L19 - Diabetic Emergencies COPY Flashcards
DIABETIC KETO ACIDOSIS (DKA)
i) what are the four key organs involved?
ii) what causes DKA?
iii) what effect does this have on the liver?
iv) how does frequency of urination change?
v) as glucose isnt being taken up from cells - name two things that happens to allow the body to get fuel? what does this result in (acid/base balance)
vi) how does the body try and compensate? (2)
vii) name two things that can set DKA off
i) liver, adipose tissue, skeletal muscle and kidneys
ii) very low insulin
iii) insulin will usually stop the liver producing lots of glucose but lack of insulin means the liver keeps producing glucose
iv) wee lots - so dehydrated and thirsty
v) body will burn muscle and fat to get fuel
- this results in acidosis due to ketone build up
vii) body tries to compensate for acidosis by
1) weeing out K+
2) breathing out co2 to get rid of acid (pear drop smell)
vii) missed insulin and alcohol can set off DKA
DKA PATHOPHYSIOLOGY
i) how does the pancreas not making insulin affect the urine? what two things can this result in?
ii) name an effect of mild dehydration and severe dehydration
iii) what fatal event can this cause?
iv) how is free fatty acid breakdown affected? what does this result in?
v) which two main events result in acidosis and ketosis?
i) pancreas doesnt make insulin > hyperglycaemia
- this can result in glycosyuria and hyperosmolality
ii) glycosyuria can cause dehydration and electrolyte (K+) loss
- mild = renal failure (AKI)
- severe = CV shock
iii) can cause CV collapse
iv) increase in FFA breakdown to ketones
- results in acidosis
v) acidosis = glycosyrua
ketosis = lipolysis
EFFECT OF INSULIN DEFIC ON ADIPOSE TISSUE
i) how does insulin defic affect lipolysis and esterification of fat?
ii) name one other thing that can cause this
iii) what does this result in in relation to FFAs and glycerol?
iv) what do FFA act as a substrate for in the liver? what two things does this produce?
v) which two tissues can utilise ketones as their main energy substrates?
vi) when does ketoacidosis occur (in relation to balance between KB production and utilisation)
i) insulin deficiency causes increased lipolysis and reduced esterification of fat
ii) glucagon and adrenaline excess can also cause inc lipolysis and reduced esterification
iii) results in excess FFA and glycerol breakdown from triglycerides
iv) FFA act as a substrate for ketone body synthesis in the liver
- this produces acetoacetate/hydroxybutyrate and acetone
v) the brain and muscle can utilise ketones as energy substrates
vi) KA results when KB production exceeds the rate of utill by brain/muscle and renal clearance
DKA - METABOLIC DERANGEMENT
i) how is the acidosis buffered by the body at a cellular level? (what is exchanged for what) what does the kidney then excrete?
ii) which channel allows this buffering?
iii) how is the acidosis managed at a respiratory level?
iv) how is acidosis managed at a renal level? is this a fast or slow response?
v) what electrolyte disturbances does this result in? (2)
i) K+ is exchanged for H+
- H+ in to be conjugated and K+ out
- high K+ levels in blood therefore kidney excretes K+
ii) potassium hydrogen pump allows this
iii) hyperventilation as H+ stim resp centres
- want to breathe off O2 (fast breathing = tachypnoea)
iv) renal excretion of H+
- slow response
v) results in potassium and sodium depletion as well as dehyration
DKA - PRECIPITATING FACTORS
i) what two things principally ppt DKA
ii) name three infections assoc with DKA
iii) what % of undiagnosed T1DM present with DKA?
iv) name two other precip factors
v) which drug class may ppt DKA?
i) relative or absolutely insulin deficiency
ii) viral illness, pneumonia, UTI
iii) 50%
iv) MI and error/missed insulin admin
v) steroids
DKA - SYMPTOMS AND SIGNS
i) name three symptoms and three signs that hyperglycaemia and dehydration cause
ii) name three symptoms and three signs that acidosis causes
iii) what is a normal pH range?
i) hypergly and dehydration
- symptoms = thirst, polyuria, weakness, malaise, drowsy
- signs = dry mouth, sunken eyes, postural/supine hypertension, hypothermia/coma
ii) acidosis
- symptoms = N&V, abdo pain and breathlessness
- signs = facial flush, hyperventilation and smell of ketones on breath
iii) 7.35-7.45
DKA - CLINICAL FEATURES
i) what age is most common?
ii) what is the principal ppt cause?
iii) what will serum sodium be?
iv) what will blood glucose be?
v) what will serum bicarb be? will there be an acidosis or alkalosis?
vi) what will serum ketones be?
