Week 11/12
Minutes
PBL 10: Can I drink beer?
Trigger 1:
What we know?
Young man
Ambulance- E.D w
Mother
Semi-conscious
What we need to
know?
Hypotheses?
Is there a scale of
consciousness?
D- overdose? Illicit & other, poison, alcohol,
How long has he been
semi-conscious for?
I-infection-meningitis-encephalitis, cerebral malaria, viral,
bacterial, protozoa agents.
M- malnutrition, disturbed electrolytes (Na+, K+, Ca2+, Cl-),
dehydration, hyperglycemia, Hormonal?-hypothyroidism,
Kidney failure->urea->toxic, createnine.
T- trauma, head injury, brain tumour, Epileptic seizure?
O- stroke (lack of oxygen)-genetic, diabetic. Anaemia.
Cardiovascular issue (reduced perfusion to the brain).
P- attempted suicide? Overdose drugs.
Trigger 2:
What we know?
Steven, 19y.o
Lives at home
Plays football 2x wk
V. social
Unwell for couple of days
Loosing weight recently
Always thirsty
No medication
What we need to know?
What are the types of
diabetes?
Hypotheses?
Diabates: Increased urine output to excrete, increased thirst.
Dehydration: Hyponatremic (primarily due to loss of ions, esp Sodium- would t), hypernatremic
(loss of water), isonatremic (combination of both- most common form of dehydration).
Renal Failure- failure of excretory fn. Failure of acid secretion- conscious levels. Chronic renal
failure?
Thyroid disorders: endocrine, can cause hypo/hyperglycaemia.
Thyroid disorders- weight loss, crisis- heart failure.
Semicomatose + increased urine output-> diabetes mellitus, diabetes insipidus.
Trigger 3
What we know?
What we need to know?
Hypotheses
Week 11/12
Level of consciousness- 11 What is the Glasgow coma
Glascow coma scale.
scale?
No sign of trauma
Breathing rapidly
Breath smells of acetone
BP 96/68
HR 128Bbp/min
Resp rate- 22 per minute
Blood glucose is 28mmol/L
(RR: 3.5-5.5 mmol/L).
A urine dipstick test
indicates glucose and
ketone bodies.
Minutes
Hypovolemic shock?
Metabolic acidosis
Hypovoelemic shock?
Glasgow coma scale:
Eye response- spontaneous (highest score of 4), verbal command (3), pain (2), no response (1)
Motor response- Obey verbal command (6), pain response (5), withdraws from pain stimulus (4),
abnormal flexion (3), extensor response (2), No (1).
Verbal response- Oriented and converse (5), orientated but confused (4), inappropriate words (3),
incomprehensible (2), No (1).
Minimum=3, max 15.
ACUTE MANAGEMENT
DRSABC: Oxygen through cubital fossa, fluids- start with normal saline.
Below GCS of 8- incubate.
GCS 11 probably able to hold his airway himself. Unlikely to give us his history.
Tracheal deviation? Look for breathing saturation monitor, give oxygen.
C-circulation, check pulse rate, bp. Check carotid pulse, femoral pulse (harder on obese patient).
IV fluids-
Blood glucose levels:
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Blood glucose levels = normally 3.6 and 5.8 mM
Lack of insulin-> decreases efficiency of peripheral glucose utilization and augments glucose
production, raising plasma glucose to 30-120mg/L.
Increased blood glucose- more glucose to filter in renal tubules than can be reabsorbed, excess in
urine. Normally when above 18 (threshold).
Causes dehydration- glucose doesn’t diffuse easily thru pores of the cell membrane, increased
osmotic pressure extracellular causes water diffusing out of cells.
Thus polyuria- excretes water.
Inc glucose -> inc pyruvate -> inc avetly CoA -> Free fatty acids -> H+ -> ketone bodies -> co2 -> utilised in
brain.
Ketone bodies:
Ketone breath- sweet, fruity odour. Excess glucose -> greater pyruvate-> greater acetyl coA-> converted
into ketone bodies (all occurring in the liver). Acetone (volatile compound evaporates at room temp)
Week 11/12
Minutes
broken down and smell is lost in breath and urine. Usually in the breath when there is excess. Fruity odour.
When dehydrated, will find ketone bodies in urine. If increases more so, will excrete via breath.
Rapid breathing: increased ketone bodies (CCOO already donated their proton) causes ketone acidosis.
Excess ketones breaks down-> increased CO2 as a byproduct, produced all in the liver-> results in increased
breathing to excrete CO2.
Wednesday:
QUESTIONS?
What mechanisms underly the development of acidosis?
Metabolic acidosis caused by severe vomting, diabetes mellitus, strenuous exercise (increased lactic acid)
and uremic acidosis (renal failure).
Diabetes mellitus: abnormal fat metabolism, due to the inability of the cells to preferentially use glucose
due to inadequate insulin-> excess keto acids dissociation leads to increased H+ in plasma.
Insulin deficiency results in
-triglceride synthesis decreased.
-lipolysis increased
-results in large scale mobilisation of fatty acids from triglyceride stores.
The increased blood fatty acids are largely used by cells as their energy source. Increased liver use of fatty
acids results in the release of excessive ketone bodies into the blood, causing ketosis.
