Endocrinology and Electrolye Disturbances Flashcards
(105 cards)
1
Q
What is the pathophysiology behind Addisons (primary adrenal insufficiency)?
A
Destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency
2
Q
What are some of the causes of Addisons ?
A
- Autoimmunity
- Adrenal metastases (eg from lung, breast, renal cancer)
- Lymphoma
- HIV
3
Q
What are the causes of secondary adrenal insufficiency?
A
- Iatrogenic - long-term steroid therapy -> suppression of the pituitary–adrenal axis
4
Q
What are some of the signs and symptoms of adrenal insufficiency?
A
- Lean, tanned, tired, tearful ± weakness, anorexia, dizzy, faints, flu-like myalgias/arthralgias.
- Mood: depression, psychosis.
- GI: nausea/vomiting, abdo pain, diarrhoea/constipation, salt craving
- Pigmented palmar creases & buccal mucosa
- Postural hypotension
5
Q
What tests/ investigations should be performed for suspected Addisons crisis?
A
- Morning serum cortisol
- Short acth stimulation test (Synacthen® test)
- Plasma cortisol
- Serum ACTH
- ↓Na+ & ↑K+ (due to ↓mineralocorticoid)
- ↓glucose (due to ↓cortisol).
- uraemia, ↑Ca2+, eosinophilia, anaemia.
- Plasma renin/ aldosterone
- CT/MRI
6
Q
What electrolye changes do you expect to see in Addisons?
A
- ↓Na+ & ↑K+ ↓glucose (due to ↓cortisol)
- ↑ ACTH
7
Q
How do you treat Addisons?
A
- Hydrocortisone: Replace steroids: ~15–25mg daily, 2–3 doses
- Fludrocortisone↓Na+, ↑K+: po from 50–200mcg daily
- Do not abruptly stop steroid use!
8
Q
How is addisonian crisis managed?
A
- Bloods: cortisol, ACTH, UE (but treat more urgently than needed)
- Hydrocortisone 100mg IV STAT
- IV fluid bolus for hypotension
- Monitor blood glucose (be aware of hypoglycaemia)
- Continuing treatment
- Glucose IV if hypoglycaemic
- IV fluids
- Hydrocortisone, 100mg/8h IM or IV - change to oral steroids after 72h
- Fludrocortisone - if adrenal disease
9
Q
What are some of the causes of Cushings syndrome?
A
ACTH dependent causes
- Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
- Ectopic ACTH production (5-10%): e.g. SCLC
ACTH independent causes
- iatrogenic: steroids
- adrenal adenoma (5-10%)
- adrenal carcinoma (rare)
- Carney complex: syndrome including cardiac myxoma
- micronodular adrenal dysplasia (very rare)
- Pseudo-Cushing’s
- mimics Cushing’s
- often due to alcohol excess or severe depression
- causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
- insulin stress test may be used to differentiate
10
Q
What are some of the sx of cushings syndrome?
A
Round in the middle with thin limbs:
- Round “moon” face
- Central Obesity
- Abdominal striae
- Buffalo Hump (fat pad on upper back)
- Proximal limb muscle wasting
High levels of stress hormone:
- Hypertension
- Cardiac hypertrophy
- Hyperglycaemia (Type 2 Diabetes)
- Depression
- Insomnia
Extra effects:
- Osteoporosis
- Easy bruising and poor skin healing
11
Q
What are some of the investigations that will be used for Cushings?
A
Overnight dexamethasone suppression test: patients with Cushing’s syndrome do not have their morning cortisol spike suppressed
24 hr urinary free cortisol
Insulin stress test is used to differentiate between true Cushing’s and pseudo-Cushing’
Other:
- FBC (raised white cells) and electrolytes (potassium may be low if aldosterone is also secreted by an adrenal adenoma)
- MRI brain for pituitary adenoma
- Chest CT for small cell lung cancer
- Abdominal CT for adrenal tumours
12
Q
How is Cushings Syndrome mxd?
A
The main treatment is to remove the underlying cause (surgically remove the tumour)
- Cushings disease - Trans-sphenoidal (through the nose) removal of pituitary adenoma
- Surgical removal of adrenal tumour
- Surgical removal of tumour producing ectopic ACTH
Adrenal tumour - laparoscopic adrenalectomy
Medical Mx: metyrapone + ketoconazole
13
Q
Describe the thyroid HPPA
A
14
Q
What basic thyroid function tests are requested for hypo and hyperthyroidism?
