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Medicine year 4 CDM > Block 6: Hyponatraemia, basics and T1D > Flashcards

Block 6: Hyponatraemia, basics and T1D Flashcards

1
Q

Rhythm of ACTH axis

A
  • Increased CRH and ACTH pulses in day
  • CRH is released in pulsatile manner
  • Reduced pulses at night
  • Cortisol maximum at 0900
  • Cortisol minimum at midnight
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2
Q

Regulation of ACTH secretion

A
  • Stress and cicadian rhythm causes release of Serotonin, Glutamate, Histamine and Catecholamine. Acts on Hypothalamus
  • Hypothalamus releases Corticotrophin releasing hormone (CRH) →
  • Anterior Pituitary releases ACTH (adrenocorticotrophic hormone) →
  • Adrenal gland released Cortisol
  • Cortisol inhibits Pituitary and Hypothalamus (negative feedback)
  • GABA is inhibitory on hypothalamus
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3
Q

Rhythm of GH axis

A
  • Pulsatile release
  • Few pulses in day
  • Most of GH secreted during sleep- peak 2am
  • High mean GH in acromegaly
  • GH effects mediated via IGF-1
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4
Q

Regulation of GH secretion

A
  • Hypothalamus releases GHRH (growth hormone releasing hormone) →
  • Anterior Pituitary releases GH (growth hormone) →
  • Liver releases IGF-1 (insulin like growth factor 1)
  • Hypothalamus can release Somatostatin which inhibits pituitary
  • GH inhibits Hypothalamus
  • IGF-1 inhibits Pituitary and Hypothalamus (negative feedback)
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5
Q

Pituitary gonadal axis in women- cyclical

A
  • In follicular phase oestrogen surge leads to LH release
  • In mid-late luteal phase LH pulses cause progesterone release
  • Positive feedback during mid-cycle LH/FSH surge
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6
Q

Regulation of LH and FSH secretion

A
  • Hypothalamus releases GnRH →
  • Pituitary releases LH and FSH →
  • Gonad (ovary/testis) releases testosterone (negative), oestrogen and progesterone (negative and positive)
  • Prolactin inhibits pituitary
  • Testosterone, oestrogen and progesterone inhibit pituitary and Hypothalamus
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7
Q

Effects of LH and FSH

A
  • Males FSH- Spermatogenesis
  • Males LH- Testosterone production
  • Females FSH- follicle development
  • Females LH- Ovulation
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8
Q

Hormones- storage, release, transport and action

A
  • Hormones can be stored as complexes (e.g thyroid hormones as thyroglobulin) or as prohormones (e.g. insulin- proinsulin)
  • Release in response to trophic hormones (ACTH, TSH, autonomic nervous stimulation, or external stimuli (daylight) or metabolic (glucose)
  • Transported via specific binding proteins (e.g. sex hormone binding globulin, cortisol binding globulin, growth hormone binding protein) or non-specific such as albumin (e.g.thyroid hormone)
  • Free unbound hormone biologically active- unbound and bound hormones normally exist in equilibrium. As more free hormone is required its released from the bound globulin
  • Act via receptors on cell membranes triggering intracellular pathways (e.g. insulin) or acts intracellularly at the nucleus (e.g. steroids, thyroid hormone) as its absorbed into the cell
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9
Q

Principles of investigating Endocrine disease

A
  • Measure hormone levels at the right time of day
  • If you think a hormone is lacking stimulate it
  • If you think a hormone is being produced in excess supress it
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10
Q

Thyroid hormone system

A
  • Hypothalamus releases TRH into portovenous system→
  • Anterior pituitary releases TSH →
  • Thyroid releases Thyroxine (T4) and Triiodothyronine (T3)
  • T4 and T3 have negative effect on pituitary and Hypothalamus
  • Hypothalamus releases Somatostatin and Dopamine which inhibits the pituitary
  • You assess system by measuring TSH, free T4 and free T3. TRH not helpful as too low
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11
Q

Hormone levels in Thyroid disease

A

Primary Endocrine disease (thyroid): End organ damage (thyroid). There is low T4 and T3, as there is no negative feedback there is high TSH and TRH

Secondary Endocrine disease (thyroid): Pituitary insufficiency. Low TSH causes low T4 and T3. As no inhibitory effect high TRH.