Ketone bodies include several different acids: such as acetoacetic acid, that result from incomplete
breakdown of fat during hepatic energy production. Therefore this developing ketosis leads to progressive
metabolic acidosis.
Acidosis supresses the brain, and if serious enough can lead to diabetic coma and death.
How does the body deal with metabolic acidosis?
Compensatory mechanism is increased ventilation to blow off extra, acid-forming CO2. Exhalation of one of
the ketone bodies (acetone)- fruity smell. Ketosis more likely to develop in a type 1 diabetic.
How is acid-base balance regulated?
H+ + HCO3 - <-> H2CO3 <-> H2O + CO2
Should do full blood count:
Haemoglobin- may have a bleed
White cell countHyperkalaemia- give glucose and insulin to treat.
Insulin receptor: Insulin triggers uptake of potassium so when glucose comes in swaps for potassium, needs
potassium in the cell to allow for glucose to come into the cell. Involved in membrane potential.
Give insulin- takes up potassium in cell. Put him into hypokaelmic (with treatment need to monitor closely
as hypokalemic can occur).
Trigger 4
What we know?
Venous blood biochem:
Glucose 25.3 (NR: 3.2-7mmol/L)
β-hydroxybutyrate 4mmol/L (NR:
0.18mmol/L)
Osomolarity 310 (NR:275-295)
What we need to know?
What is beta-hydroxybutyrate?
-a ketone body
(need to know all three ketone bodies!) acetone, betahydroxybyturate, acetoacetate.
Week 11/12
Minutes
Sodium 138 (NR: 135-145mmol/L)
Potassium: 4.8 (3.5-4.5mmol/L)
Arterial blood:
Why is potassium raised?
Can fluctuate severly as insulin decreases potassium levels by
redistributing it into the cells. Is not a co-transporter.
pH 6.97 (7.35-7.45)
paO2 126 (80-100mmHg)
paCO2 21 (NR: 36-44mmHg)
HCO3 5 (NR: 21-28mmol/L)
Why do patients become hyperkalemic? Pathophysiology.
Why is he hyperventilating? High hydrogen is sensed via
chemoreceptors, resulting in increased resp rate.
H+ + HCO3 - <-> H2CO3 <-> H2O + CO2
Blood levels show we have low HCO3 (Le Chateliers principle) as trying to use up H+ by blowing of CO2
(respiratory rate increased).
pH acidic as acidosis.
paCO2 lower as blowing off.
paO2 high as increased respiratory rate.
Trigger 5:
What we know?
IV fluids and insulin
infusion treated.
Electrolytes and blood
gasses, glucose
monitored closely.
8hrs in hosp-slightly
improved and speaking
coherently.
Initially his K+ levels fellrequires frequent
monitoring of K+ levels.
What we need to know?
What is the management of acidosis?
Usually diabetic acidosis patients go to ICU- very serious. K+ levels monitoring,
insulin infusion given
Management (ABC): treat diabetes, shock, acidosis (fluids, insulin), underlying
condition (infection caused the onset? Ie give antibiotics to treat condition)
Does he have an underlying treatment? Flu-like symptoms?
Last minute resort- give bicarbonate. When ABC mechanisms aren’t improving.
What are the mechanisms underlying the patients improvement?
-back into homeostasis
-fluids- improved
-Insulin- helped glucose uptake in cells.
What is the continued management of diabetes?
Trigger 6:
What we know?
2 days later stabilised.
Insulin-dependent diabetes
Questions re lifestyle
Can I play sport?
Drink beer?
Can I put glucose in my
coffee instead of sugar?
What about some extra
calories to put weight back
on?
What we need to find out?
Can he drink beer?
Beer- high calories, drink in moderation.
What does Stephen need to do to control his diabetes?
-look for signs of hyper/hypoglycaemia
-monitor diet, blood glucose level, insulin units to inject.
-Lifestyle, medication compliance, exercise (recommended 1hr
daily, adrenaline->promotes uptake of glucose into cells).
-diabetics have high risk of myocardial infarction, cerebrovascular
incident (stroke). Thus change of lifestyle, exercise important.
Week 11/12
Minutes
-High glucose weakens blood vessels, promotes atherosclerosis.
Microvascular disease, peripheral neuropathy.
- Eyes (retinopathy – cataracts)
- Kidneys
- Nerves- loose sensation in legs in later stages. Vasovasorum
affected (microvascular, small blood vessels supplying nerves)
- Peripheries
Trigger: Closure
Leaves hosp 4 days later.
Management plan in place.
GP apt in a couple of days.
Information kit from diabetes Australia is given to him while in hosp.
Registers w national diabetes supply scheme.
NEED TO KNOW TOPICS?
Osmalality vs Osmolarity- Marty
Ketone bodies- Sylvie
What are the precipitators to diabetic acidosis? Ie septic, infection etc. –Joe
Metabolic Acidosis- Rebecca/Jess
What are the buffers in our body? Not just bicarbonate there are others –Raph
Why patients get hyper and hypokalemia?-Sam
Clinical-diabetes three broad principles of management-Hannah
Draw a man with pointing out problems associated with diabetes ie brain, eyes-Vic