Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Main Conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

T1DM

Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system

A
  • Absolute deficiency of insulin resulting in raised glucose levels
  • Childhood
  • BMI below 25
  • Weight loss
  • Polydipsia
  • Polyuria
  • Can initially present as DKA (Vomitting, Abdo pain, keto breath, Kussmaul respiration)

Diagnosis

  • Random Glucose (or 75gOGTT): 11.1 mmol Fasting: 7.0 mmol
  • If pt ASYMPTOMATIC above criteria must be met on 2 separate occassion
  • HbA1c not as effective in T1DM due to nature of presentation
  • C-peptide levels and diabetes-specific autoantibodies are the investigations of choice. CPeptide=LOW
  • Other Antibody tests: antiGAD, ICA, IAA

Management

  • HbA1c monitor every 3-6m, Target: below 48mmol
  • Daily self monitoring of Blood sugar (4x Daily, mealtime, sleep time)
  • Target: Below 7mmol before meals and waking up.
  • SC Insulin
  • Multiple daily injection basal-bolus insulin regimens, (Background, long-acting insulin injected once a day
    Short-acting insulin injected 30 minutes before consuming carbohydrates    )
  • Injecting into the same spot can cause lipodystrophy So you can get insulin pumps but may be complicated to use for some patients, or cycle injection sites
  • NICE recommend considering adding metformin if the BMI >= 25 kg/m²

Side Fx Insulin

  • Hypoglycaemia
  • Weight gain
  • Lipodystrophy

polyuria and polydipsia are due to water being ‘dragged’ out of the body due to the osmotic effects of excess blood glucose being excreted in the urine (glycosuria).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T2DM

A
  • Relative deficiency of insulin due to an excess of adipose tissue.
  • Polydipsia
  • Polyuria

Diagnosis

  • Random Glucose (or 75gOGTT): 11.1 mmol Fasting: 7.0 mmol
  • If pt ASYMPTOMATIC above criteria must be met on 2 separate occassion
  • HbA1c of greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus
  • A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG) - offer them oral glucose tolerance test
  • HbA1c should be checked every 3-6 months until stable, then 6 monthly

Misleading HbA1c results can be caused by increased red cell turnover

  • haemoglobinopathies
  • haemolytic anaemia
  • untreated iron deficiency anaemia
  • suspected gestational diabetes
  • children
  • HIV
  • chronic kidney disease
  • people taking medication that may cause hyperglycaemia (for example corticosteroids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

T2DM Treatment Pathway

Should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)

A

First line

  1. Lifestyle Intervention
    • Metformin ( titrated up slowly to minimise risk of GI upset)
  3. add SGLT-2 Inhibitor (dapagliflozin) if CVD risk or Heart failure

Gliclazide, a sulfonylurea, is often used second-line if metformin is not tolerated

Second Line

  • Considered if blood glucose >58mmol
    1. Metformin (+/-SGLT2inhib) + DPP-4 inhibitor (gliptin) or pioglitazone or sulfonylurea (Gliclazide)

Thrid Line

  1. Metformin + 2 of the above drugs
  2. Metformin + Insulin
    - NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need
    - metformin should be continued.

Fourth Line

  1. Metformin + Insulin + GLP1 mimetic (semaglutide/ozempic)
  • Only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months

metformin should be avoided in moderate to severe renal failure,

you can use SGLT2 as combo therapy in non CVD if NICE criteria met

Targets:

Lifestyle 48mmol
Metformin 48mmol
Treatment regimen Includes any drug which may cause hypoglycaemia (e.g. lifestyle + sulfonylurea) 53 mmol/mol (7.0%)
Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%) 53 mmol/mol (7.0%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MoA Diabetic Drugs

A
  • Biguanide: Metformin
    Increases insulin sensitivity
    Decreases hepatic gluconeogenesis
  • SGLT2 Inhib: Dapagliflozin
    Inhibits reabsorption of glucose in the kidney
  • DPP4 inhib: Sitagliptin
    Increases incretin levels which inhibit glucagon secretion
  • Thiazolidinedione: Pioglitzone
    Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
  • Sulfonylurea: Gliclazide
    Stimulate pancreatic beta cells to secrete insulin
  • GLP1 agonists: Semaglutide
    Incretin mimetic which inhibits glucagon secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Side Effects of Diabetic Drugs

