Void first prior to sexual intercourse
6. Shower instead of bathtub
1. Urinary retention
7. Cotton underwear
2. Females
8. Increase water intake !!! up to 2-3 liters per
3. Poor perineal hygiene ( front to back )
day
4. Catheterize patient
9. Acidify the urine
5. Tampoon user
10. Analgesic as ordered
6. Menstruation
- NSAIDS ( after meals )
7. Psychotic patients
- Bladder analgesic
8. Sexual intercourse
Phenazopyridine – discolorations of urine
9. Bath tub
11. Antibacterial drugs as ordered
10. Nylon underwear
-cortrimoxazole , quinolones .
11/15/21  Urinary frequency
Urinary tract obstruction
Focus – stones on urinary tract = urolithiasis URETER
Types of stones Stoned fall  Ureter = Urotherolithiasis
1. Calcium stones  Most painful site of stone

- Calcium phosphate  Severe pain
- Calcium oxalate  Colicky
2. Uric acid  CVA & flank area radiating to the
3. Struvites tight and genitalia
4. Cystines  Hematuria
What type of stones may develop in having  Gross/microscopic
frequent Infection
Note : pag may hematuria = may problem in
ETIOLOGY : urinary tract ( = Urotherolithiasis )
- No exact etiology
RF: ND DX :Ureter
a. Family history - Acute pain
b. Hypercalcemia - Altered elimination pattern :urination
c. Gout
d. Males
:read book
- How this developed

 Supersaturation of urine (¯ water &
solutes )
KIDNEY
form = Nephrolithiasis
 Pain CVA & plank area
 Hematuria
 Gross/microscopic
HYDRONEPHROSIS = edema in kidney
URINARY BLADDER
form = Cystolithiasis
 Pain hypogastric area & low back
 Hematuria
 Gross/microscopic Hesitancy
 Dysuria
 Dribbling sensation
DIAGNOSTICT TEST 4. Restrict sodium rich food – sodium excretion of

1. Urinalysis calcium ( stone formation )
- Hematuria 5. Restrict protein ( because protein excretion of
- Pyuria calcium also )
- Proteinuria 6. If stone uric acid the patient should avoid
- Cast avoid purine rich food
- Crystals 7. If stone is oxalate  avoid oxalate containing
2. KUB x-ray ( kidney Ureter …) food
3. IVP - intravenous pyelography 8. If stone is calcium  avoid Ca rich food is not
4. CT stonography recommended unless the patient has true
5. Stone analysis hypercalcemia
6. Ultrasound 9. Avoid UTI
7. MRI 10. Removal of stone
8. Culture of the urine – to know if there is a. Drug therapy – Rowatinex /sambong
infection b. ESWL – extra corporeal shockwave
lithotripsy ( pulverize the stone )
c. Laparoscopic surgery
d. Open surgery
11. Pain reliever – narcotics or non narcotic
GOALS:
1. Relieve the pain – severe
2. Prevent infection
3. Improve urination
4 phases :AKI
RENAL FAILURE
MANAGEMENT :
1. oral fluid intake up to 3L/Day
2. If stone is acid – alkalinize the urine /
alkalinizing food
- Loss of kidney function
3. If thew stones is alkaline , acidify the urine /
acidifying food ( acid ash diet )
A. Acute renal failure
 sudden loss of kidney function
 reversible 2. Oliguric phase
 non progressive =oliguria(¯urine output <30ml/hr: azotemia )
 acute Kidney injury (AKI)
- sudden impairment of kidney function 3. Diuretic phase
- reversible Nephrons start to recoverurine output but
- non progressive there is still azotemia
B. Chronic renal failure
 Gradual 4. Recovery phase
 Progressive loss of kidney function 6 mos to 1 yr or more reversible
 Irreversible
 Chronic kidney disease ( CKD)
- Gradual
- Progressive impairment in kidney function
- Irreversible
ACUTE KIDNEY INJURY (AKI)
CAUSES:
a. Pre renal
- ¯ blood flow to the kidneys
Ex.
= Shock
b. Intra renal
- The kidneys are diseased
Ex.
- Acute pyelonephritis
- Acute glomerulonephritis
- Nephrotoxic effects of drug
- Acute tubular necrosis
c. Post renal
- Obstruction to the flow of urine
- Stone
- Tumor
- Strictures( congenital lesions)
1. Initial phase CHRONIC KIDNEY DISEASE ( CKD)