A
- Hyperthyroidism: Ask for T3, t4, and TSH. All will have ↓TSH (except the rare tsh-secreting pituitary adenoma). Most have ↑T4, but ~1% have only raised T3.
- Hypothyroidism suspected or monitoring replacement ℞ T4 and TSH. T3 not very useful. TSH varies through the day (monitor at same time)
- Other
- Thyroid autoantibodies: Anti-TPO: may be increased in autoimmune thyroid disease (Hashimotos or Graves)
- TSH receptor antibody: GRAVE
- USS: for goitre (use FNA to look for cancer)
- Isotope scan: cause of hyperthyroidism
15
Q
What are some of the sx of thyrotoxicosos/ hyperthyroidism?
A
Thyroidism
- Tremor
- Heat intolerance/ high HR
- Yawning
- Restlessness
- Oligomennorhoea
- Intolerance to heat
- Diarrhoea
- Irritability/ insomnia
- Sweating
- Muscle wasting
Also: weight loss but increased appetite. Alopecia and urticaria
16
Q
What are the signs of hyperthyroidism?
A
- Pulse fast/irregular HR (AF or sinus rhythm)
- HT and flow murmur
- warm moist skin
- fine tremor
- Hyperreflexia
- palmar erythema
- thin hair
- lid lag
- lid retraction (exposure of sclera above iris; causing ‘stare’,
- There may be goitre: thyroid nodules; or bruit depending on the cause
17
Q
What are the signs unique to Graves’ disease?
A
- Eye disease: exophthalmos, ophthalmoplegia.
- Pretibial myxoedema: oedematous swellings above lateral malleoli: the term myxoedema is confusing here.
- Skin changes: dermopathy
- Thyroid acropachy: extreme manifestation, with clubbing, painful finger and toe swelling, and periosteal reaction in limb bones.
18
Q
What tests are used for hyperthyroidism?
A
- ↓TSH (suppressed), ↑: t4, and t3
- There may be mild normocytic anaemia, mild neutropenia (in Graves’)
- ↑esr, ↑Ca2+, ↑lft.’
- Subclinical
19
Q
What is Graves and how does it occur?
A
- Patients are often hyperthyroid but may be, or become, hypo- or euthyroid.
- Cause: circulating igg autoantibodies binding to and activating g-protein-coupled thyrotropin receptors, which cause smooth thyroid enlargement and ↑hormone production
20
Q
What are the primary and secondary causes of hyperthyroidism?
A
-
Primary:
- Graves’ disease (younger women)
- Toxic multinodular goitre (older women)
- Solitary toxic adenoma
- Subacute thyroiditis
- Iodine overload
-
Exogenous:
- TSH secreting pituitary tumour
- Others:
- Subacute de Quervain’s thyroiditis
- Drugs: amiodarone, lithium (hypothyroidism more common)
- Postpartum
- TB (rare)
21
Q
How is hyperthyroidism diagnosed?
A
- Have a low threshold for doing tfts!
- ↑TSH ↓T4
- In rare secondary hypothyroidism: ↓t4 and ↓tsh or ↔ due to lack from the pituitary
22
Q
How is hyperthyroidism treated?
A
Drugs:
- Sx control: β-blockers (eg propranolol 40mg/6h) for sx control
- Anti thyroid meds:
- Titration: carbimazole 20–40mg/24h po for 4wks, reduce according to TFTS every 1–2 months
-
Block-replace: Carbimazole + levothyroxine simultaneously. Use for Graves.
- Carbimazole SE: agranulocytosis (↓↓-neutrophils -> dangerous sepsis): sore throat/mouth ulcers. Must stop and get an urgent FBC if signs of infection
-
Radioiodine (131I): ci: pregnancy, lactation, active hyperthyroidism - risk of thyroid storm.
- Requires lifelong thyroxine replacement
- Thyroidectomy: Risk of damage to recurrent laryngeal nerve (hoarse voice) and hypoparathyroidism (hypocalaemia)
23
Q
What is thyroiditis?
A
- Inflammation of the thyroid gland either caused by viral infection, medication (amiodorone) and following childbirth
- Hypothyroid phase follows the initial toxic hyperthyroid phase
24
Q
What are the complications of hyperthyroidism?