Drug Classes

  • Biguanide: Metformin
  • SGLT2 Inhib: Dapagliflozin
  • DPP4 inhib: Sitagliptin
  • Thiazolidinedione: Pioglitzone
  • Sulfonylurea: Gliclazide
  • GLP1 mimec: Semaglutide
A

- Sulfonylurea: Gliclazide: Hypoglycaemia Weight gain yponatremia

  • Biguanide: Metformin: Gastrointestinal upset
    Lactic acidosis
  • SGLT2 Inhib: Dapagliflozin: Urinary tract infection
  • DPP4 inhib: Sitagliptin: increased risk of pancreatitis
  • Thiazolidinedione: Pioglitzone: Weight gain
    Fluid retention
  • Sulfonylurea: Gliclazide
    Hypoglycaemia Weight gain Hyponatraemia
  • GLP1 mimec: Semaglutide: Nausea and vomiting
    Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ramadan + Diabetic Treatment Regiment

A

Metformin: one-third before sunrise (Suhoor) and two-thirds after sunset (Iftar)
Sulfonylureas: after iftar
Gliclazide: Bigger dose after iftar
Pioglitazone: no adjustment is needed for patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Diabetic Sick Day rules

A

T1DM

  • if a patient is on insulin, they must **not **stop it due to the risk of diabetic ketoacidosis
  • Drink 3L water
  • eat as normal
  • monitor blood sugars closely

T2DM

  • metformin: stop treatment if there is a risk of dehydration, to reduce the risk of lactic acidosis.
  • sulfonylureas: may increase the risk of hypoglycaemia
  • SGLT-2 inhibitors: check for ketones and stop treatment if acutely unwell and/or at risk of dehydration, due to the risk of euglycaemic DKA
  • GLP-1 receptor agonists: stop treatment if there is a risk of dehydration, to reduce the risk of AKI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ketoacidosis

complication of existing type 1 diabetes mellitus, very rarely it occurs in T2DM

A

Predisposing Factors

  • Incorrect Insulin Regiment, MI, Infection, Missed Insulin Dose

Pathophysiology

  • Uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

Presentation:

  • Vomitting
  • Polydypsia, Polyuria, Dehydration
  • Abdo pain
  • keto breath
  • Kussmaul respiration

Diagnosis

  • Blood Glucose >11mmol
  • Ketones: >3mmol
  • pH < 7.3
  • bicarbonate < 15 mmol/l

Managment

  • IV Fluids: isotonic saline
  • IV infusion Insulin at 0.1 unit/kg/hour
  • potassium may need to be added to the replacement fluids
  • IV Dextrose once Glucose below 14mmol
  • long-acting insulin should be continued, short-acting insulin should be stopped

Further

  • Resolution: pH>7.3, Ketones <0.3
  • Watch out for Cerebral Oedema in Children
  • ketonaemia and acidosis should have been resolved within 24 hours. If this hasn’t happened the patient requires senior review from an endocrinologist

Complications may occur from DKA itself or the treatment:
gastric stasis
thromboembolism
arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
acute respiratory distress syndrome
acute kidney injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hyperosmolar Hyperglycaemic State

Compared to DKA, HHS comes on over many days, and consequently, the dehydration and metabolic disturbances may be more extreme

A

Predisposing Factors

  • intercurrent illness
  • dementia
  • sedative drugs
  • Pathophysiology
  • hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion

Presentation

  • clinical signs of dehydration
  • polyuria
  • polydipsia
  • Lethargy
  • N&V
  • focal neurological deficits

Diagnosis

  • No set criteria
  • Blood Glucose 30mmol
  • raised serum osmolarity (> 320 mosmol/kg)
  • no ketonaemia or acidosis

Management

  • IV 0.9% sodium chloride solution
  • No insulin unless blood glucose stops falling while giving IV fluids
  • VTE Prophylaxis

Complications

  • vascular complications may occur due to hyperviscosity:
  • such as myocardial infarction
  • stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Maturity onset diabetes of the young (MODY)

