Final Exam Blueprint Flashcards
priorities of care for patient with peripheral neuropathy
SAFETY
assess sensation, mobility, wounds
avoiding extreme temperatures, soaking feet, and poorly fitting shoes
teach patients to check their feet DAILY
which organ is most affected by blood glucose?
brain
cannot store glucose and uses a LOT for functioning, so important to maintain blood glucose control
s+s of DKA, what type of onset + associated with which DM?
- rapid onset
- CBG >300
- ketones in urine
- acidosis (low pH)
- kussmaul breathing
type 1
interventions for DKA
- ABC (don’t intubate b/c kussmaul helping to blow off CO2)
- telemetry
- fluids (NS for CBG >250, D5 1/2 NS CBG <250)
- potassium (slowly to prevent heart issues)
s+s of HHS, what type of onset + associated with which type of DM?
- gradual onset
- CBG >600
- profound dehydration
- hyperosmolar state (>320)
type 2
higher mortality rate
interventions for HHS
- ABC
- telemetry
- fix osmolarity SLOWLY (avoid neuro complications)
- fluids (1/2 NS b/c of osmolarity)
would you expect weight loss or weight gain with DKA? why?
would you expect hypo or hypertension?
weight loss b/c of hyperglycemia –> body breaking down fat –> diuresis
HYPOtension b/c of fluid loss
DM diagnostic for fasting glucose
> 126 on 2+ occasions
DM diagnostic for HgA1C
> 6.5%
DM diagnostic for non fasting glucose
> 200 w/symptoms of hyperglycemia
DM diagnostic for glucose tolerance test (preggos)
> 200
and increased risk of developing TIIDM later on
what is normal fasting glucose? and when is best time to take this?
80-110
morning labs after NPO
what is normal HgA1C?
<4-6%
what is HgA1C that indicates risk of Diabetes?
5.7-6.4%
re: urinalysis, what would you see present in urine with early stage diabetic nephropathy?
albumin
s+s of hyperglycemia
“hot and dry, sugar’s high”
kussmaul breathing, weight loss, 3 P’s, fatigue, hypotension, blurred vision
s+s of hypoglycemia
“cool and clammy, need some candy”
diaphoretic, tremors, tachycardia, irritability, confusion, hunger, fatigue, nausea
what are the 3 P’s r/t hyperglycemia and describe why they occur (KISS)
- polyphagia: cells starving
- polyuria: diuresis r/t hyperglycemia
- polydipsia: secondary to polyuria and dehydration
compare type 1 DM with type 2 DM
- type 1: autoimmune, beta cells destroyed + don’t produce insulin; complication: DKA
- type 2: insulin resistance; often treated with lifestyle mods + oral drugs, sometimes insulin; complication: HHS
expected ABG values for DKA
pH low (<7.35) CO2 low (<35) HCO3 low (<22)
expected lab findings for pyelonephritis
- WBCs elevated
- presence of RBCs in urine
- presence of bacteria in urine
- culture: E. coli
deficiencies for hypoparathyroidism
- vitamin D
- Calcium
- magnesium (maybe)
- PTH
comfort interventions for post lithotripsy
pain management: ice packs, tylenol, NSAIDs
dietary restrictions for acute glomerulonephritis
K+ and protein
how should fluids be increased with acute glomerulonephritis?
output from the day before + 500-600mL
s+s of hypothyroidism
- low HR, BP, RR
- fatigue
- sleeping a lot
- anorexia
- weight gain
- intolerance to cold
- depression
- thickened tongue (changes in speech)
- edema in eyes/face
- dry skin
T3 + T4 levels for:
hypothyroidism
hyperthyroidism
hypo = low = low T3+T4
hyper = high = hight T3+T4
s+s of hyperthyroidism
- high HR, BP, RR
- intolerance to heat
- insomnia
- weight loss
- excess hunger
- dry brittle hair
- hot, moist skin
- irritability
- tremors
- diaphoresis
main complications/manifestations of FES
- brain: HA, confusion, seizure, altered LOC
- lungs: dyspnea, breathlessness, tachypnea how it’s similar to PE
- skin: petechiae
(up to 72 hours after long bone fracture or hip/knee arthroplasty)
s+s of PE
- dyspnea
- low O2
- tachypnea
s+s of acute glomerulonephritis (5)
- fluid overload issues*
1. edema
2. BP
3. decreased urination
4. weight gain
5. respiratory issues
what history is good to collect for acute glomerulonephritis?
recent infection (strep within 10 days)
how would we know acute glomerulonephritis is resolving and patient is getting better?
weight loss, less edema, increased urine output, no respiratory issues
3 body systems mainly affected by malignant hypertension
- brain (stroke)
- kidneys (failure)
- heart (failure)
what s+s would you see in the brain related to malignant hypertension?
- change in LOC
2. HA
what s+s would you see in the kidneys related to malignant hypertension?
- uremia
- decreased GFR
- increased BUN/creatinine
what s+s would you see in the heart related to malignant hypertension?
- EKG changes
- dyspnea
- fluid retention/weight gain
what is tx for malignant hypertension? how slow should we do this?
reduce BP with antihypertensives
25% reduction in 2-6 hrs
s+s of hyperparathyroidism
“mneumonic” + it’s s+s, plus 3 extras
= hypercalcemia (serum)
= hypocalcemia (bones)
“bones, grones, stones, moans”
bone fractures, GI issues (constipation, N/V), kidney stones, irritability, lethargy, confusion
waxy pallor, weakness, cardiac issues
patient teaching for hyperparathyroidism (3)
- 3-4L H2O/day
- injury prevention (b/c of hypocalcemia in bones)
- monitor cardiac fxn
s+s of PKD
- HTN
- Edema
- distended abdomen
- pain
- low GFR
- increased BUN/creatinine
- kidney stones
- dysuria
- nocturia
- foul smelling urine
- cola colored urine
- bloody urine
- cysts in other areas of body
re: PKD and cysts forming in other areas of the body, what’s our concern with the brain? what might be a s+S of this?
aneurysm
HA!
what is an early sign of PKD?
+ what is a late sign of PKD?
early: nocturia (can’t regulate urine)
late: edema (periorbital edema is an example –> notify provider)