vii) what is the approx % mortality rate and what treatment are patients usually discharged with?
i) mostly young T1DM
ii) absolute or relative insulin deficient
iii) sodium = normal or low
iv) blood glucose will be up but not loads - usually <40mmol
v) bicarb will be <14 (low) = ACIDOTIC (high H+ and low HCO3)
vi) ketones will be high
vii) 5% mortality and patients are often discharged with insulin
CASE HX - DKA
i) name two things a patient may look and one thing they may smell of
ii) what is kussmaul respiration?
iii) what will bicarbonate levels likely be?
iv) which can be looked at in the blood to measure ketones? what should ketone levels be?
v) what may WBC be?
i) look drowsy and flushed
- smelling of ketones (pear drop breath)
ii) kussmaul respiration = hyperventilating to get rid of excess co2
iii) very low bicarb levels
iv) plasma hydroxybutyrate to measure ketones
( should be less than 3)
v) WBC may be raised
DKA - MANAGEMENT
i) what is the first step? (2)
ii) how is fluid balance corrected?
iii) what parameter needs to be lowered? how is this done?
iv) name three electrolytes that need to be monitored
v) what may be given prophylactically to prevent clots?
vi) what may the patient also be at risk of? (vomit to lungs)
what may be given for this?
vii) what three principal things are given to correct DKA
i) confirm diagnosis and check for precipitating causes
ii) correct fluid balance with IV saline + potassium (consider urinary catheter)
iii) lower glucose - using IV insilin at 0.1 unit/kg/hr
iv) monitor potassium, sodium and ketones
v) prophylac LMW heparin to prevent clots (dehydration may cause blood to be thick)
vi) may be at risk of aspiration - if yes consider an NG tube
vii) give insulin, give fluids, give K+
DKA - RECOVERY
i) what levels would expect to be seen for pH, ketones in urine
ii) what diet should be followed
iii) what type of insulin should the patient be on?
i) normal pH and ketones <2
ii) normal diet resumed
iii) switch from IV insilin to normal subcutaneous insulin
HYPEROSMOLAR HYPERGLYCAEMIC STATE (HHS)
i) do you have insulin?
ii) do you get raised ketones? why?
iii) what is the liver doing?
iv) what group of people are most vulnerable to this?
v) what symptom can be very characterstic of HHS? why?
i) you have some insulin but not enough
ii) dont get raised ketones as there is no muscle and fat breakdown
iii) liver is still producing lots of glucose
iv) elderly are most vulnerable
v) get dehydration - because blood glucose is very high (wee out glucose and drag water with it)
HHS - CLINICAL FEATURES
i) what is the most common age range?
ii) name the common precipitating causes
iii) what will serum sodium usually be? why?
iv) what will blood glucose be?
v) what will serum bicarb be? is the patient acidotic?
vi) what will serum ketones be?
vii) what is approx % mortality? what is the main cause?
viii) is there an absolute insulin deficiency?
ix) what is the subsequent course of action? (2)
i) >40yrs
ii) steroids, diuretics, sugar
iii) high serum sodium as dehydrated
iv) high blood glucose >40mmol/l
v) bicarb and pH will be normal (not acidotic)
vi) ketones will be 0 (dont breakdown muscle or fat)
vii) 30% mortality due to thromboses
viii) no absolute insulin deficiency
ix) diet and tablet controlled
HHS - CASE HISTORY
i) name three common symptoms a patient may present with
ii) how may the patient look? (2)
iii) what will blood glucose be?
iv) will the patient be acidotic?
v) what will osmolality be? (high or low)
i) polyuria, polydipsia, tiredness
ii) may look drowsy and pale
iii) high blood glucose
iv) patient wont be acidotic
v) very high osmolality (usually maintained in tight control 280-300)
HHS - MANAGEMENT
i) what is the first thing that needs to be addressed? how is this done?
ii) how is glucose lowered?
iii) which two main electrolytes need to be monitored?
iv) what should be given to prevent clotting?
i) the dehydration
- rehydrate the patient using saline and potassium IV
ii) glucose is lowered by IV insulin
iii) sodium and potassium
iv) LMW heparin
HYPOGLYCAEMIA
i) what blood sugar level classes as hypo?
ii) when does the clinical syndrome associated with hypogly start to develop?
iii) how may a patient present when they are
a) asymptomatic b) mild symptomatic, c) severe symptomatic
iv) what is the most serious classification of patient presentation
i) <4mmol/l
ii) when the nervous system begins to get glucose deficient
iii) a) asymp = awake or sleeping
b) mild asymp = pt can treat themselves
c) severe symp = third party help needed (can lose driving lic)
iv) most serious = coma and convulsions