A
- CVS: HF, Angina, AF
- Osteoporosis
- Ophthalmopathy
- Gynaecomastia.
25
What are the signs of hypothyroidism?
Tiredness; sleepy, lethargic; ↓mood; cold-disliking; ↑weight; constipation; menorrhagia; hoarse voice; ↓memory/cognition; dementia; myalgia; cramps; weakness.
26
What are the signs of hypothyroidism?
* **bradycardic**
* **r**eflexes relax slowly
* **a**taxia (cerebellar)
* **d**ry thin hair/skin
* **y**awning/drowsy/coma
* **c**old hands
* **a**scites ± non-pitting oedema (lids; hands; feet) ± peri-cardial or pleural effusion
* **r**ound puffy face/double chin/obese
* **d**efeated demeanour
* *i*mmobile ± ileus; ccf
* Also: neuropathy; myopathy; goitre
27
What are some of the causes of hypothyroidism? What are some that are seen in kids?
* **Causes of primary autoimmune hypothyroidism:**
* Primary atrophic hypothyroidism,
* Autoimmune: Hashimotos
* Iatrogenic: Post-thyroidectomy + radioiodine treatment
* Pregnancy
* Drugs: Antithyroid drugs, amiodarone, lithium, iodine.
* **Children**:
* **Neonatal hypothyroidism** caused by **iodine deficiency** -\> cretinism + mental retardation
* **Familial thyroid dyshormogenesis**
* **Secondary**: Not enough tsh v. rare
28
How is hypothyroidism managed?
* **Healthy and young:**
* **Levothyroxine** (t4), ***50–100ug/24h*** po; review at 12wks. Adjust 6-weekly by clinical state and to normalize but not suppress TSH (keep tsh \>0.5mu/L). Wait ~4wks before checking TSH to see if a dose change is right.
* *If T4 raised, but TSH still high: poor complicance*
* *If T4 raised but TSH too low: over replacment*
* Elderly or ischaemic heart disease:
* **Levothyroxine:** ***25ug/24h***; ↑dose by 25mcg/4wks according to TSH
* **Discontinue amiodorone:** Thyroidectomy may be needed if amiodarone cannot be discontinued
* if managing 2ndary hypo: T4 should be replaced to upper part of normal limit
* If pt remains symptomatic despite normal thyroid function investigate other pathology
29
What is subclinical hypothyroidism?
Normal T4 but elevated TSH
Think of it as assymptomatic hypothyroidism
30
How do you manage subclinical hypothyroidism?
* **Assymptomatic** - treatment may not be needed - thyroid function can revert back to normal - repeat testing
* Treat if:
1. **If TSH \> 10U/L** - start thyroxine even if assymptomatic - high likelihood of progressing to frank hypothyroidism
2. **If pregnant: TSH 5-10miU/L** - start thyroxine
3. **If +ve for thyroid antibodies** - annual thyroid function test
31
What thyroid results would be expected for different hyper/ hypo conditions, thyroiditis etc?
Subclinical hyperthyroidism - Suppressed TSH/ normal T3 + T4
32
How does PTH hormone work?
* ↑osteoclast activity releasing Ca2+ and PO43− from bones
* ↑Ca2+ and ↓PO43− reabsorption in the kidney
* active 1,25dihydroxy-vitamin d3 production is ↑. Overall effect is ↑Ca2+ and ↓PO43−.
33
How do you get hyperparathyroidism?
* Primary: solitary adenoma, hyperplasia of all glands, parathyroid cancer.
* Secondary: ↓Ca2+, ↑pth (appropriately)
34
What are the signs of **hypercalcaemia**?
*‘Bones, stones, groans, and psychic moans.’*
* Abdominal pain
* Vomiting
* Constipation
* Polyuria; polydipsia
* Depression
* Anorexia
* Weight loss
* Tiredness
* Weakness
* Hypertension
* Confusion
* Pyrexia
* Renal stones; renal failure
35
What ECG changes are seen of hypercalcaemia?
↓qt interval.
36
What are the causes of hypercalcaemia?