A
  • A group of inherited genetic disorders affecting the production of insulin.
  • Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Latent autoimmune diabetes of adults (LADA)

A
  • The majority of patients with autoimmune-related diabetes present younger in life. There are however a small group of patients who develop such problems later in life.
  • These patients are often misdiagnosed as having T2DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of Raised Bloodsugar (hyperglycaemia)

Other than Diabetes

A
  • Pancreatitis
  • haemochromatosis
  • Glucocorticoid use (Prednislone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Complications of Diabetes

DOUBKE CHECK THIS CARD NOT ALL IS ACCURATE

A

Diabetic retionopathy: cotton wool spots (‘soft exudates’ - represent areas of retinal infarction)panretinal laser photocoagulation, VEGF inhibs
Peripheral Neuropathy: Sensory loss, glove stock distribution, treat with gapapentin, TCA (amitryptaline) , Duloxetine, pregablin
Gastric Neuropathy: Gastroparesis treatment: metoclopramide, domperidone
Diabetic Nephropathy albumin:creatinine ratio (ACR), reduce protein, start ACE Inhib to control BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hormone Axis Phsiology

Thyroid, Adrenal, GH, Parathyroid Axis’ -ve feedback loops

The hypothalamus releases hormones that stimulate the pituitary gland. The pituitary gland has an anterior and posterior part.

A

Thyroid Axis
* Hypothalamus -> TRH -> AP -> TSH ->Thyroid Gland -> T3 +T4

Adrenal Axis

  • Hypothalamus -> CRH -> AP -> ACTH -> Adrenal Glands -> Cortisol (stress hormone)

Growth Hormone Axis

  • Hypothalamus -> GHRH -> AP -> GH -> Liver -> IGF1

Parathyroid Axis (different)

  • Low Ca2+ -> Parathyroid Glands -> PTH Hormone -> Bone Resorption, less Ca2+ secreted in kidneys, PTH also stimulates the kidneys to convert vitamin D3 into calcitriol, the active form of vitamin D. Vitamin D promotes calcium absorption from food in the intestine.

Anterior Pituitary

  • ACTH
  • TSH
  • FSH
  • LH
  • GH
  • Prolactin

Posterior Pituitary

  • Vasopressin/Anti Diuretic Hormone
  • Oxytocin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

AUTOIMMUNE

Hyperthyroidism

aka thyrotoxicosis

Graves most common cause
Others incl.:

  • Amiodarone use
  • Toxic multinodulare goitre
  • Initial stages of De Quervians + Post Partum Thyroditis (these later become hypo)
A

Signs

  • Weight loss
  • Manic Restlessness - Tachycardic + Palipitations
  • Heat intolerance - sweating
  • Pretibial myoxedema
  • Oligomennhoria - infrequent periods
  • Diarrhoea
  • Anxiety + Tremor
  • High output cardiac failure in elderly

Ix

  • Low TSH + High T4 (High T3 but irrelevant)
  • Anti TPO antibodies

Management

  • Propranalol - initial symptom management
  • Carbimazole - watch out of agranulocytosis (reduced granulocytes- neutrophils)

Agranulocytosis can present with symptoms such as fever, chills, sore throat, mouth ulcers, and severe infections.

Subclinical hyperthyroidism is an entity which is gaining increasing recognition. It is defined as:

  • normal serum free thyroxine and triiodothyronine levels
  • with a thyroid stimulating hormone (TSH) below normal range (usually < 0.1 mu/l)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Grave’s Disease

Most common cause of thyrotoxicosis/Hyperthyroidism

Common in F - 30-50y

A

Signs

  • typical features of thyrotoxicosis (heat intolerance, palpitations, Pretibial myoxedema etc)
  • Exopthalmos - Big eyes
  • Opthalmoplegia
  • Thyroid acropachy: 1. digital clubbing 2. soft tissue swelling of hands + feet 3. periosteal new bone formation

Ix

  • TSH receptor stimulating antibodies raised
  • anti-thyroid peroxidase antibodies (75%) raised
  • Thyroid scintigraphy: diffuse, homogenous, increased uptake of radioactive iodine

