Endo - DKA, Addison's Disease, Primary and Secondary Hyperaldosteronism Flashcards
DKA - what is it?
It is when excess glucose cannot be removed due to lack of insulin, therefore glucose is not taken up by cells to be metabolised
Instead uncontrolled lipolysis occurs, which results in free fatty acids, that are then converted to ketone bodies
This then leads to severe acidosis and hyperglycaemia
DKA - which diabetes does it occur mainly in?
Mainly Type 1 DM
DKA - what are the most common precipitating triggers?
- Missed insulin dose
- Infection
- Surgery
- M.I.
- Pancreatitis
DKA - what is the clinical presentation?
- Abdo pain
- Polyuria, polydipsia
- Pear drop smell on breath
- Gradual drowsiness, vomiting and dehydration
- Kussmaul respiration - deep and laboured breathing pattern
DKA - what are the blood components you test for and what result is indicative of DKA?
- Glucose >11mmol/L or known DM
- pH <7.3
- Bicarbonate <15mmol/L
- Ketones >3mmol/L or ketones + + on dipstick
DKA - what is the management?
FIGPICK
Fluids - 1L isotonic saline in 1st hour, then add K+ every 2 to 4h after
IV Insulin - 0.1unit/kg/hr infusion
Glucose - start when at least <14mmol/L alongside saline to avoid hypos
Potassium replacement - never infuse >10mmol hour
Infection
Chart fluid balance
Ketones - monitor
DKA - when is DKA defined as being resolved?
When:
pH >7.3
blood ketones < 0.6 mmol/L
bicarbonate > 15.0mmol/L
DKA - what are the complications due to incorrect fluid therapy
Iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
Cerebral oedema - especially in kids and young adults
DKA - what are some complications?
ARDS
AKI
Thromboembolism
Addison’s Disease - what is it?
Also called PRIMARY ADRENAL INSUFFICIENCY
Autoimmune destruction of the adrenal cortex, causing less aldosterone and cortisol to be produced
Leads to primary hypoadrenalism
Addison’s Disease - what are the causes?
Autoimmune (80%)
TB - most common cause worldwide
Adrenal metastases
HIV
Addison’s Disease - what are the symptoms?
Bronze skin
G.I. - Abdo pain, constipation
MSK - weakness, myalgias
NEURO - dizzy, syncope
PSYCH - tearful, anorexia
Addison’s Disease - what are the signs?
Pigmented buccal mucosa
Vitiligo
Postural hypotension
Shock
Addison’s Disease - what are the investigations?
Definite investigation:
- ACTH stimulation test. Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM
- AD excluded if 30
If ^^^ not readily available - 9am serum cortisol test
Addison’s Disease - what are the electrolyte imbalances seen?
HYPOGLYCAEMIA - due to low cortisol, because cortisol is responsible for breaking down glycogen into glucose
HYPONATRAEMIA
HYPERKALAEMIA
Addison’s Disease - what is the management?
Given combination of:
Used to replace cortisol
1. HYDROCORTISONE - 20-30mg daily
Used to replace aldosterone
2. FLUDROCORTISONE - to correct postural hypotension
Secondary adrenal insufficiency - what is it and what are the causes
Secondary adrenal insufficiency caused by inadequate ACTH stimulating the adrenal glands, results in decreased cortisol being released.
Usually result of loss or damage to the pituitary gland.
Due to congenital underdevelopment (hypoplasia) of the pituitary gland, surgery, infection, loss of blood flow or radiotherapy.
Primary Hyperaldosteronism (Conn’s syndrome) - what is it?
Primary Hyperaldosteronism is when too much aldosterone is produced, independent of the RAAS system
Primary Hyperaldosteronism (Conn’s syndrome) - what is the levels of Renin like?
Serum renin is low as it is suppressed by high BP
Primary Hyperaldosteronism (Conn’s syndrome) - what are the causes?
Adrenal adenoma - called Conn’s syndrome when this is the cause
Bilateral adrenal hyperplasia
Adrenal carcinoma - rare
Genetics - Familial hyperaldosteronism
Primary Hyperaldosteronism (Conn’s syndrome) - symptoms and signs?
Often asymptomatic
Signs of hypokalaemia - weakness, cramps, polyuria
High BP
Primary Hyperaldosteronism (Conn’s syndrome) - what investigations can you do?
Check renin and aldosterone levels and do a renin/aldosterone ratio
1. HIGH aldosterone and LOW renin - PRIMARY Hyperaldosteronism
- HIGH aldosterone and HIGH renin - SECONDARY Hyperaldosteronism
Check K+ for hypokalemia
Blood gas analysis - alkalosis
Look for cause like adenoma so CT, MRI, renal doppler US
Primary Hyperaldosteronism (Conn’s syndrome) - what is the management?
Hyperplasia - Aldosterone Antagonists, Spironolactone or Eplerenone
Conn’s - Spironolactone pre-op
Laparoscopic adrenalectomy
Adrenal carcinoma - surgery
Primary Hyperaldosteronism (Conn’s syndrome) - what is Secondary Hyperaldosteronism?
It is where excessive renin stimulates excessive aldosterone production
Primary Hyperaldosteronism (Conn’s syndrome) - Secondary Hyperaldosteronism causes?
Occurs due to kidney BP being lower than rest of body BP, so the juxtaglomerular cells detect low BP, therefore producing more renin, so causes of this include:
- Renal artery stenosis
- Renal artery obstruction
- Heart Failure
Primary Hyperaldosteronism (Conn’s syndrome) - Secondary Hyperaldosteronism investigations?
CT angiogram
Doppler US
Magnetic resonance angiography (MRA)
Primary Hyperaldosteronism (Conn’s syndrome) - Secondary Hyperaldosteronism treatment?
Need to treat underlying cause
Renal artery stenosis - Percutaneous renal artery angioplasty via the femoral artery