Injury acute tubular necrosis
ETIOLOGY :
AKI- repeated bout  CKD ETIOLOGY impaired kidney function
Most common …
1. Hypertension
2. Diabetes mellitus
= nephropathy
CLASSIFICATION
GFR(glomerular filtration rate )= 125 ml/min
Stage of CKD
Stage 1
- GFR>90ml/min
- Impaired kidney function /normal or high
NURSING DIAGNOSIS: IKF
GFR
- Fluid volume excess
- Activity intolerance/ fatigue
Stage 2
- Ineffective tissue perfusion
- GFR 60 – 89 ml/min – Mild
- Risk for cardiac arrest
- Imbalance nutrition less than body
Stage 3
requirements
- GFR 30 – 59 ml/min – moderate
- Risk for impaired skin integrity
DIAGNOSTIC TEST :IKF
Stage 4
1. Kidney function test – BUN & creatinine
- GFR 15 – 29 ml/min – severe
2. GFR – 125ml/min
Stage 5
3. Ultrasound
- GFR <15 ml/min
4. KUB
- ESRD/ESKD – uremia /uremic syndrome
5. Ct scan
( collection of S/SX referrable to severe
6. MRI
uremia , this is multi system affection , this
7. Culture
can only see on end stage
8. Urinalysis
9. Biopsy
Note :ESRD / ESKD
10. Cystoscopy / ureterocystoscopy
- Nervous – confusion
- Uremic psychosis – altered LOC
- Respiratory system – pulmonary edema
- Hematologic system – anemia ,
thrombocytopenia
MANAGEMENT:
- Integumentary system – ashen gray color ,
1 modality of treatment for both acute &
uremic frost
chronic = Dialysis
- Digestive system – uremic fetor , ammonia
like breath
S/SX:
- Musculoskeletal system – renal
- Oliguria
osteodystrophy , deformity
- Azotemia
IMPAIRED KIDNEY FUNCTION - Edema
- Anemia Note:
- HPN No diuretics if patient is on end stage (ESRD) need
- Fatigue na ng dialysis
- Hyper K ( immediate indication of dialysis ) 2. HPN – antihypertensive drug
- Hyper P Ex. Ace inhibitors
- Hyper M Quinapril
- Hypo Cal AIIR blockers – losartan , candesartan
- 3. Hyperkalemia
- Metabolic acidosis a. Insulin IV
b. Glucose IV
>push K into the cells
c. calcium gluconate
- Antagonize the effect of K on cardiac
cells
d.kayexalate
4. Metabolic acidosis
a. Sodium bicarbonate (Na HCO3)
5. Hyperphosphatemia
a. AIOH ( antacids)
b. Amphojel – bind PO4 to be remove from
the body ( phosphate binding agents
6. Hypocalcemia
a. Calcium
b. Vit D supplements
7. Anemia
a. Erythropoietin parenteral
b. (epogen (epocinon ( epoetin alfa)
c. Ferrous sulfate supplements
Nursing intervention:
MEDICAL MANAGEMENT : 1. Restrict fluid
1. Edema – diuretics 2. Restrict sodium
Ex. Loop D = furosemide
3. Monitor I&O - Sudden changes in the fluid and
4. Monitor VS electrolyte levels feeling of wellness
5. Weigh patient daily is felt a day after the dialysis
6. Promote rest periods b. …..
7. Diet c.
- restrict Na
- K , P , Mg rich food
- Restrict fats
- carbohydrates
8. Provide safety measure
9. Sin care
10. Assess for symptoms of bleeding / other
conditions
Modalities of treatment
2 dialysis for acute and chronic
1. Dialysis
a. Peritoneal dialysis
Goals :PD
1. Remove toxic waste
2. To re istablish fluid and electrolyte balance
3 types of PD
1. Acute intermittent PD ( AIPD)
2. Continuous ambulatory PD (CAPD)
3. Continuous cyclic PD (CCPD)
Principle :
1. Osmosis – from concentration to ¯
concentration
2. Simple diffusion
Note: This happen through semipermeable
membrane peritoneal membrane
RISK FACTORS : PD
1. Peritonitis
2. Primary peritonitis
3. Secondary peritonitis – rupture of
appendix ( surgery )
Possible complication !!!!! 4. Perforate ulcer ( correct by surgery )
a. Dysequillibrium
- assess for patency

