Final Flashcards
Lab value for serum creatinine and what kind of test is it?
What is creatinine
How does it compare to BUN
What do different levels mean?
0.6-1.3mg/dl blood test
A waste product from mm and protein. It is not reabsorbed in the kidneys and is there for a reliable indicator of kidney function.
It is more accurate than BUN
Increase=inflammation or infection, kidney damage
Decrease=malnutrition
BUN level and what type of test
What is BUN
What are the non renal factors that can increase it-7
10-20mg/dl Blood
Blood urea nitrogen
Infections, GI bleeds, Trauma, Athletic activity, mm breakdown, dehydration, steroids.
What is GFR normal value and what kind of test?
What does it say about kidney function?
How accurate is it?
> 90ml/min It is based on creatinine, age, sex, and race and it estimates the GFR.
If it is decreased then we have decreased kidney function
It is very accurate because it measures GFR and that is the best indicator of kidney function.
AKI
What is most common cause
What is most common cause of death?
Acute tubular necrosis
Infection
Prerenal AKI What is oliguria from? What is happening in the kidney? What do we treat? What can it lead to?
Decreased volume of blood not damage to parenchyma
Because of low BP kidneys are trying to raise BP by saving NA+ and H2O RAAS
Fix cause and hydrate
Intrarenal AKI
Drugs that are hard on the kidneys 9
Aminoglycocides-(CIN), Antibiotics, Contrast, NSAIDS, ACE inhibitors (pril) Hemoglobin and myoglobin- from damaged cells. Metformin, Dig, Opioids.
What is the most common cause of intrarenal AKI
Acute tubular nephrosis from sepsis or nephrotoxins most common
others-Major surg, hypovolemia, shock, blood transfusion, mm injury
What other things can cause AKI besides drugs?
Glomerular nephrosis, systemic lupis erythmatosus
What are urinary casts?
Clumps of cells and blood cells found in urine when kidneys are not working.
What are the stages of AKI 4
Initiation, Oliguric, Diuretic, recovery
RIFLE STAGING AKI
RIsk SC increases X1.5 or GFR Dec by 25% UOP-<0.5ml/kg/hr for 6 hours
Injury SC up X2 or GFR Down by 50% uop <0.5ml/kg//hr for 12 hours
Failure SC up X3 or >4mg/dl with acute rise of >/= 0.5 or GFR down by 75%
UP- <0.3 ml/kg/hr for 24 hours or anuria for 12 hours
Loss- Persistant acute kidney fail complete loss of function >4 weeks UOP same as fail
End- Complete loss of kidney function > 3months
Value for oliguric
<400ml/day
What defines oliguric stage value
When does it happen-3
How long does it last
Prognosis?
A reduction of urine output of less than 400ml a day. Usually happens within 1-7 days of injury but if ischemia is present than 24 hours. If from drugs it might be a week.
10-14 days up to months
Longer=poor prognosis
Oliguric phase in prerenal looks like
Low perfusion to the kidneys activates RAAS- Na+ and H2O retention =Low urine Na+ and High Specific gravity.
Describe diuretic phase of AKI UOP WHy? One thing How long Two more things
UOP- 1-3 lt sometimes 5 or more. It is from osmotic diuresis from high urea concentration. Kidneys can excrete waste but cant concentrate it. Can last 1-3 weeks. BUN and creatine start to stabilize.
Hypoeverything
Recovery phase of AKI
starts when?
What does recovery look like 4
Starts when GFR starts to increase and BUN and c start to decrease Major improvement in first 1-2 weeks. Full recovery can take 2 months.
Older adults less likely to recover, can progress to CKD
Care for AKI 10
eliminate cause-drugs dose blockage Nutrtion-add cal increase carbs decrease fat and prot Possible restrictions in electrolytes loop diuretics- zides fluids-replace what was lost- Daily output plus 600m Dialysis- can help with hyperk+ Weights, IO, Prevent infection Skin checks mouth care
drug for AKI
drugs tx for Hyperk
Loops-lasix zides, manitol, Na+ bicarb Ca+ gluconate Glucose Insulin Kayexalate- If these fail or there are neuro s/s dialyze
Complications of Dialysis 8
Hypotension, MM cramps Loss of blood hepatitis Steal syndrome- ischemia distal to fistula Tachycardia vision changes nausea mental changes
Drugs that are hard on the kidneys 9
Aminoglycocides-(CIN), Antibiotics, Contrast, NSAIDS, ACE inhibitors (pril) Hemoglobin and myoglobin- from damaged cells. Metformin, Dig, Opioids.
Drugs that are hard on the kidneys 10
Aminoglycocides-(CIN), Antibiotics, Contrast, NSAIDS, Ibprophen, ACE inhibitors (pril) Hemoglobin and myoglobin- from damaged cells. Metformin, Dig, Opioids.