Management

  • referred to secondary care for ongoing treatment.
  • Propranalol - initial symptom management
  • Carbimazole - watch out of agranulocytosis (reduced granulocytes- neutrophils)
17
Q

Hypothyroidism

underactive thyroid

1mary Hypothyroidsm: Issue with thyroid gland itself
2ndry Hypothyroidism: Issue with pituitary gland which secretes the TSH

A

Hashimoto’s thyroiditis - most common cause in the developed world
Others incl.: Iodine deficieny (common in developing world), lithium or amiodarone use, de Quervain’s or Post Partum thyroiditis. Secondary causes incl. Pituitary failure, Coeliac, downsydnrome, turner’s

Signs

  • Weight gain
  • Lethargy
  • Dry (anhydrosis), cold, yellowish skin
  • Dry, coarse scalp hair, loss of lateral aspect of eyebrows
  • Non pitting oedema
  • Constipation
  • Menorrhagia - heavy periods
  • Decreased Deep tendon reflexes
  • Carpal Tunnel Syndrome

Ix

  • Primary: High TSH low T4
  • Secondary: Low TSH Low T4
  • Sick euthyroid syndrome: Low TSH Low T4

Management

  • Primary: levothyroxine to replace the underlying deficiency.
  • starting dose of levothyroxine should be lower in elderly patients and those with ischaemic heart disease.
  • 25 in elderly 50-100mg in normal
  • monitor after 8-12 weeks
  • women with established hypothyroidism who become pregnant should have their dose increased ‘by at least 25-50 micrograms levothyroxine’ due to the increased demands of pregnancy
  • Interaction with iron and calcium carbonate (levothyroxine less available) so ask patients to go easy with spinach and milk and if they do then eat thyroxine 4hr apart

Side-effects of thyroxine therapy

  • hyperthyroidism: due to over treatment
  • reduced bone mineral density
  • worsening of angina
  • atrial fibrillation
18
Q

Hashimotos Thyroditis

chronic autoimmune thyroiditis leading to hypothyroidism

A

Signs

  • features of hypothyroidism (weight gain, cold intolerance, constipation, dry, non pitting oedema)
  • goitre: firm, non-tender
  • anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies

Associations

other autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo
Hashimoto’s thyroiditis is associated with the development of MALT lymphoma

19
Q

Thyroglossal cyst

Differential for goitre

A

Features
* usually midline, between the isthmus of the thyroid and the hyoid bone
* moves upwards with protrusion of the tongue
* may be painful if infected
* common in <20y

20
Q

Thyroid Cancer

4 main types

Features of hyperthyroidism or hypothyroidism are not commonly seen in patients with thyroid malignancies as they rarely secrete thyroid hormones

A

Papillary

  • 70%
  • common in Young females

Follicular

  • 20%
  • split in to Adenoma & carcinoma
  • Adenoma: Usually present as a solitary thyroid nodule
  • Carcinoma: Vascular invasion predominates

Management of papillary and follicular cancer

  • total thyroidectomy
  • followed by radioiodine (I-131) to kill residual cells
  • yearly thyroglobulin levels to detect early recurrent disease

Medullary

  • 5%
  • Cancer of parafollicular (C) cells, secrete calcitonin, part of MEN-2
  • Serum calcitonin levels often raised
  • Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.

Anaplastic

  • difficult to treat
  • pressure symptoms
  • Most common in elderly females
  • Local invasion is a common feature
  • Treatment is by resection where possible, palliation may be achieved through isthmusectomy and radiotherapy. Chemotherapy is ineffective.

Pressure Symptoms Due to the aggressive nature of anaplastic thyroid cancer, pressure symptoms can be more pronounced and may include severe difficulty swallowing (dysphagia), difficulty breathing (dyspnea), a feeling of fullness or pressure in the neck, hoarseness, or changes in voice quality

21
Q

Cushing’s Syndrome

Cushing syndrome is a condition marked by excessive cortisol levels, with Cushing’s disease specifically denoting this syndrome caused by a pituitary adenoma producing excess adrenocorticotropic hormone (ACTH).

A

Cushing’s syndrome refers to the features of prolonged high levels of glucocorticoids in the body.

