DKA features [7]
Polyuria, polydipsia
Abdominal pain/ vomiting/ nausea
Hyperventilation/ Kusmal breathing
Tachycardia, hypotensive
Reducing GCS
Succussion/ gastric splash
Ketone breath
Features of severe DKA
GCS < 12
pH <7.2
O2 < 90%
Ketones > 7 ?
Investigations in DKA
Bloods
- U+Es: hypokalaemia,
- Glucose, HBA1c
- FBC= infection
- VBG
- CRP, culture
Ketones
ECG
Urine dip/ urinalysis
Imaging
- CXR if infective signs
Initial management of DKA
Analgesia for pain
IV fluid resus
- Saline 0.9% 1L over 1 hours
- K+ if hypokalaemic
Fixed-rated insulin
- 0.1mg/ Kg
- Until glucose reaches 14 mmol/L
- Stop short acting insulin, continue long-acting
Oxygen if hypoxic
Further management of DKA
When glucose reaches 14mmol/L
- Start dextrose 10%
- Give insulin 30mins after first feed
Give K+
- Monitor at least 4 hourly
Transition to variable rate insulin
- When significant clinical improvement
- Stop dextrose and saline
- Overlap with Long actin insulin
- Stop IV insulin after 2nd meal
Precipitating factors for DKA [5]
Poor glycaemia control
Acute infection
- UTI
- Pnuemonia/ respiratory tract
Surgery
Stress
Trauma
Life-threatening complications of DKA [3]
Cerebral oedema
Hypokalaemia
Aspiration pnemonia
Addison’s disease
- Presentation
Low cortisol features
- Hypotension
- Weight loss
- Fatigue
Low mineralocorticoid features
- Polydipsia, polyuria
- Postural hypotension
Hyperpigmented skin
Initial Investigations for addison’s disease
Standing and sitting BP
BMI
Bloods
- U+Es= low na, raised K+
- Glucose= low
9am salivary cortisol
- Low
Special investigations for addison’s disease
SynACTHen test
- Low cortisol production
Abdominal ultrasound
- rule out CAH
Risk factors for addison’s disease
Family Hx
Autoimmune endocrinological disease
- T1 DM
- Thyroid disease
Post infective
- TB
- HIV
- Disseminated fungal infection
Addisonian crisis
- Features
Acute, abdominal pain
- Vomiting/ nausea
Lethargy
Altering consciousness
Examination and investigative findings for addisonian crisis
Hypotension
Hyponatraemia, hypoglycaemia
Hyperkalaemia
Management of addisonian crisis
Analgesia for pain
A-E
- IV fluid saline resuscitation
IV hydrocortisone
- > 6= 100mg
- > 1= 50mg
- <1= 25mg
IV hydrocortisone in 5% glucose over 24 hours by IV infusion.
What enzyme is the most common deficient in congenital adrenal hyperplasia?
21-hydroxylase
- Converts progesterone into aldosterone + cortisol
- In CAH backlog of progesterone is pushed down the testosterone synthesis pathway.
Less common
- 11-beta hydroxylase
Presentation of CAH
Precocious puberty
Salt wasting
- low weight/ failure to thrive
- fatigue
- Hyponatraemia, hypokalaemia
Hypoglycaemia
Severe
- Virilisation of genitals in females (clitomegaly)
- Amenorrhea (females)
- Deep voice
Complications of gigantism [5]
Hyperhidrosis
Recurrent headaches
Cardiomyopathy
Hypopituitarism
Thyroid cancer
_______ inhibits the release of growth hormone
Somatostatin
GH acts on the liver to release ______
IGF-1
What genetic conditions are associated with gigantism?
Multiple endocrinological neoplasia type 1
Neurofibromatosis
McCune Albright syndrome
Features of gigantism
Intracranial
- Headache
- Visual disturbance
MSK
- Tall stature/ high velocity growth
- Carpal tunnel
- enlarged hands, feet
Skin
- Thicker, oily
- Skin tags
- Hyperhidrosis
Development
- Delayed puberty
Metabolic
- Hyperglycaemia
- Hypertension
Diagnostic tests for gigantism
Plasma IGF-1
Oral glucose tolerance test
- 75g glucose does not lower GH levels <1mcg/L
Imaging
- Pituitary MRI
Management of gigantism
Somatostatin analogues= octreotide IM
- Reduce GH production
- Started before surgery
2nd line
- Carbogoline (dopamine agonist)
Surgery
- Transphenoidal hypophysectomy
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Acute respiratory illness33
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Miscellaneous53
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Gastroenterology30
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Development and developmental disorders63
-
Neurology and cardiology29
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Oncology1
-
Acute and chronic respiratory illness20
-
Surgery17
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Infection66
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Neonatal/ prematurity36
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Emergency conditions6
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Endocrine23
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ENT31
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Cardiology40
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MSK and rheum18