* Most common: **malignancy** (eg from bone metastases: breast, kidney, lung, thyroid, prostate, ovary, colon, myeloma, **PTHrP**)
* **Primary hyperparathyroidism.**
* **Others**: sarcoidosis, vit D intoxication, thyrotoxicosis, lithium, tertiary hyperparathyroidism, milk-alkali syndrome, and familial benign hypocalciuric hypercalcaemia
37
Which cancers secrete PTHrP?
* Breast carcinoma
* Renal cell cancer
* Small cell lung cancer
38
What investigations are used for hypercalcaemia and what do we expect them to show?
* The main distinction is malignancy vs 1° hyperparathyroidism.
* **Malignancy**: ↓albumin, ↓Cl−, alkalosis, ↓K+, ↑PO43−, ↑alp.
* **Hyperparathyroidism**: ↑PTH
* Other investigations: FBC, protein electrophoresis, cxr, isotope bone scan, 24h urinary Ca2+ excretion (for familial hypocalciuric hypercalcaemia).
39
How is hypercalcemia treated acutely?
1. Dehydrated? Give iv **0.9% saline**
2. **Bisphosphonates**: These prevent bone resorption by inhibiting osteoclast activity.
1. **Pamidronate: single dose**. Infuse slowly, eg 30mg in 300mL 0.9% saline over 3h via a largish vein. Max dose 90mg
2. **Zoledronic acid:** more effective in reducing serum Ca2+. Single dose 4mg iv (diluted to 100mL, over 15min) across 1 wk.
3. **Demusomab**
3. **Chemotherapy:** malignancy.
4. **Steroids:** sarcoidosis, eg **prednisolone** 40–60mg/d.
5. **Salmon calcitonin:** now rarely used.
40
How is hypercalcemia treated more long term?
* **Cinacalcet** - increased sensitivity of PT cells to calcium -\> reducing PTH secretion and reversing hyperparathyroidism + hypercalcaemia secondary to that
* **Calcitonin**
* **Desunomab** - calcium lowering therapy with reabsorptive agents
* Avoid medications that worsen hypercalcaemia : e.g., *thiazide diuretics, calcitriol [(1,25-dihydroxyvitamin D)], calcium supplementation, antacids, lithium*
41
What are the sx and signs of hypocalcaemia?
*SPASMODIC*
* Spasms (carpopedal spasms = Trousseau’s sign)
* Perioral paraesthesiae
* Anxious, irritable, irrational
* Seizures
* Muscle tone ↑ in smooth muscle—hence colic, wheeze, and dysphagia
* Orientation impaired (time, place, and person) and confusion
* Dermatitis (eg atopic/exfoliative)
* Impetigo herpetiformis (↓Ca2+ and pustules in pregnancy—rare and serious)
* Chvostek’s sign; choreoathetosis; cataract; ccardiomyopathy (long qt interval on ecg).
42
What are some of the causes of hypocalcaemia?
43
How would you treat hypocalcaemia?
* **Mild**: Give calcium 5mmol/6h po
* **CKD**: **Alfacalcidol**, eg 0.5–1mcg/24h po.
* **Severe:** Give 10mL of 10% **calcium gluconate IV** over 30 mins
44
What are some of the symptoms of **hypernatraemia**?
* Lethargy
* Confusion
* Irritability
* Weakness
* Thirst
* Coma
* Fits
* Dehydration
* Diorrhoeah and vomiting
45
What are some of the signs of hypernatraemia?
* Reduced JVP
* Orthostatic hypotension
* Oliguria
* Dehydration signs
46
What are some of the causes of hypernatraemia?
* Diabetes insipidus
* Dehydration
* Osmotic diuresis
* Fluid loss without H20 replacement: burns, diarrhoea, vomiting
* Primary aldosteronism
* Iatrogenic: incorrect fluid replacement
47
How is **hypernatraemia** managed?
* Free water losses
* Oral or IV fluids
* If IV: **Dextrose 5% in water** is recommended - monitor for **hyperglycaemia**.
* **Avoid saline** - unless they are severely hypotensive or in shock
* Diabetes Insipidus: **desmopressin**
* 2nd: RRT
* Inadequate free water intake: oral or IV fluids, treat underlying cause
* 2nd: loop diuretic
* 3rd: RRT
48
What are the symptoms of **hyponatraemia**?
*Think less coordinated and aware*
* Reduced perception
* Gait disturbance
* Ataxia
* Headache
* Confusion
* Seizures
* Weakness
* Irritability
* Reduced GCS
49
What are the signs of **hyponatraemia**?