Feautures

  • Round face (known as a “moon face”)
  • Central obesity
  • Abdominal striae (stretch marks)
  • Buffalo Hump on back
  • Proximal Myopathy
  • Male pattern facial hair in women (hirsutism)
  • Easy bruising and poor skin healing

Causes of Cushing’s Syndrome: CAPE

  • C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
  • A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
  • P – Paraneoplastic syndrome from small cell lung cancer
  • E – Exogenous steroids (patients taking long-term corticosteroids)

Investigations

  • overnight (low-dose) dexamethasone suppression test
  • A hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance.

Management

  • Trans-sphenoidal (through the nose) removal of pituitary adenoma
  • Stop Steroids but taper it instead of stopping abruptly

Pseudo-Cushing’s

  • mimics Cushing’s
  • often due to alcohol excess or severe depression
22
Q

Acromegaly

excess growth hormone secondary to a pituitary adenoma in over 95% of cases. A minority of cases are caused by ectopic GHRH or GH production by tumours e.g. pancreatic.

A

Features

  • coarse facial appearance, spade-like hands, increase in shoe size
  • large tongue, prognathism, interdental spaces
  • excessive sweating and oily skin: caused by sweat gland hypertrophy
  • Galactorrhoea
  • headaches, bitemporal hemianopia
  • Complications: Cardiomyopathy, HTN, Diabetes

Investigations

  • Serum IGF-1 levels first line
  • Oral Glucose Tolerance test done secondary to confirm diagnosis (GH above 2)

Management

  • Trans-sphenoidal surgery is the first-line treatment for acromegaly i
  • if contrainicated
  • octreotide (somatostatin analogue): inhibits GH
  • External irradiation is sometimes used for older patients or following failed surgical/medical treatment

6% of patients have MEN-1

The growth hormone suppression test involves consuming a 75g glucose drink with growth hormone tested at baseline and 2 hours following the drink. The glucose should suppress the growth hormone level. Failure to suppress growth hormone indicates acromegaly.

23
Q

primary hyperaldosteronism

Conn’s Syndrome: primary hyperaldosteronism caused by adrenal adenoma

Hyperaldosteronism refers to high levels of aldosterone. Conn’s syndrome refers to an adrenal adenoma producing too much aldosterone.

A

Causes

  • bilateral idiopathic adrenal hyperplasia - most common
  • adrenal adenoma: 20-30% of cases
  • familial hyperaldosteronism

Features

  • Hypertension
  • hypokalaemia - muscle weakeness
  • metabolic alkalosis

Ix

  • treatment resistant hypertension warrants ix for primary hypealdosteronism
  • plasma aldosterone/renin ratio is the first-line investigation (high aldo + low renin)
  • high-resolution CT abdomen and adrenal vein sampling used for source
  • Normal CT = adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia

Management

  • adrenal adenoma: surgery (laparoscopic adrenalectomy)
  • bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
24
Q

Addison’s Disease

Primary Hypoadrenalism

Autoimmune destruction of the adrenal glands is the most common cause of primary hypoadrenalism in the UK, accounting for 80% of cases.
This is termed Addison’s disease

other causes of hypoadrenalsim

  • tuberculosis
  • metastases (e.g. bronchial carcinoma)
  • HIV
A
  • reduced cortisol and reduced aldosterone

Features

  • lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
  • hyperpigmentation (especially palmar creases) - bronze
  • vitiligo
  • loss of pubic hair in women
  • hypotension
  • hypoglycaemia
  • hyponatraemia and hyperkalaemia may be seen
  • Crisis: collapse, shock, pyrexia

Ix

  • ACTH stimulation test (short Synacthen test)
    Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug
  • an ACTH stimulation test is not readily available (e.g. in primary care) then sending a 9 am serum cortisol can be useful:
    Under 500ml warrants synachthen test

Management

  • both glucocorticoid and mineralocorticoid replacement therapy
  • Hydrocortisone - 2/3times daily given mostly earlier on
  • Fludrocortisone
  • steroid card issued
  • patients should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis

Management of intercurrent illness

  • in simple terms the glucocorticoid dose should be doubled, with the fludrocortisone dose staying the same