- What medication is commonly used as a phosphate binder in CKD
- What medication is commonly used as a phosphate binder in CKD
- What are the advantages of an AVF compared to compared to an AVG
Less likely to clot and less likely to become infected. Hear a bruit (whooshing) and feel a thrill.
Below list 5 complications of MG as a result of the muscle weakness in specific muscle groups.
What crisis and what are the s/s?
- ptosis/facial drooping
- difficulty with speech
- issues with chewing food
- problems with swallowing
- difficulty breathing (increased risk for aspiration and infections).
Other complications: fatigue, risk of falls/injury
These complications are associated with the lack of Ach and subsequent progressive muscle weakness. Muscle weakness in the face, neck and chest are especially concerning because they are vital for eating/swallowing/breathing.
Myasthenic Crisis-Exacerbation, worsening of mm weak like swallowing and breathing
RA
Rheumatoid arthritis is a systemic autoimmune disease that is characterized by inflammation of connective tissue in diarthrodial (synovial) joints. The person will have fever, fatigue and potentially organ involvement. Joint stiffness is a common symptom and can last several hours. There is a genetic predisposition associated with RA. Unlike osteoarthritis, those with RA experience periods of remission and exacerbation.
You are doing patient teaching on the treatments used in RA. Explain in layman’s terms to the patient the types of drug therapy used in RA, how they work and any side effects of the drug therapy.
DMARDs (Disease Modifying Antirheumatic Drugs) are the main treatment for slowing the disease progression and decreasing the risk for joint erosion or deformity. Methotrexate is the preferred DMARD. Methotrexate side effects include bone marrow suppression and hepatoxicity. Lab monitoring must take place -therapeutic levels can be reached in 4-6 weeks.
These are for life
Use Aggressively
Cross Match and what do results mean
Used to determine existence of antibodies agains donor mix r serum with d lymphocytes
negative is safe
positive is not safe and means cytotoxic antibodies to the donor
CD4 levels
Normal
Healthy
AIDS
800-1200
>500
<200
kaposi sarcoma
HIV lesions all over and very different
Oral Hairy leukopenia
epstine bar painless white raised lesions on lateral tongue
4 opportunistic infections with HIV
PCP pnemonia, mycobacterium TB, Cytomegalovirus, toxoplasmosis
about Myasthenia gravis
AUTOIMMUNE disorder of neuromuscular junction marked by fluctuating weakness that increases with mm use.
Etiology of MG 3
Antibodies attach ACh receptors and stimulate mm contraction
can cause thymus hyperplasia
increase in day and some relief at night
Clinical manifestations of MG effects 6 areas 3 s/s 2 other things one test
Weakness that effects eyes, eyelids, chew, swallow, speak and breathe,
Pitosis, double vision, fading voice,
NO SENSORY LOSS, normal reflex,
EYE test
What is MG crisis?
What are we most concerned about?
Acute exacerbation of mm weakness triggeref by triggers most importantly- Respiratory infection/steroids
Breathing issues and aspiration
Pharmacology of fibromyalgia: How do tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs) work in the treatment of fibromyalgia? How do muscle relaxers work to treat fibromyalgia?
Two common drug tx
One last thing
TCAs and SSRIs are used to relieve pain and helping with depression and treat insomnia that comes with the debilitating nature of extreme pain. Muscle relaxers also help reduce pain/spasms and treat sleeping difficulties. Non-pharmacological treatments include massage and stretching to help with muscle pain.
Lyrica, symbolta
NO OPIOIDS
- What are the clinical manifestations of acute transplant rejection
Fever, flu like symptoms, pain and tenderness at the sight of transplant. Signs of organ failure (hypertension, fluid retention, BUN and CR up). Days to month after transplant. Want a negative cross match, positive BAD!
● S/s acute HIV/chronic/AIDS
○ Acute: flu-like
○ Chronic: no s/s - asymptomatic
○ Chronic (active): night sweats - fever - flu-like - malaise - dia
Heat cramps
describe
s/s 5
casue 1
tx 4
teach 2
severe cramps in lg mm groups fatigued by heavy work
brief and tend to follow heavy work or exercise.
N/tachy/pallor/weaness/diaphoresis
dehydrated
rest/hydrate with Na+ and water elevation massage
avoid strenuous activity for 12 hours and increase electrolytes
Heat exhaustion
s/s 12
1 tx
prolonged exposure to heat over hours or days
fatigue/N/V/extreme thirst/ anxiety/hypoten/tachy/high temp/ dilated pupils/mild confusion/ash color/diaphoresis
moist sheet/ambiant cooling/IV fluids
Heat Stroke
Describe
s/s 7
tx-8
and two considerations
serious results from failure of hypothalmic thermoregulation process.
diaphoresis, vasodilation, tachypenia, sweat glans stop functioning increase in temp rapidly
cerebral edema and hemorrhage from heat
ABC reducing core temp monitoring dysR, 100%O2, ECG monitoring, pulse ox. correct e and coagulation
Prevent shivering/ watch for rabdo-watch urine
how to cool heat stroke?