* Reduced UO
* Reduced skin turgor
* Increased fluid intake
* Altered mental status, seizures or coma
* Orthostatic hypotension
* ? Oedema
* ? Crackles on auscultation
50
What are some of the Ix performed for hyponatraemia
* Serum osmolality
* Urine osmolality
* Urine sodium
* Thyroid function
* Assessment of cortisol (morning cortisol or synacthen test)
51
What are the different types of hyponatraemia you can get? What is the most common?
* Hypovolaemic
* Euvolaemic
* Hypervolaemic
* Most common: hypotonic (hypoosmolar) hyponatraemia
52
What are the main causes of hypervolaemic hyponatraemia? How would we treat this?
* CHF
* Liver Cirrhosis
* Nephrotic Sx
* AKI/ CKD
* *Think anything with oedema!*
* *Treatment:* Fluid correct +/- furosemide
53
What are the causes of hypovolaemic hyponatraemia? How is it treated?
* **Third space losses:** pancreatitis, hypoalbuminaemia, burns, BO
* **Recent excessive fluid:** diarhoea, vomiting
* **Renal losses:** thiazide like diuretics, addisons, osmotic diuresis
* ***Treatment**: IV fluids (0.9% saline at 1-3ml/kg/hr + K+ if needed (check U+E)*
54
What are some examples of euvolaemic hyponatraemia?
* Hypothyroidism
* Primary polydipsia
* Gluccorticoid deficiency - adrenal insufficiency
* *SIADH*
55
What is SIADH? When should we suspect it?
* Syndrome of inappropriate ADH secretion
* Suspect in pt with very concentrated urine + hyponatraemia, + no oedema, hypovolaemia, diuretics
* Suspect when low plasma osmolality
56
What are some of the causes of SIADH?
* **Malignancy**: SCLC, thyoid, pancreatic, prostate, lymphoma
* **CNS disorders:** stroke, guillaine barre, abscess, meningoencephalitis, haemorrhage (subdural/ subarachnoid), head injury, neurosurgery
* **Chest disease:** SCLC, pneumonia, TB, abscess
* **Endocrine disease:** hypothyroidism
* **Drugs**: opiates, carbemezapine, SSRI, tricyclics, cytotoxics, psychotropics, sulphonylureas
57
How is SIADH treated?
* Treat the cause
* Restrict fluid, loop diuretics
* Consider **salt +/- loop diuretics** if severe
* Drugs:
* **Demeclocycline:** ADH antagonist
* **Tolvaptan:** vasopressor receptor antagonist
58
How is hyponatraemia treated chronically and acutely?
* A**cute (within 48 hours)** + symptomatic:
* GIve 3% hypertonic saline IV boluses
* +/- **furosemide**
* **Chronic (**48 hours)****
* If having seizures - Hypertonic saline
* Otherwise isotonic saline + furosemide
* If chronic + assymptomatic: water restriction + stop offending drug
59
What is hyperkalaemia?
* 5-6mmol/L K+
* A plasma potassium \>6.5mmol/L - emergency
60
What are the causes of hyperkalaemia?
* Rhabdomyolysis
* Acidosis/ DKA
* K+ rich diet
* CKD/ AKI
* Drugs: spironolactone, ARB/ AceI, amiloride, NSAIDs, heparin, LMWH, ciclosporin
* Burns
61
What are the symptoms of hyperkalaemia?
* Fatigue
* Palpitations
* Light headness =\> poss syncope
* Arrythmia
* Weakness
62
What ECG changes are seen with hyperkalaemia?
* Tall tented T waves
* Absent/ flattened P waves
* Slurred ST segment - sine wave
* Prolonged QRS
* 3Bs: bradycardia, block, bizarre
63
How would you treat **hyperkalaemia**?
* **IV Calcium Gluconate 10mg 10% over 5-10 minutes** - protect heart
* **IV fast acting insulin (**actrapid) in **IV glucose/ dextrose 50% 50mls**
* **Salbutamol** 5-10mg nebulised
* Eliminating K+from the body
* IV **Calcium Resonium**
* **Furosemide** 20-80mg
* **Dialysis** if persistent
* If acidotic: **sodium bicarbonate**
64
What is hypokalaemia?
