scenarios/medications/disease Flashcards
RE/4 case A:
Mr E. Toh was brought into your ED collapsed and unresponsive. He looks unkempt and smells of alcohol.
On examination, he is pale and his BMI is 17. He feels cold and clammy. There was no sign of trauma or injury. His blood pressure was 110/78 mmHg and his heart rate was 75 beats per minute.
His test results are as follows.
Sodium 144 mmol/L (135-145) Potassium 5.1 mmol/L (3.5-4.5) Chloride 107 mmol/L (95-108) Bicarbonate 9 mmol/L (24-31) Creatinine 210 umol/L (35-85) Glucose 2.1 mmol/ L (5.0 -7)
Liver Function tests Bilirubin 2.4 mg/dL (0.3-1.1) AST 315 U/L (14-48) ALT 56 U/L (40-120) GGT 800 U/L (9–48) Albumin 18 g/L(35-55)
possible reasons for low glucose?
malnourishment
reason:
clinical picture suggests malnourishment and liver damage from alcohol abuse
liver damage
- increased bilirubin, AST, GGT indicate liver damage
malnourishment (especially since liver screwed LOL, alcohol abuse, and tissues also screwed)
- low BMI, protein, glucose (and low glycogen)
- increased creatine indicate muscle proteolysis/cachexia (when muscle break down, creatine phosphate -> creatine + ATP)
metabolism as a whole is screwed (therefore, bicarbonate and sodium affected)
cold and clammy
- adrenergic response to hypoglycemic
acute hypoglycemic event likely cause of unconsciousness and unkemptness
NOTE:
METFORMIN AND SULFONYLUREAS CAN INDUCE HYPOGLYEMIA BUT!! DOES NOT CAUSE LIVER/KIDNEY DAMAGE AND DOES NOT ACCOUNT FOR OTHER PARTS OF CLINICAL PICTURE (E.G. CACHEXIA)
SULFONYLUREA USE CAN BE DETECTED BY C-PROTEIN LEVELS AT A HYPOGLYCEMIC STATE
- insulin should not be produced in hypoglycemia
- sulfonylurea would still induce insulin
METFORMIN have increased risk of metabolic ketoacidosis
-THERFORE, CANNOT BE USED WITH PRE-EXISTING ORGAN FAILURES
medication:
sulfonylurea (drug class) use for what
treat type 2 DM
sulfonylurea will induce insulin!
note: examples of sulfonylurea
- Glibenclamide aka glyburide
medication: metformin
when CANNOT use metformin?
when there is PRE-EXISTING ORGAN FAILURES
why? increased risk of metabolic ketoacidosis
how increase metabolic ketoacidosis? not sure but theory is because of inhibition of gluconeogenesis and stimulation of fatty acid oxidation
when differentiating between pt using sulfonylurea and pt being malnourished, what should they do
c-peptide level when pt hypoglycaemic
if sulfonylurea: c-peptide high
recap: hypoglycaemic -> low insulin, c-peptide = insuline levels
why c-peptide instead of insulin?
- insulin half life short, difficult to measure
RE/4 case A:
Mr E. Toh was brought into your ED collapsed and unresponsive. He looks unkempt and smells of alcohol.
On examination, he is pale and his BMI is 17. He feels cold and clammy. There was no sign of trauma or injury. His blood pressure was 110/78 mmHg and his heart rate was 75 beats per minute.
His test results are as follows.
Sodium 144 mmol/L (135-145) Potassium 5.1 mmol/L (3.5-4.5) Chloride 107 mmol/L (95-108) Bicarbonate 9 mmol/L (24-31) Creatinine 210 umol/L (35-85) Glucose 2.1 mmol/ L (5.0 -7)
Liver Function tests Bilirubin 2.4 mg/dL (0.3-1.1) AST 315 U/L (14-48) ALT 56 U/L (40-120) GGT 800 U/L (9–48) Albumin 18 g/L(35-55)
why unable to mount glucose?
low glycogen stores
reason: low BMI, smells of alcohol -> alcoholic, likely to be malnourished and neglect proper food intake
hypoglycemic -> search for glucose by using glycogen stores
RE/4 case B:
A 11 year old girl was seen in the outpatient clinic. Her mother reports she is always complaining of being weak and has episodes of sweating. These symptoms are improved by eating. She is developmentally slow and attends Special Education. She only started sitting at 14 months and walked at the age of 3.
On examination she has normal blood pressure, temperature and pulse rate. But she is 25 kg. She has an enlarged liver which is firm. There is no splenomegaly. The rest of the examination is normal.
She complains of sweating and feeling unwell. You take a blood sample and these are the results.
Hypoglycaemia Low pH High Lactate High Triglycerides High ketones High free fatty acids
What does the presence of hypoglycaemia and high blood ketones suggest?
(what disease)
insufficient glucose synthesis aka Von Gierke’s disease [FOM TBL 1]
- glucose-6-phosphate deficiency, cannot break down glycogen
reason:
cannot be insufficient insulin (since she has hypoglycaemia)
cannot be too much insulin (since she has high blood ketones)
brain can only use glucose and ketone. since there is insufficient glucose synthesis, body produce more ketone
recap:
insulin decrease glucose, DECREASE ketone also
NOTE: CORI DISEASE (type3 glycogen storage disease) is milder than Von Gierke’s
- CORI: insufficient debranching enzyme, also caused by buildup of glycogen
RE/3:
Pemberton’s test for what
used to evaluate venous obstruction in pt’s with goiters
pembertons sign = facial plethora during bilateral arm elevation
- caused by SVC compression (more significant to cause sign)
RE/4 case C:
A 26 year old Chinese woman has been losing weight over the past few months. She has been thirsty and passing a lot of urine. 2 days prior to admission she had a fever, runny nose and sore throat. This morning she complained of abdominal pain and vomited after eating breakfast. When her mother went to check on her in her room 2 hours later, she found her unconscious on the floor.
