Endocrine Core Conditions

Question 1

What is diabetic ketoacidosis?

Answer 1

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

Question 2

How is DKA characterised?

Answer 2

Absolute insulin deficiency (hyperglycaemia)
Ketonuria
Acidosis

Question 3

What is DKA the most common complication of?

Answer 3

Acute hyperglycaemic complication of diabetes

Question 4

What are the causes of DKA?

Answer 4

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

Question 5

What are the signs & symptoms of DKA?

Answer 5

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

Question 6

What is the pathophysiology of DKA?

Answer 6

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

Question 7

How are ketone bodies formed?

Answer 7

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

Question 8

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

Answer 8

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

Question 9

What is the mechanism of Kussmaul breathing?

Answer 9

Deep laboured breathing

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

Question 10

What is the treatment of acute DKA?

Answer 10

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

Question 11

In DKA what are the indications for ICU admission?

Answer 11

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

Question 12

How is acute DKA differentiated from mild/moderate DKA?

Answer 12

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

Question 13

How is mild/moderate DKA treated?

Answer 13

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

Question 14

How is DKA investigated?

Answer 14

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

Question 15

What is severe DKA characterised by?

Answer 15

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

Question 16

What definition is given when DKA is resolved?

Answer 16

Blood ketones <0.6mmol/L

Venous pH >7.3

Question 17

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

Answer 17

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

Question 18

Define HHS

Answer 18

Hyperglycaemic hyperosmolar state

Inc plasma osmolarity due to extreme dehydration and increase blood concentration

Question 19

What is HHS a complication of?

Answer 19

Diabetes type 2

Question 20

What are the causes of HHS?

Answer 20

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

Question 21

What are the signs & symptoms of HHS?

Answer 21

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

Question 22

What is the pathophysiology of HHS?

Answer 22

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

Question 23

What characteristics differentiate HHS from other diabetic complications?

Answer 23

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

Question 24

How is HHS treated?

Answer 24

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

Question 25

How is hyponatraemia defined?

Answer 25

Serum conc <135mmol/L | Most common electrolyte disorder

Question 26

What are the causes of hypoN?

Answer 26

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

Question 27

What are the signs & symptoms of hyponatraemia?

Answer 27

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

Question 28

How is hyponatraemia managed?

Answer 28

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

Question 29

What is Na homeostasis controlled by?

Answer 29

``` ADH from posterior pituitary Kidneys Aldosterone Vasopressin Thirst ```

Question 30

What is the pathophysiology of Na retention/excretion?

Answer 30

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

Question 31

What is the pathophysiology of SIADH & hypoNatraemia?

Answer 31

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

Question 32

Define hyperkalaemia

Answer 32

Serum conc >6.0mmol/L

Question 33

What are the causes of hyperkalaemia?

Answer 33

``` 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 ```

Question 34

What are the signs & symptoms of hyperkalaemia?

Answer 34

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

Question 35

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

Answer 35

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

Question 36

What is the management of hyperkalaemia?

Answer 36

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

Question 37

Causes of hypoglycaemia in non-diabetics?

Answer 37

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

Question 38

What are the causes of hypercalcaemia?

Answer 38

Malignancy Drugs Hyperparathyroidism Sarcoidosis

Question 39

What are the ECG signs of hypercalcaemia?

Answer 39

Short QT Prolonged QRS Flat T waves