Addisonian crisis

Causes

  • sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
  • adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
  • steroid withdrawal

Management

  • hydrocortisone 100 mg im or iv
  • 1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
  • continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
  • oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
25
Q

2ndry Hypoadrenalism

A

Secondary adrenal insufficiency results from inadequate adrenocorticotropic hormone (ACTH) and a lack of stimulation of the adrenal glands, leading to low cortisol. This is the result of loss or damage to the pituitary gland. Secondary adrenal insufficiency can be due to:

  • Tumours (e.g., pituitary adenomas)
  • Surgery to the pituitary
  • Radiotherapy
  • Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
  • Trauma
26
Q

Diabetes Insipidus

A lack of antidiuretic hormone (cranial diabetes insipidus)
A lack of response to antidiuretic hormone (nephrogenic diabetes insipidus)

A

Cranial DI

  • Causes: idiopathic, post head injury, pituitary surgery, haemochromatosis, DIDOMAD

Nephrogenic DI

  • Causes: Genetics, hypercalcaemia, hypokalaemia, Lithium (reduced kidnys response to ADH)

Features

  • Polydipsia
  • Polyuria

Ix

  • high plasma osmolality, low urine osmolality - dilute urine
  • a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
  • Water Deprivation test
    patient avoids all fluids for up to 8 hours before the test (water deprivation). After water deprivation, urine osmolality is measured. If the urine osmolality is low, synthetic ADH (desmopressin) is given. Urine osmolality is measured over the 2-4 hours following desmopressin.

Management Nephrogenic

  • Thiazides
  • Low salt/protein diet

Management Cranial

  • Desmopressin

Water Deprivation results

  • polydipsia: High Urine Osmolality
  • Cranial Low Urine Osmolality - corrected after Desmopressin
  • Nephrogenic: Low Urine Osmalilty - not corrected after Desmopressin
27
Q

SIADH Secretion

Syndrome of inappropriate ADH secretion

hyponatraemia secondary to the dilutional effects of excessive water retention

A
  • Excessive release of antidiuretic hormone (ADH), also known as vasopressin -> leads to water retention, volume expansion, and dilutional hyponatraemia

Causes

  • Small Cell Lung cancer
  • Stroke, SAH
  • TB, Pneumonia
  • Sulfonylureas, SSRI, TCA, Carbamazipene

Ix

  • Urine osmolality: Urine osmolality is inappropriately high (>100 mOsm/kg) in relation to serum osmolality, as the kidneys should normally dilute urine in the setting of low serum osmolality.
  • Urine sodium concentration: Urine sodium concentration is typically high (>40 mmol/L) due to the action of ADH on the renal tubules.

management

  • fluid restriction
  • correction must be done slowly to avoid precipitating central pontine myelinolysis
  • demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH

this increase in body fluid volume does not lead to the expected signs of fluid overload, such as oedema or hypertension, because the excess fluid is uniformly distributed throughout all body fluid compartments.

28
Q

Hyperparathyroidism

Primary hyperparathyroidism is caused by excess secretion of PTH resulting in hypercalcaemia.

A

Causes

  • 85%: solitary parathyroid adenoma

Features

  • Around 80% of patients are asymptomatic and are diagnosed on routine blood tests
  • polydipsia, polyuria
  • depression
  • anorexia, nausea, constipation
  • peptic ulceration
  • pancreatitis
  • bone pain/fracture
  • renal stones
  • hypertension

Ix

  • Raised Ca, Raised PTH, Reduced K
  • pepperpot skull on Xray

Management

  • the definitive management is total parathyroidectomy
  • not suitable for surgery: calcimimetic ‘mimics’ the action of calcium on tissues by allosteric activation of the calcium-sensing receptor

Bones, Stones, abdo Groans & psychic moans

29
Q

Hypoparathyroidism

Primary hypoparathyroidism

  • decrease PTH secretion
  • e.g. secondary to thyroid surgery
  • low calcium, high phosphate
  • treated with alfacalcidol
A

Features

  • tetany: muscle twitching, cramping and spasm
  • perioral paraesthesia
  • Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
  • Chvostek’s sign: tapping over parotid causes facial muscles to twitch
30
Q