* K+ \<2.5mmol/L - requires urgent treatment
* Note that hypokalaemia exacerbates digoxin toxicity.
65
What are the signs of hypokalaemia?
* Fatigue
* Constipation
* HT
* Paralysis
* Proximal muscle weakness
* Worsened glucose control in diabetes
66
What ECG changes would you expect to see with hypokalaemia?
* U waves
* small or absent T waves
* prolonged PR interval
* ST depression
67
What are the causes of hypokalaemia?
* Extra renal losses - inadequate intake, gut losses
* Redistribution
* Refeeding syndrome
* Primary or secondary hyperaldosteronism
* Renal losses
Hypokalaemia with alkalosis
* vomiting
* thiazide and loop diuretics
* Cushing's syndrome
* Conn's syndrome (primary hyperaldosteronism)
Hypokalaemia with acidosis
* diarrhoea
* renal tubular acidosis
* acetazolamide
* partially treated DKA
68
How would you treat hypokalaemia?
* Magnesium replacement
* Oral K+ replacement
* IV K+ replacement in 0.9% saline (avoid dextrose)
69
What is hyperosmolar hypoglycaemic state? What is its diagnostic criteria
* Happens with Type 2 DM (elderly pt)
* Hypovolaemia
* Marked hyperglycaemia (30mmol/L or more) without significant hyperketonaemia (\< 3mmol/L), ketonuria (2+ or less) or acidosis (pH\>7.3, bicarbonate\> 15mmol/L)
* Osmolality usually 320mosmol/kg or more
* Volume depletion without significant ketoacidosis
* Dehydration
* Minimal acidosis
70
What are some of the symptoms of Hyperosmolar hyperglycaemic state?
* Polyuria and polydipsia
* Weight loss
* Weakness
* Dehydration signs: dry mucous membranes, poor skin turgor, tachycardia, hypotension, seizure. **SHOCK**
71
What are some of the investigations for Hyperosmolar hyperglycaemic state?
* Urinalysis
* Plasma glucose
* Serum/ urine ketone
* Bloods: FBC, UE, +Ca2+, Mg2+, P043-, LFT
* Serum osmolality
* Anion gap
* ABG/ VBG - lactate, bicarb, pH
* Plasma osmolality
* HbA1C
72
How would we manage Hyperosmolar hyperglycaemic state?
1. IV fluids: 0.9% saline
2. Give K+ when urine starts to flow
3. Fixed rate Insulin - if glucose remains high - if blood glucose does not fall by 5mmol/L/hr
1. Use the presence of ketonaemia to determine - 3B hydroxybutyrate
1. \>1mmol - start insulin
2. \<1mmol/l - no insulin
4. Avoid hypoglycaemia in 1st 24 hrs
1. Aim for CBG 10-15mmol/L
2. If CBG \<14 mmol/L - start glucose 10% at 125ml/hr
5. DVT prophylaxis - if tolerate
6. Cathetar - then monitor fluid input + output
7. Examine feet - avoid ulcers
73
What are the symptoms of hyperglycaemia?
* Polyuria
* Polydipsia
* Unexplained weight loss
* Diabetes nephropathy/ neuropathy/ retinopathy
74
What are the symptoms of hypoglycaemia?
blood glucose concentrations \<3.3 mmol/L - autonomic symptoms (causes the release of glucagon and adrenaline):
* Sweating
* Shaking
* Hunger
* Anxiety
* Nausea
blood glucose concentrations below \<2.8 mmol/L - neuroglycopenic symptoms
* Weakness
* Vision changes
* Confusion
* Dizziness
75
What investigations are used for hyperglycaemia?
* Random blood glucose
* eGFR, FBC, UE
* Urine dipstick
* HBA1c
* Ketones
* Albumin and creatinine ratio
76
What investigations are used for hypoglycaemia?
* Urine dipstick
* Bloods: FBC, UE, CRP, LFT, insulin, sulphonylurea
* Cortisol (serum)/ ACTH
* Thyroid: TSH, T4
77
What is diabetes insipidus?
* Metabolic disorder characterised by an absolute or **relative inability to concentrate urine**, resulting in the production of large quantities of dilute urine
* Two types:
* **Central**: reduce synthesis of ADH +/or reduced release from HPPA
* **Nephrogenic**: Insensitivity of kidneys to ADH
* Characterised by: polyuria, polydipsia and hypotonic urine
78
What are the sx of addisonian crisis and when should it be suspected?