Sick euthyroid syndrome: low TSH and free T4 (not due to pituitary)

Primary endocrine disease (Thyroid excess): High T4 and T3 causes inhibitory effect causing low TRH and TSH

Secondary endocrine disease (pituitary excess- pituitary tumour): High TSH causes High T4 and T3 results in inhibitory effect causing low TRH

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12
Q

Cortisol stimulation

A

Give Syncacthen either IV or IM then wait an hour, Cortisol should then rise >600 nmol/L. 400-600 is borderline. If fault at adrenal gland ACTH is high, if fault in pituitary ACTH is low

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13
Q

Cortisol suppression

A

When you think there’s excess. Do urinary free cortisol or plasma cortisol (levels dependent on time of day to confirm high levels. Then do Dexamethasone suppression test given late at night and test in morning. Normal is <50nmol/L. In Cushing’s it will be slightly suppressed and in ectopic ACTH syndrome and adrenal tumour wont be at all. If in doubt prolong till 2 days or high dose dexamethasone for 4 days

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14
Q

Hormone tests for Hormone excess

A
  • Cushing’s syndrome – measure hormone levels & dexamethasone suppression tests
  • Acromegaly – measure hormone levels & oral glucose tolerance test (suppression)
  • Thyrotoxicosis – measure hormone levels
  • Hyperprolactinaemia – measure hormone levels
  • Insulinoma – simultaneous fasting glucose & insulin levels
  • Phaeochromocytoma – plasma & urine catecholamine levels, no suppression test
  • Hyperparathyroidism – simultaneous plasma calcium & parathyroid hormone levels
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15
Q

Hormone tests for hormone deficiencies

A
  • Addison’s disease – measure hormone levels & synacthen stimulation test
  • Growth hormone deficiency – measure hormone levels & stress stimulation e.g.exercise
  • Hypothyroidism – measure hormone levels
  • Hypogonadism – measure hormone levels: FSH, LF, oestrogen, testosterone
  • Secondary amenorrhoea – measure hormone levels
  • Diabetes insipidus (ADH insufficiency) – water deprivation test or hypertonic sodium chloride infusion test (stimulation)
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16
Q

Non-medication approaches in Endocrinology

A
  • Surgery: removal of functioning tissue i.e. pituitary tumour. Removal of whole gland i.e. thyroid, adrenal
  • Destructive therapy i.e. radiotherapy- often used as adjunct to surgery in pituitary tumours, given orally in thyroid
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17
Q

Medication for hormone excess: Block release of hormone

A
  • Somatostatin analogues for growth hormone excess in Acromegaly
  • Dopamine receptor agonists for hyperprolactinaemia
  • Diazoxide prevents insulin release from b cell tumours in pancreas
  • Gonadotrophin releasing hormone (GnRH) modulators prevent LH/FSH release
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18
Q

Prolactin secretion

A
  • Hypothalamus releases TRH →
  • Pituitary releases Prolactin →
  • Breasts secrete milk
  • Oestrogen also increases Prolactin production
  • Dopamine is inhibitory on the pituitary. Dopamine receptor agonists can suppress prolactin release and pituitary tumours
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19
Q

Medication for hormone excess: block hormone production

A
  • Antithyroid drugs block iodination of tyrosine
  • Ketoconazole and metyrapone block steroid biosynthesis i.e. Hydrocortisone in Crushing’s
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20
Q

Medication for hormone excess: block hormone action

A
  • Tamoxifen is a selective oestrogen receptor modulator (SERM)
  • Cinacalcet is a parathyroid hormone receptor blocker
  • a & b adrenoceptor blockers used in phaeochromocytoma and b blockers in hyperthyroidism
  • Pegvisomant is a growth hormone receptor blocker in Acromegaly
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21
Q