b. Hemodialysis - palpate for thrill
- Most common done today - auscultate bruit
- Can go under peritoneal dialysis
note :ilalagay mo sa chart or bed sa bed ni patient
- no bp monitory
- no blood extraction on the site of pistula
( sasabihin mo kung saang arm )
2. Renal transplant
- ESRD
- Most effective
Goals : HD - Most cost effective
1. to remove nitrogenous wastes
2. To remove excess water DRUGS : CKD/ESRD
PRINCIPLES : HD Note : Hindi sila pang treatment pang delay lang to
1. osmosis ng dialysis gets mo
2. simple diffusion 1. Ketoanalogue – amino acids
3. ultrafiltration - Can maintain the creatinine level
dialyzer – artificial kidney 2. Kremezine
 Emergency dialysis - Who cannot under go dialysis
- insertion of J tube in the central vein agadagad
 Elective dialysis - It remove the waste products
- Av osmosis – artery vein connect
( adsorbent
a. AV fistula
DONOR :
b. Av graft ( can see patients vein go bigger )
- Dead
- Living donor – healthy / tissue
compatibility
SURGERY :
- Nephrectomy
- Position – lateral
- Post op monitor – every 15 mi,n,
every 30 min every hour until stable
room pain reliever
- Discharge teaching – monitor kidney
function test every 6 months or
annual
PATIENT – recipient : RT
- Supine
- Location – pelvis / iliac crest
POST Op: RT
- Monitor every 15, 30 mins / hours
Until stable
- Monitor urine output hourly
GOALS: RT
- To prevent rejection
= Immunosuppressant drug
a. Steroids
 withraw gradually after 3-4
months
( more possible infection)
b. Cyclosporine- for life to prevent
infection
 Reverse isolation
 Avoid crowded places
 Avoid sick people
- To prevent infection
( fever , tenderness over the graft ,
leukocytes )
!!!!!!!!!
Monitor kidney function
Live a healthy lifestyle

NCMB Midterm 312 Lec

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NCMB 312 LEC Midterm

- Sized ng palm ng patient

-it may cause Osmotic Diuresis

- protenate or 5% albumin in isotonic saline PROMOTE HEALING

TYPES SKIN GRAFTS

The infection process

Insidance of disease  Pathogenicity ______________________

VERTICAL TRANSMISSION – mother to child

5. Portal entry of organism into human

VACCINE Minimum age at fisrt Number of doses Minimum interval Reason

Varicella vaccine 12 moths 2 3 months Protection against

1. Fluid volume excess (FVE)

Risk for injury

a. Central Venous Pressure (CVP)

1.  fluid IVF/ ORS

Yung sodium na pumasok lalabas uli

o Neurons – functional unit PROBLEM

Stimulus will open up for sodium = sodium

1. Restrict sodium rich food

1.  Na & water - 3.5 – 5.5 meq/L

MANAGEMENT : hyponatremia ETIOLOGY :hyperkalemia

(sa outside of the cell inc. concentration

o Muscle cells B. Hypokalemia

1.  K rich food (When it expose to UV sunlight =cholecalciferol (vit

a. ionized calcium a. Hypercalcemia

DIAGNOSTIC TEST :hypercalcemia

1. Altered electrolyt imbalance

1. serum calcium level

1. inc. calcium rish food

Acid base imbalances - Low ph  acidosis

Pag tumataas yung H ion bumababa Ph

HCO3 – 22- 26 meq/L ( kussmaul’s respiration)

Pag normal anion dap problem  nasa CL/HCO3

Etiology  dec. HCO3 / acid pH -  = acidosis

Respiratory acidosis Regulation of acid / base

Etiology :  pCO2  pH 7.35 – 7.45

Respiratory Alkalosis pH 7.31  pCO2 49  HCO3 24 (N)

Ex.(N) pH 7.39 pCO2 49  HCO3 27 

(Ph is normal )= fully/ compensated

(PCO2 ) respiratory acidosis compensated

Thickness – 3 – 2.5 cm thick

Note: pag nag kaka chronic kidney D. nag shrishrink

Upper back /plank area ang masakit –> upper urinary

Low back / hypogastrict area – >lower urinary tract

Urinary bladder / uretra  problem is on hypogastric /

 Kidney punch test Kidneys / urether  costovertibral angle / plank area

Effective filtration presure ( EEFP)

EFP = hp – (op + tp)

Efp ( ex. Kunwari lamng )

Efp = 40 ( the pressure will go where )tubules

( pag may stones jaan tataas ang tubular pressure

- Fluid na lumabas ( na filtrate ) = Ultrafiltrate

Normal urine output

RBC papasok sa glomerulus – afferent arteriole 3. Water regulation

5. Regulation of acid based balance

Etiology Etiology : glomerulonephritis

Autoimmune – antibodies are formed against onw

1. Calcium stones  Most painful site of stone

- How this developed