Sx: shock, postural hypotension, oliguria, weak, confused, comatose
## Footnote
*Predict on someone who has been previously taking long term steroids but has forgotten to stop taking thm*
79
What are the symptoms of Diabetes Insipidus?
* Polyuria
* Polydipsia
* Hypotonic urine
* Sx of hypernatraemia
* Sx of thirst and dehydration
80
What are some the causes of Diabetes Inspidus?
* Vascular: haemorrhage
* Infection: meningoencephalitis
* Trauma: pituatary surgery, craniopharyngoma, pituatary stalk lesions, traumatic brain surgery
* Autoimmune
* Metabolic: hypercalcaemia, hypokalaemia
* Idiopathis (\<50%)
* Congenital: defects in ADH gene
81
What investigations are used for diabetes insipidus?
* Bedside: urine dipstick
* Bloods: FBC, UE, CRP, electrolyes: Na (↑) , K (↓), Ca2+ (↑), nitrogen (↑)
* 24 hour urine collection (polyuria)
* Serum (↑)/ urine osmolality (↓)
* ***\*Water deprivation test -*** dehydrate pt for 8 hours then monitor weight loss/ serum/ urine osmolality hourly
* ***ADH stimulation test***
* MRI ? - To find cause
82
How is diabetes insipidus treated?
1. **IV fluids** - to maintain UO.
1. Do not try to correct hypernatraemia quickly as you risk cerebral oedema + brain damage
2. **Desmopressin** 2ug IM
3. Nephrogenic - **bendroflumethiazide**
83
What is DKA? What diagnostic criteria must the pt have?
* Commonly affect T1 patient
*
Diagnostic Criteria
* Significant ketonuria (≥ 2+) or blood ketone \> 3mmol/L
* Blood glucose \> 11mmol/L or known diabetes mellitus
* Bicarbonate \< 15mmol/L and/or venous pH \< 7.3
Diabetic ketoacidosis (DKA) is defined as the accumulation of ketone bodies in the blood of patients with diabetes mellitus, which results in metabolic acidosis. This is indicative of acute metabolic decompensation and is a medical emergency.
84
What is the pathophysiology behind DKA?
* Increased glucose but no insulin for it to be taken up by
* Body enter a starvation like state where alternative meabolism pathways are utilised
* Glucose turned into ketones -\> ketoacidosis -\> acidosis + hyperglycaemia
85
What Ix should be used for the diagnosis if DKA?
* Bloods: cap/ lab glucose, FBC, UE, CRP, bicarbonate, ketones, amylase/ lipase
* VBG/ ABG: lactate, bicarb, pH
* ? ECG/ CXR
86
How would you manage DKA?
1. ABC
2. 2 wide bore cannulaes
3. IV fluids: 0.9% saline
* If SBP\< 90 give a bolus
* Otherwise give 1L bags over 1hr
* Add K+ once they start passing urine
4. Insulin: 50u fixed rate human insulin to 50ml of saline.
* Infuse this at 0.1units/kg/hr
* Continue until pH \>7.3 or ketones (cap) \>0.6mmol
* After this continue with variable rate (sliding scale) insulin
5. K+ replacement - review U+E
6. Cathetar
7. Avoid hypoglycaemia
* When glucose \<14mmol/L start infusing 10% glucose to run alongside saline (same pump)
8. Continue fixed rate insulin until ketones \<0.6mmol/L
87
What is a myoxoedema coma? What symptoms characterise it?
Hypothyroidism emergency
* Bradycardia
* Hyporeflexia
* Hypothermia
* Seizures
* Coma
* Reduced glucose
88
How would you treat myxodema coma?
* Oxygen
* Correct hypoglycaemia
* Give T3 5-20ug/12h IV slowly - may get manifestations of IHD
* Hydrocortisone 100mg 8h IV
* Warm patient (avoid hypothermia)
89
What is thyrotoxic storm?
What are the symptoms?
How would you manage it?
* Hyperthyroid emergency
* Severe hyperthyroidism
* Management
* IV fluids
* Bloods
* Sedate: **chlorpromazine**
* **Propanolol** high dose
* Possibly high dose **digoxin** to slow the heart
* **Carbimazole**
* **Hydrocortisone**/ **dexamethasone**
* If infection: co-amox
90
How do you treat phaeochromacytoma?