Medical treatment for hormone deficiency principles

A
  • Not possible to reproduce pulsatility
  • Can replace cyclically e.g. induction of ovulation
  • Diurnal variation for steroid replacement (higher dose at 9am, lower at 4pm) in Addison’s
  • Relate to requirement (e.g. insulin bolus before meals) i.e. T1D
  • Most hormones given orally
  • Some have to be by injection (e.g. insulin)
  • Care with drug interactions (e.g. oral iron & antacids reduce T4 absorption)
22
Q

Hyponatraemia

A
  • Na <135 mmol/L
  • 15-20% of hospital admission
  • Predictor of complications and death in Heart disease, Cirrhosis and Neurological disorders
  • Causes increased hospital stay
23
Q

Classifying Hyponatraemia

A
  • Either too little water sodium or too much water
  • Mild: 130 - 135 mmol/l
  • Moderate: 125 - 129 mmol/l
  • Profound: <125 mmol/l
  • Acute: exists <48h
  • Chronic: exists for at least 48h- assume chronic if don’t know
24
Q

Clinical features of Hyponatraemia

A
  • Symptoms: None, Headache, Nausea, Vomiting, Muscle cramps, Lethargy
  • Signs: Disorientation, seizures, coma, cerebral oedema, death
  • Symptoms aren’t dependent on Na+ levels as can be tolerated differently
25
Q

Adaption to hyponatraemia

A
  • Brain with hyponatraemia in hypotonic state get water influx this causes oedema which increases risk of coma
  • Rapid adaption: if there’s slow increase in hypotonia you get a rapid adaption. Loss of Na+, K+ and chloride channels and ions. Causes water loss
  • Slow adaption: loss of organic osmolytes which takes water with it, reduces oedema
26
Q

Causes of hyponatraemia

A
  • Hyperglycaemia
  • Addisons
  • SIADH
  • Reduced renal free water clearance
  • Pseudohyponatraemia (plasma with higher level of solute): Hypertriglyceridemia, non-physiological osmolyte
  • Sodium depletion: diuretics, salt wasting, Nephropathy, Hypoadrenalism, Central salt wasting, extra renal loss (gut loss)
  • Excess water intake: dipsogenic DI, sodium free hyperosmolar irritant solution, dilute infant feeding formula, IV therapy
27
Q

Hyponatraemia: reduced renal free water clearance

A
  • Hypovolaemia: Drugs, Renal failure, Portal hypotension & ascites, Hypoalbuminaemia, Sepsis and vascular leak, Central salt wasting, Fluid sequestration
  • Cardiac failure
  • Nephrotic syndrome
  • Hypothyroidism
  • Hypoadrenalism
  • SIADH
  • Nephrogenic SIADH
28
Q

Diagnosis of SIADH

A
  • Hyponatraemia
  • Clinical euvolaemia
  • Serum osmolality <275 mOsmol/kg.
  • Urine Osmol >100mOsm/Kg: Submaximal dilution. Urine is concentrated
  • Urine Na >30 mmol/L
  • No recent diuretic use
  • Absence of: hypotension and hypovolaemia. Non-osmotic AVP release, oedema, adrenal, thyroid and renal insufficiency
  • Management is fluid restriction
29
Q

Causes of SIADH

A
  • drug induced: SSRI, Carbamazepine, Phenothiazine, TCA’s etc
  • CNS: inflammatory, tumour, infection
  • Tumour-associated: Small cell lung carcinoma
  • Chest disease: infection, inflammatory (sarcoidosis), structural
30
Q

Investigations of SIADH

A
  • Urine investigations: sodium and osmolality
  • Plasma: osmolality, LFT’s, bone panel, TFT, 9am cortisol
  • Radiology: CXR, CT of chest/abdo/pelvis if SIADH confirmed
31
Q