Hypercalcaemia

Causes

  • sarcoidosis
    other causes of granulomas may lead to hypercalcaemia e.g. tuberculosis and histoplasmosis
  • vitamin D intoxication
  • acromegaly
  • thyrotoxicosis
A
  • ‘bones, stones, groans and psychic moans’
  • corneal calcification
  • shortened QT interval on ECG
  • hypertension

Management

  • initial management of hypercalcaemia is rehydration with normal saline,
31
Q

Hypocalcaemia

A
  • tetany: muscle twitching, cramping and spasm
  • perioral paraesthesia
  • if chronic: depression, cataracts
  • ECG: prolonged QT interval
  • Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
  • Chvostek’s sign: tapping over parotid causes facial muscles to twitch

Management

  • severe hypocalcaemia (e.g. carpopedal spasm, tetany, seizures or prolonged QT interval) requires IV calcium replacement
    the preferred method is with intravenous calcium gluconate, 10ml of 10% solution over 10 minutes
32
Q

Hyperkalaemia

Causes

  • acute kidney injury
  • drugs: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin
  • metabolic acidosis
  • Addison’s disease
  • rhabdomyolysis
  • massive blood transfusion
A

ECG

  • Peaked or ‘tall-tented’ T waves (occurs first)
  • Loss of P waves
  • Broad QRS complexes
  • Sinusoidal wave pattern

Management

  • Stabilisation of the cardiac membrane
  • IV calcium gluconate
  • does NOT lower serum potassium levels

Short-term shift in potassium from extracellular (ECF) to intracellular fluid (ICF)
* compartment
* combined insulin/dextrose infusion
* other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium

33
Q

Hypokalaemia

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 diabetic ketoacidosis
A

Features

  • muscle weakness, hypotonia
  • hypokalaemia predisposes patients to digoxin toxicity - care should be taken if patients are also on diuretics

ECG features

  • U waves
  • small or absent T waves
  • prolonged PR interval
  • ST depression
  • long Qt
34
Q

Prolactinoma

size (a microadenoma is <1cm and a macroadenoma is >1cm)

A
  • Prolactinomas are a type of pituitary adenoma, a benign tumour of the pituitary gland.

Features
In Women

  • amenorrhoea (absence of periods)
  • infertility
  • galactorrhoea
  • osteoporosis

In Men

  • impotence
  • loss of libido
  • galactorrhoea - milk from nipples

Both

  • visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
  • Headaches
  • hypopituitarism

Diagnosis

  • MRI

Management

  • dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland
  • Surgery in failed medical management
35
Q

Phaechromocytoma

A
  • tumour of the adrenal glands that secretes unregulated and excessive amounts of catecholamines (adrenaline).

Presentation

  • Anxiety
  • Sweating
  • Headache
  • Tremor
  • Palpitations
  • Hypertension
  • Tachycardia

Diagnosis

  • Plasma free metanephrines
  • 24-hour urine catecholamines
  • CT/MRI for tumour

Management

  • Alpha blockers (e.g., phenoxybenzamine or doxazosin)
  • Beta blockers, only when established on alpha blockers
  • Surgical removal of the tumour

Adrenaline is produced by the chromaffin cells in the medulla (middle part) of the adrenal glands. Adrenaline is a catecholamine hormone that stimulates the sympathetic nervous system and is responsible for the “fight or flight” response.

A phaeochromocytoma is a tumour of the chromaffin cells that secretes unregulated and excessive amounts of adrenaline. In patients with a phaeochromocytoma, the adrenaline tends to be secreted in bursts, giving intermittent symptoms.

36
Q

Carcinoid Tumour

A
  • Usually occurs when metastases are present in the liver and release serotonin into the systemic circulation

Features

  • flushing (often the earliest symptom)
  • diarrhoea
  • bronchospasm
  • hypotension
  • right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
  • other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome

Investigations

  • urinary 5-HIAA
  • plasma chromogranin A y

Management

  • somatostatin analogues e.g. octreotide
  • for diarrhoea: cyproheptadine may help

Main Conditions (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions