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ACC > Endocrine Core Conditions > Flashcards

Endocrine Core Conditions Flashcards

1
Q

What is diabetic ketoacidosis?

A

Acute metabolic complication of diabetes (type 1) which is potentially fatal

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2
Q

How is DKA characterised?

A

Absolute insulin deficiency (hyperglycaemia)
Ketonuria
Acidosis

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3
Q

What is DKA the most common complication of?

A

Acute hyperglycaemic complication of diabetes

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4
Q

What are the causes of DKA?

A

Inadequate insulin therapy
Infection (release of epinephrine which releases glucagon- inc blood glucose levels & need for alternative energy-ketones)
MI/stroke
Drugs: Steroids, 2nd gen antipsychotics, thiazides

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5
Q

What are the signs & symptoms of DKA?

A 
Polyuria
Polyphagia
Polydipsia
N&V
Weakness
Weight loss
Kussmaul breathing
Acetone (pear drop breath)
Sunken eyes
Altered consciousness/ mental status
Acute cerebral oedema
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6
Q

What is the pathophysiology of DKA?

A

1) Reduction in net circulating insulin
2) Causes elevation of counter hormones (Glucagon, cortisol, growth hormone)
3) Lead to inc gluconeogenesis, hepatic & renal glucose production & impaired glucose utilisation in peripheral tissues
4) Hyperglycaemia & hyperosmolarity
5) Insulin deficiency leads to release of FFA from adipose tissue, hepatic fatty acid oxidation, formation of ketone bodies
6) Ketonaemia & acidosis

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7
Q

How are ketone bodies formed?

A

Lipolysis (fat broken down into free fatty acids)
FFA sent to the liver where they are turned into ketone bodies
-Acetoacetic acid
- Beta hydroxybutyric acid

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8
Q

What are the pro’s and con’s of ketones?

A

Pro’s: Can be used for the body for energy
Con’s: Make the blood more acidic (Kussmaul respiration), more K+ in the blood (hyperK) but reduced stores, high anion gap

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9
Q

What is the mechanism of Kussmaul breathing?

A

Deep laboured breathing

Body tries to reduce CO2 intake and therefore the acidity of the blood

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10
Q

What is the treatment of acute DKA?

A 
IV fluids: Isotonic saline (0.9% NaCl)
When p.glucose 11.1 change to 5% dextrose w/0.45% NaCl
Consider ICU
IV insulin (FRIII)
IV Potassium Phosphate when K+ <3.5
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11
Q

In DKA what are the indications for ICU admission?

A 
Haemodynamically unstable (AKI)
Cariogenic shock (HF)
Altered mental status
Pregnant
Oliguria/anuria
Sats <92% room air/ <90s after 2L fluid
Respiratory insufficiency
HCO3 <10
Severe acidosis <7.1
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12
Q

How is acute DKA differentiated from mild/moderate DKA?

A

Absence of:
Orthostatic/supine hypoT
Dry mucous membranes
Poor skin turgor

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13
Q

How is mild/moderate DKA treated?

A

IV fluids: Isotonic saline >1hour add potassium phosphate if levels <3.5
Insulin when K+ >3.5

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14
Q

How is DKA investigated?

A

3 features for diagnosis:

  • Plasma glucose: >11mmol OR known DM1
  • ABG: pH <7.3, bicarb <10s >15m
  • Urinalysis: Glucose & Ketones ++ OR blood ketones >3

Other: Bloods: U&E, lactate, anion gap, electrolytes

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15
Q

What is severe DKA characterised by?

A 
Blood ketones >6
Bicarb <5
pH <7
HypoK <3.5
GCS <12
O2 <92% on room air
sBP <90
HR >100, <60
Anion gap >16
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16
Q

What definition is given when DKA is resolved?

A

Blood ketones <0.6mmol/L

Venous pH >7.3

17
Q

How often should obs be done on a patient with DKA?

A

Sugars, Potassium, Bicarb every 2 hours for first 6 hours

18
Q

Define HHS

A

Hyperglycaemic hyperosmolar state

Inc plasma osmolarity due to extreme dehydration and increase blood concentration

19
Q

What is HHS a complication of?

A

Diabetes type 2

20
Q

What are the causes of HHS?

A 
Infection
CVA/MI
Trauma
Non-compliance to medication
Drugs (Thiazides, steroids, beta blockers)
21
Q

What are the signs & symptoms of HHS?