Diagnostic algorithm for Hyponatraemia: move down

A
  • Exclude Non-hypotonic hyponatraemia i.e. hyperglycaemia Glucose test
  • Hypotonic hyponatraemia: do urine osmolality
  • <100 mOsmol/Kg- dilute urine: primary polydipsia, inappropriate IV fluids, low solute intake
  • > 100 mOsmol/Kg (not trying to dilute urine): Urine Na
  • <30mmol/L Na+- trying to retain Na+: low effective atrial volume, heart failure, cirrhosis/portal hypertension, Nephrotic, Hypoalbuminaemia, third space loss, GI loss, previous diuretic use
  • > 30 mmol/L Na+: Diuretic or ACEi. If not diuretics or ACEi : SIADH, low effective volume, salt wasting nephropathy, vomiting, hypoadrenalism
32
Q

Management of Hyponatraemia: severe

A
  • Hyponatraemia exclude hyperglycaemia i.e. serum glucose
  • In severe symptoms give fluids straight away otherwise do urine osmolality and work out cause
  • Hyponatraemia with severe symptoms: hypertonic saline to restore serum sodium concentration to a safe level (dont give too much). 150 mls of 3% saline over 20 minutes. Aim for increase in sodium 8-10mmol/L over 24 hours
33
Q

Management of Hyponatraemia: not severe

A
  • Acute hyponatraemia with mild or no symptoms: Stop non-essential parenteral fluids and medications associated with hyponatraemia and treat underlying cause
  • Chronic hyponatraemia without moderate or severe symptoms: Stop non-essential supplementary fluids and medications that can provoke hyponatraemia and treat underlying cause
  • Hyponatraemia secondary to hypervolaemia: fluid restriction is recommended to prevent further fluid overload.
  • Hyponatraemia due to syndrome of inappropriate antidiureis (SIADH): fluid restriction
  • Hyponatraemia secondary to hypovolaemia: extracellular volume is restored with infusion of 0.9% saline.
34
Q

Complications of rapid correction of chronic hyponatraemia: osmotic demyelination syndrome

A
  • Neurology: Quadriplegia, Opthalmoplegia, Pseudobulbar palsy, Coma
  • Pathology: De-myelination, necrosis
35
Q

Symptoms of T1D

A

Polyuria, Nocturia, New onset enuresis, Polydipsia, Unintentional weight loss, Fatigue, Blurred vision, Extreme hunger, Irritability/mood changes

36
Q

T1D diagnosis and vaccine

A

Most children are diagnosed between 9-14

Vaccines: annual immunisation against influenza, immunisation against pneumococcal infections if they are taking insulin or oral hypoglycaemic medication

Diagnosis= fasting plasma glucose >7.0 mmol/l or 2 hour plasma glucose >11.1 mmol/l. Fasting C-peptide is low or undetectable.

37
Q

T1D: monitoring for complications and associated conditions

A
  • Thyroid disease at diagnosis and annually thereafter until transfer to adult services
  • Diabetic retinopathy annually from 12 years
  • Moderately increased albuminuria (albumin:creatinine ratio [ACR] 3–30 mg/mmol; ‘microalbuminuria’) to detect diabetic kidney disease, annually from 12 years
  • Hypertension annually from 12 years
  • Annual foot assessment from the age of 12 years
  • Screen for Coeliac at diagnosis and there after if symptoms arise.
38
Q

T1D: tests at diagnosis

A
  • Insulin antibodies,anti-GAD antibodiesandislet cell antibodiesto test forantibodiesassociated with destruction of thepancreasand the development of type 1 diabetes
  • FBC, U&E, laboratory glucose, HBA1c
39
Q

What are the different insulin regimes

A
  • Multiple daily injection basal–bolus insulin regimens: injections of short-acting insulin or rapid-acting insulin analogue before meals, together with 1 or more separate daily injections of intermediate-acting insulin or long-acting insulin analogue.
  • Continuous subcutaneous insulin infusion (insulin pump therapy): a programmable pump and insulin storage device that gives a regular or continuous amount of insulin (usually a rapid-acting insulin analogue or short-acting insulin) by a subcutaneous needle or cannula.
  • One, two or three insulin injections per day: these are usually injections of short-acting insulin or rapid-acting insulin analogue mixed with intermediate-acting insulin.
40
Q

What is the normal target range for HbA1C

A

HbA1c target level of 48 mmol/mol (6.5%) or lower is ideal to minimise the risk of long-term complications. On diagnosis tends to be >48.