Remove clothing, wet sheet, fan, icepacks to glabrous surfaces
Hypothermia described
Core temp below 95
most heat is lost from head thorax and lungs and wet clothing increases heat loss by 5x and immersion in cold water by 25x
MIld hypothermia
Degrees
s/s
tx
93-95 degrees shivering lethargy confusion mild heart rate changes
passive rewarming-warm blankets get out of wet clothes.
Mod hypothermia
86-93
ridgid bradycardia from hypotension, bradypenia
Active external rewarming-heat lamps bear hugger
Severe hypothermia
below 96 Pupils fixed and dilated absent reflexes heart rate and respiratory rate VERY slow almost can’t detect -appear dead so they need to be warmed to 86 degrees before pronounced dead
Active Internal warming-warm fluids- chest tubes IV cath
Hypothermia outcomes 5
Kidney failure, clots, dysR, hypoxia metabolic acidosis
Chronic fitigue syndrome diagnosis
and one thing
Profound fatigue longer than 6 moths Post exertional malase- crashing unrefreshing sleep and one Cognitive impairment-brain fog Orthostatic intolerance no labs or tx plan
What is a late sign of kidney failure
Dec urine output
ABC
○ airway - breathing - circulation - disability (AVPU) - environ - full set VS - Get stuff (LMNOP) - Hx (SAMPLE) - Heat to Toe - Inspect post surfaces
- What is the purpose of decontamination area
– get off patient and protect staff, right outside hospital
- What is disasters triage?
Black/Dead, not breathing (agonal), Red/Need help right away, Yellow/Need treatment, Green/Walking wounded
Rule of nines
Head- 4.5% x 2
Trunk 18% X2
legs 9%x2
Arms 1.5% X2
Genitals -1%
Fluid replacement for burns called?
adults
peds
electrical and rabdo?
after 24hr
one thing about all
the parkland
2ml/kg/TBSA
3ml/kg/TBSA
4ml/kg/TBSA
33%
1/2 in first 8hrs then other 1/2 in 16 hrs
- What should a patient be intubated?
Can’t protect own airway, can’t maintain own breathing, i.e. burns to neck, burns to face, too fatigued, apnea, blocked airway. GCS <8
- What is dobutamine used for in shock
increase contractility and cardiac output along with norepi. ○ (MAP <65 not corrected via IVF)
○ 30mL (kg)
○ positive inotropic med
○ inc contractility and CO
- What is the priority intervention for sepsis?
Blood cultures before antibotics, Fluid 30ml/kg
- What interventions are included in the VAP bundle?
a. Head of bed up 30-45
b. Don’t change out circuit
c. CHG oral
d. Sedation vacation q24
e. Subglottic suction
What do you watch for PEEP
HypoTN, Barotrauma
SEPSIS bundle 4
○ O2
○ IVF bolus (30mL x kg)
○ cultures
○ IV abx
Absolute Neutrophil count
Determines if a pt is neutropenic or not
WBC count x % of neutrophils
Change percent to decimal
Neutropenic= <1000
<500 is severe
What is HSCT
risks
Hint-One risk effects which three areas
Bone marrow transplant with high doses of chemotherapy and radiation then healthy stem cells infused. Intense procedure
Risks=Infection, graft vs host (Skin Liver, GI), bleeding, can be fatal
can come from peripheral blood of donor
What is Multiple Myeloma
More common in 3
Cancerous plasma cells that proliferate in bone marrow and destroy bone. There is an overproduction of plasma cells that don’t make antibodies like they should. Instead they make Monoclonal antibodies that are undifferentiated and ineffective. They produce cytokines and infiltrate bone marrow a Decrease in antibodies= an increased risk of infection. pancytopenia.
Men, blacks, 65-74
S/s of Multiple Myeloma 8
Slow and insidious, skeletal pain in pelvis Ribs, Spine
Osteoporosis
Osteolytic lesions from osteoclasts
can compress spine
Hypercalcemia-Seizures, AMS, Confusion, Cardiac dysR,
Kidneys renal stones, obstruction, fail, nephrosis,
Hyper-viscosity syndrome-Worse on kidneys, and organs from M prots
Bone marrow dysfunction-Pancytopenia
- What is the treatment for tumor lysis syndrome
increase fluids, allopurinol, sodium bicarb
- What lab diagnoses are used to assess DIC? What is the priority
fix the cause
a. FSP
b. platelets
c. INR
d. D Dimer
Normal WBC cout
4000 to 11000
Map
2xd+sbp/3
N 70-100
Myasthenia crisis triggers
Tx
Res infection, illness, surg, distress, pregnancy,
Corticosteroids
Cd4 counts
N 800-1200
500 problematic
Aids 200
Creatinine
Bun
Gfr
C 0.6-1.3
Bun 10-20
GFzr 125