On presentation to the emergency department her blood results were as follows:
Blood Glucose 28 mmol/L
pH 7.18 (normal range 7.35-7.45)
Bicarbonate 5 mmol/L (normal range 22-26)
Potassium 2.9 mmol/L (normal range 3.5-5.0)
Betahydroxybutyrate 5 mmol/L (normal <1)
what diagnosis?
diabetic ketoacidosis
reason:
- DKA Indicative of T1DM
- Blood glucose elevated → hyperglycaemia and diabetes
- pH lower → acidosis
- Bicarbonate low → because bicarbonate used to buffer the H+ excess from the DKA (search bicarbonate equation)
- Potassium low → from preamble, the woman has been passing out a lot of urine → passing out K+
- Urine + Thirsty → polydipsia and polyuria
note: beta hydroxybutyrate is a ketone
3 major ketone bodies
- betahydroxybutyrate
- acetoacetate
- acetone
RE/4 case C:
A 26 year old Chinese woman has been losing weight over the past few months. She has been thirsty and passing a lot of urine. 2 days prior to admission she had a fever, runny nose and sore throat. This morning she complained of abdominal pain and vomited after eating breakfast. When her mother went to check on her in her room 2 hours later, she found her unconscious on the floor.
On presentation to the emergency department her blood results were as follows:
Blood Glucose 28 mmol/L
pH 7.18 (normal range 7.35-7.45)
Bicarbonate 5 mmol/L (normal range 22-26)
Potassium 2.9 mmol/L (normal range 3.5-5.0)
Betahydroxybutyrate 5 mmol/L (normal <1)
The AE staff have given the patient 500 ml N saline over the first 30 minutes and sends the patient up to the ward with a N Saline drip, 500 ml over the next 1 hour. The patient has received no other intravenous or oral medications. The houseman wants to start insulin straight away to bring down the glucose levels. However, the registrar on call cautions against that.
why?
we have to wait until potassium is ok, if not it will worsen hypokalemia
reason: insulin shifts potassium into cells by stimulating activity of Na+-H+ antiporter on cell membrane, promoting entry of sodium into cells.
leads to activation of Na+-K+ ATpase, causing electrogenic influx of potassium -> lower blood K+ (hypokalemia)
RE/4 case D:
A 62 year old patient has type 2 diabetes for 16 years. He was on Janumet 50/1000 bd and Glipzide 10 mg bd. His HBA1c was 9.8% and his fasting glucose was 9 mmol when he visited his General practitioner.
He has brought his home capillary glucose readings
His General Practitioner started him an Empagliflozin 25 mg. 2 weeks later, he is found by his daughter lying on the bathroom floor, unconscious. His Blood results are as follows
Blood Glucose 12 mmol/L
pH 7.18 (normal range 7.35-7.45)
Bicarbonate 5 mmol/L (normal range 22-26)
Potassium 2.9 mmol/L (normal range 3.5-5.0)
Betahydroxybutyrate 5 mmol/L (normal <1)
diagnosis?
diabetic ketoacidosis
reason: this pt is T2DM, DKA not common in T2DM
NOTE: empagliflozin (sodium-glucose cotransporter inhibitor) effect
- DKA despite being T2DM (known side effect)
- blocking uptake of Na and glucose -> reduced conc gradient -> pee out more water!!
- inhibit glucose resorption in kidney -> more glucose release-> conc gradient is water out -> dehydration
- build up of ketones (because more renal glucoses, shift from carbs to FA utilisation)
medication: advice for those taking empagliflozin
drink lots of water, dont hold in urine, clear urine often and dont eat when sick
NOTE: empagliflozin (sodium-glucose cotransporter inhibitor) effect
- DKA despite being T2DM (known side effect)
- blocking uptake of Na and glucose -> reduced conc gradient -> pee out more water!!
- inhibit glucose resorption in kidney -> more glucose release-> conc gradient is water out -> dehydration
- build up of ketones (because more renal glucoses, shift from carbs to FA utilisation)
medication: “-gliflozin”
suffix of what group of inhibitors?
SGLT2i
= sodium-glucose cotransporter 2 inhibitor
medication: empagliflozin usually given for what
T2DM!
those with insulin RESISTANCE
NOTE: empagliflozin (sodium-glucose cotransporter inhibitor) effect
- DKA despite being T2DM (known side effect)
- blocking uptake of Na and glucose -> reduced conc gradient -> pee out more water!!
- inhibit glucose resorption in kidney -> more glucose release-> conc gradient is water out -> dehydration
- build up of ketones (because more renal glucoses, shift from carbs to FA utilisation)
disease: what disease has the following signs
mucous membrane pigmentation, skin pigmentation, darkening of hair,
freckling, vitiligo, pigment accentuation at nipples & friction areas, pigment concentration in skin creases & in scars
hypotension
loss of weight emaciation - anorexia, vomiting, diarrhea
muscular weakness
low circulating cortisol, high levels of ACTH and MSH
Addison’s disease
reason: adrenal cortex failure
low cortisol, negative feedback reduced thus high levels of ACTH and MSH
high levels of MSH -> pigmentation
no cortisol and no aldosterone => low blood pressure
disease: what disease has these signs
red cheeks moon face buffalo humps bruisability ecchymoses (easily bruised) thin skin red striae high BP thin arm and legs pendulous abdomen poor wound healing osteoporosis proximal myopathy
Cushing’s disease
pendulous abdomen but thin arms and legs = lemon on stick = centripetal obesity (due to fat redistribution)
* increased fat production, decreased proteins