A 
Altered mental state
Polyuria &amp; polydipsia
Weight loss
Poor skin turgor (dehydration)
Dry mucous membranes
Mental status alterations
22
Q

What is the pathophysiology of HHS?

A

1) Glucose is a polar molecule so cannot passively diffuse across cell membranes
2) Glucose acts as a solute
3) High levels of glucose in the blood (hyperosmolar state)
4) Water diffuses from cells into blood vessels
5) Leads to total body dehydration

23
Q

What characteristics differentiate HHS from other diabetic complications?

A

Hypovolaemia
Hyperglycaemia >30mmol/L
Osmolality >320
NO acidosis/ketones

24
Q

How is HHS treated?

A

Fluids: IV 0.9% NaCl
vasopressors: 0.5-3micro IV NorA
Potassium
Insulin

25
Q

How is hyponatraemia defined?

A

Serum conc <135mmol/L

Most common electrolyte disorder

26
Q

What are the causes of hypoN?

A

HypoV: Vol depletion, third spacing
Euvolaemic: SIADH, hypothyroid, adrenal insufficiency, meds
HyperV: Effective decreased arterial vol (cHF, cirrhosis, nephrotic syndrome), Vol overload

27
Q

What are the signs & symptoms of hyponatraemia?

A 
Headache
Confusion
Balance difficulties
Acute cerebral (coma, vomiting, altered mental state, seizures)
Pulmonary oedema
Low urine output
Orthostatic hypotension
Abnormal JVP
28
Q

How is hyponatraemia managed?

A 
Acute:
Hypertonic 3% saline infusion
Treat underlying
HypoV: Isotonic IV 0.9% saline
HyperV: Fluid restriction 1L/day, adjunct: Furosemide
29
Q

What is Na homeostasis controlled by?

A 
ADH from posterior pituitary
Kidneys
Aldosterone
Vasopressin
Thirst
30
Q

What is the pathophysiology of Na retention/excretion?

A

1) Drink water
2) Blood diluted= dec plasma osmolality
3) Hypothalamus signals pituitary to dec ADH secretion
4) Fewer aquaporins opened in distal convoluted tubule
5) Dilute urine & Na excreted

31
Q

What is the pathophysiology of SIADH & hypoNatraemia?

A

1) Body continues to excrete ADH when dec plasma osmolality
2) Dilute blood = dilute Na
3) Causing dec aldosterone production
4) More Na excreted by the kidneys
5) Water follows Na excretion by diffusion
6) Normalises fluid vol but dec Na vol

32
Q

Define hyperkalaemia

A

Serum conc >6.0mmol/L

33
Q

What are the causes of hyperkalaemia?

A 
High K+ intake
Dec k+ excretion
Renal failure
Drugs: ACEi, Spironolactone, amiloride, beta blockers
Inc cell turnover/lysis
Infection
Severe burns, rhabdomyolysis
Insulin deficiency
Metabolic acidosis
34
Q

What are the signs & symptoms of hyperkalaemia?

A

Asymptomatic
Muscle weakness or flaccid paralysis
Life-threatening arrhythmia (VT)

35
Q

What changes can be seen on an ECG due to hyperkalaemia?

A 
Prolonged PR interval
Tall tented T waves
Loss of P waves
Widened QRS complexes
Sine waves
Arrhythmias: VF, VT, PEA
Bradycardia
36
Q

What is the management of hyperkalaemia?

A 
10mls Ca gluconate 10% IV over 3mins
5-10u of Actrapid in 50mls 20% Dextrose
Nebulised Salbutamol 5mg
IV Na2CO3
IV Furosemide
Dialysis
37
Q

Causes of hypoglycaemia in non-diabetics?

A

EXPLAINS H:
Endogenous: Drugs, beta blocker/valproate/salicylate OD, OH-
Pituitary insufficiency
Liver disease
Addison’s disease
Islet cell tumours, immune, infection (sepsis, malaria)
Non pancreatic neoplasm: Fibroma, sarcoma, mesothelioma
Starvation & malnutrition
Hypothyroidism

38
Q

What are the causes of hypercalcaemia?

A

Malignancy
Drugs
Hyperparathyroidism
Sarcoidosis

39
Q

What are the ECG signs of hypercalcaemia?

A

Short QT
Prolonged QRS
Flat T waves

ACC (21 decks)

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