Cpp 3 N 4 Ex 1

Front 1

BEDSIDE GLUCOSE TESTING is good for

Back 1

More accurate in the low range

Front 2

normal values for vital signs

Back 2

Pulse is high 60-100

Blood pressure 100/60 ( 120/80)

Front 3

how to check for hyperkalemia in a ekg test?

Back 3

peaked t wave , the q starts widen

Front 4

CORRECTION FOR SERUM SODIUM The sodium level is reduced by 1.6mEq/L for every 100 mg/dL. If glucose level is over 100 mg/dL in a patient say 540 mg/dL. How to go about the correction?

Back 4

540 mg/dL – 100 mg/dL = 440 mg/dL
1.6m X 4.4 = 7.04
Corrected Sodium = 130 +7 = 137mEq/L

Front 5

Arterial blood gases:
pH: 7.20
PO2: 105 mmHg
PCO2 : 20 mmHg
HCO3-: 12 mEq/L

Back 5

ARTERIAL blood gas to determine acid/base disorder
Norma ph 7.4
Ph 7.20 acidotic
Po2 is kind of high
Pc02 is 30s 40s range so its low
Hco3- 12meq/l is low

She is hyperventilated hence the low pco2 metabolic acidosis b.c of the bicarbonate.

Front 6

SERUM OSMOLALITY. Alert patients have osm

Back 6

osm <330 mOSM/kg

kg
Serum osmolality is important b.c it correlates to mental status

Front 7

Type I diabetics have no endogenous

Back 7

insulin to oppose counter–regulatory hormones

Front 8

Precipitant events of Type 1 diabetes

Back 8

: failure to take meds, infection, emesis, other stress

Front 9

Type 1 diabetes death results from

Back 9

to OVER–correction of fluids, glucose or electrolytes

Front 10

Insulin–dependent tissues starve and cause release of counter–regulatory hormones

Back 10

Catecholamines: glycogenolysis, lipolysis and ketone formation
Glucagon: glycogenolysis and gluconeogenesis from lipolysis–> ketone formation
Cortisol: gluconeogenesis (from muscle)
GH: lipolysis and antagonizes insulin effect

Front 11

Hyperglycemia in DKA diabetics leads to

Back 11

a) osmotic diuresis –> dehydration –> hypovolcemic shock
b)hyperosmolar state –> cellular dehydration –> altered mental state

Front 12

DKA ketoacidosis leads to

Back 12

acidosis –> abdominal pain and hyperventilation

Front 13

what are the resultant changes in DKA

Back 13

Na false decrease of 1.6/100mg
K false increase 0.6 per pH of 0.1
Loss of PO4
Decreased HCO3

Front 14

DIABETIC KETOACIDOSIS (DKA)Biochemical Characteristics

Back 14

Hyperglycemia
Blood sugar > 300mg/dL
Ketonemia
Serum ketones positive at > 1:2 dilution (sodium nitroprusside test)
Acidosis
pH < 7.30
HCO3- < 15 mEq/L

Front 15

DKA is in fact an imbalance of what sort?

Back 15

endocrine

Front 16

Factors Predisposing to the Development of DKA

Back 16

Lack of adequate knowledge of the disease (2/3)
Psychological problems
Financial difficulties
Intercurrent illness (> 80%)
Infection (30-40%)
Vomiting
Myocardial infarction
CVA
Pregnancy
Other stressors

Front 17

COUNTER-REGULATORY HORMONES in response to Stress and intracellular starvation are released, those are :

Back 17

Catecholamines
Glucagon
Cortisol
Growth hormone

Front 18

Hyperglycemia in DKA results from

Back 18

Blockage of intracellular glucose transport
Counter-regulatory hormone effects

Front 19

Hyperglycemia from DKA causes

Back 19

Hyperosmolarity (affecting mental status) and Glucosuria (excess glucose in the urine, osmotic diuresis, dehydration, ketoacidosis, Hydrogen Ions, acidosis

Front 20

The classical DKA presentation is

Back 20

Diaphoresis and tachypnea

Front 21

DKA symptoms

Back 21

Early (hyperglycemia): the polys, visual changes, wt loss/weakness
Later (acidosis): N+V, acetone breath, abd pain, Kussmaul respirations (deep regular sighing), altered mental status
Terminal (hypokalemia)–>cardiac arrhythmias

Front 22

DKA MANAGEMENT

Back 22

INTRAVENOUS FLUID ADMINISTRATION
ELECTROLYTES
MONITOR USING A FLOW SHEET
INSULIN THERAPY
(BICARBONATE THERAPY)

Front 23

INTRAVENOUS FLUID ADMINISTRATION

Back 23

Lower glucose by 18%, it will normalize the ph. How you administer is normal saline. It physiological soidum. You administer as fast as you can so yo ucan dilute out
You can spread it out.

Run it into dilutional problems. Physiological . Apply a bolus of 1 L over 30 min. Fluid normalizes glucose. You wanna make sure people are peeing, otherwise we run into other problems

Front 24

DKA MANAGEMENTElectrolytes

Back 24

Potassium
Level will fall precipitously with treatment
Hold only if peaked T-waves on ECG
20-40 mEq in the first liter of fluid
½ as chloride
½ as phosphate
Monitor hourly

Front 25

DKA MANAGEMENTFlow Sheet

Back 25

Checking osmolality
People will follow based on serium chemistry
No need ot get ph multiple times. Maybe at the end of therapy. Urine output
Vital signs watch that tey are not becoming more tachychardia and mental status. If treatment is aggressivley cerebral edema can be developped b.c you decrease the glucose level to quickly.

Front 26

The most effective insulin management for DKA is

Back 26

IV

Front 27

loading dose dilemma in IV insulin DKA management

Back 27

Loading dose are not used anymore.theres no benefit of given a loading dose and then starting infussion. The danger is that you dropp the glucose too quickly thatst here reason why we don’t do loading dose
If theres high glucose you wan to decrease the rate of how glucose is goind down. You often start with half of the dose to allow slower decline. When sugar reaches 300 you have to continue you insuline therapy. To clear up the ketones. Just b.c the serum glucose reach ideal you can still be acidotic. Add dextrose to iv fluid to prevent hypoglicemia. Check acidosis by chemistry by using bicarbonate and ion gap=> when reach normal level, patient has reach normal levels.

Front 28

DKA MANAGEMENTBicarbonate Therapy complications

Back 28

Shift of oxyhemoglobin dissociation curve to the left
Hypokalemia & hypomagnesemia
Overcorrection alkalosis
Paradoxical CSF acidosis
Cerebral edema

Front 29

ICU
Age < 2 years or > 60 years
pH < 7.0
Serious concurrent illness
(Blood sugar > 1000)
Outpatient Management
Alert
No persistent vomiting
Mild acidosis, ketonemia & dehydration

Back 29

Mild dka
They have mild acidosis. It may actually clear acidosis. These are often time that are more familiar with the disease. There are many children that are monitored at home. Those that go to icu they are the extrem of ageb.c they are more susceptible to some diseases. There are no immunocompetent. If they have acidimia. If they have an MI YOU HAVE TO MANGE THE mi and the current illness. If the blood sugar is greater. You don’t want to drop from 1000 to 100.

Front 30

Laboratory evaluation of the DKA patient is complex and must be repeated

Back 30

on an hourly basis until the patient is stable