41
Q

Management for T1D

A
  • Subcutaneousinsulin regimes
  • Monitoringdietary carbohydrateintake
  • Monitoringblood sugarlevels on waking, at each meal and before bed
  • Monitoring for and managingcomplications, both short and long term
42
Q

Risk factors for T1D

A
  • Genetics: HLA-DR and HLA-DQ (coeliac)
  • Can have coeliac and other autoimmune conditions (Hashimoto’s thyroiditis, Addison’s)
  • The presence of autoantibodies to islet cells, insulin, islet antigens (IA2 and IA2-beta), glutamic acid decarboxylase (GAD), or the zinc transporter ZnT8
  • Environmental susceptibility: viral infection, cows milk, vitamin D deficiency
43
Q

T1D

A

due to autoimmune destruction of the insulin producing beta cells in the islets of Langerhans of the pancreas. A type 4 hypersensitivity reaction

44
Q

T1D complications

A
  • Hypoglycaemia:
  • Hyperglycaemia: increase insulin
  • Macrovascular: Coronary artery disease, diabetic foot, stroke, hypertension
  • Microvascular complications: Peripheral neuropathy, retinopathy, glomerulosclerosis
  • Infection: UTI, pneumonia, candidiasis, skin infections
45
Q

Hypoglycaemia

A
  • Too much insulin, not enough carbohydrate.
  • Symptoms are hunger, tremor, sweating, irritability, dizziness and pallor. In severe cases can get reduced consciousness, coma and death
  • Treat: rapid acting glucose like lucozade and slower acting carbohydrate like biscuits. If conscious use glucogel if unconscious IM glucagon
  • In hospital if catheter use IV 10% dextrose, otherwise Im glucagon
46
Q

Diabetic Ketoacidosis

A

Characterised by hyperglycaemia, acidosis and ketonaemia

Diagnosis:

  • Ketonaemia: 3mmol/L and over
  • Blood glucose over 11mmol/L
  • Bicarbonate below 15mmol/L or venous pH less than 7.3
47
Q

Causes of DKA

A

infection, dehydration, fasting. There shouldn’t be a fever in DKA, so if there is it means infection is the cause

48
Q

DKA presentation

A

smell of acetone (fruity breath), vomiting, dehydration, abdominal pain, hyperventilation (kussmaul), Hypovolaemic shock, drowsiness, coma

49
Q

DKA management

A
  • If patient is alert, not significantly dehydrated and able to tolerate oral intake without vomiting –> encourage oral intake and give subcutaneous insulin injection
  • If patient is vomiting, confused, or significantly dehydrated –> give IV fluids (initial bolus of 10ml/kg 0.9% NaCl then discuss with a senior). Then start fluid regimen. If there is evidence of shock, the initial bolus should be 20ml/kg.
  • Insulin infusion at 0.1 units/kg/hour 1hr after starting IV fluids.
  • Once glucose <14mmol 10% dextrose infusion should be started in addition to saline
  • If patient is shocked or comatose –> ABCDE approach for emergency resuscitation
  • Do not stop intravenous insulin infusion until 1 hour after subcutaneous insulin has been given.
  • Give K+ if <5.5
50
Q

DKA: cerebral oedema

A

Major complication of DKA, can occur hours after. May be due to the rapid provision of IV fluids which causes water to move from the blood into the tissues which in the brain causes swelling of the structures in the skull.

Medicine year 4 CDM (44 decks)

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