* Conservative: Hydration and reduced salt diet
* PharmacologicalABC
* **A**lpha blocker: **phenoxybenzamine**
* **B** blocker: **atenolol**
* **C**CB: **nifedepine**
* Surgery: **Excision** of tumour
91
What is Familial Hypocalcuric Hypercalcaemia?
* Rare: genetic defect in calcium sensing receptor
* Distinguished by: low urine calcium/ creatinine ratio
92
What are some of the complications of DKA?
* Cerebral oedema – especially in children and adolescents
* Hypokalaemia
* Adult Respiratory Distress Syndrome (ARDS)
* Co-morbid conditions (e.g. pneumonia)
* Acute MI
* Sepsis
93
What is the criteria for resolution of DKA?
* pH\>7.3
* Bicarbonate (HCO3-) \> 15.0 mmol/L and
* Blood ketone level \< 0.6 mmol/L (rather than \< 0.3 mmol/L)
94
What serious complication could arise in the management of DKA?
* Hypo or hyperkalaemia
* Hypoglycaemia
* Cerebral oedema
* Pulmonary oedema
95
How is hypoglycaemia managed?
In the community (for example, diabetes mellitus patients who inject insulin):
1. **Oral glucose 10-20g:** in liquid, gel or tablet form
2. Alternatively, a propriety **quick-acting carbohydrate** may be given: **GlucoGel** or Dextrogel
3. A 'HypoKit' may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
In a hospital setting:
If the patient is alert: **a quick-acting carbohydrate** may be given (as above)
Unconscious, unable to swallow:
1. SC/ IM glucagon
2. IV 20% glucose solution
96
What happens in hypopituatarism?
97
What do you test for in when assess pituatary function?
* Prolactin + TSH - any time of day
* LH + FSH - in first 5 days of menstrual cycle
* Testosterone - 0900
* IGF 1 - GH deficiency
* Insulin tolerance test - ACTH + GH reserve
* Do not perform in patients with IHD + epilepsy
Imaging
* MRI
* \< 1cm - microadenoma
* \> 1cm - macroadenoma
* PET CT - new
98
99
What can cause hyperprolactinaemia?
* Pregnancy
* Drugs
* Profound hypothyroidism
* PCOS (mild)
* Prolactinoma (\>5000)
Microprolactinomas - \<1cm
* Pituatary tumours
* Sx: menstrual disturbance, hypogonadism, galatorrhea, possible infertility
Macroprolactinimas - \>1cm
* M\>W
* Prolactin \> 5000
* Immunoassay can give inaccurate results
100
What are the causes and sx of microprolactinoma
101
How are prolactinomas managed?
* Medical: **D2 agonist - cabergoline + bromocriptine.** SE: postural hypotension.
* Tumour debulking -\> CSF leak -\> increased risk of meningitis
* Cardiac valve abnormalitis in PD
102
What are some of the sx of acromegaly?
Space Occupying Lesion
* Headaches
* Visual field defect (“bitemporal hemianopia”)
Overgrowth of tissues
* Prominent forehead and brow (“frontal bossing”)
* Large nose
* Large tongue (“macroglossia”)
* Large hands and feet
* Large protruding jaw (”prognathism”)
* Arthritis from imbalanced growth of joints
* GH can cause organ dysfunction
* Hypertrophic heart
* Hypertension
* Type 2 diabetes
* Colorectal cancer
Symptoms suggesting active raised growth hormone
* Development of new skin tags
* Profuse sweating
103
How is acromegaly Ix:d
* OGTT
* IGF1
* Prolactin: pituatary adenoma
* MRI: for tumour though small ones may not be seen
104
105
How is acromegaly mxd
* Surgery: remove tumour
* Medical
* Somatastatin analogues - **OCTREOTIDE** - monthly injections
* DOPAMINE AGONISTS - **may control GH - cabergoline / bromocriptine**
* **External beam/ stereotide radiotherapy**
* **only suitable for lesions away from the optic chiasm**
* **can take years to work**
* **SE: gradual onset hypopituatarism/ CVS disease**
* **Monitoring:**
* **colorectal cancer: COLONOSCOPY**
* **Repeat OGTT post surgery**
* **Monitor for: OSA, T2DM, CVS, sx recurrence**
