Flashcards
Endocrine Week Qs
Cards in this deck (92)
- 1What would blood tests show in primary hypothyroidsim?Low T3/4
Raised TSH/ TRH - 2Causes of Hyponatraemia?- SIADH (euvolaemic hyponatraemia)
- Adrenal Crisis (hyponatraemia and hypoglycaemia)
- Renal loss
- Extra renal loss (diarrhoea and vomiting)
- Excess water intake
- Cardiac failure
- Nephrotic syndrome
- Hypovolaemia - 3What type of hyponatraemia is SIADH?Dilutional
Euvolaemic
Inability to dilute urine (raised urine osmolality)
Low plasma osmolality. - 4Symptoms of hyponatraemia?- Headache
- Confusion
- Lethargy
- Anorexia
- Seizure
- Reduced GCS
- Myoclonus
- Hyporeflexia - 5Treatment of SIADHFluid restrict = 500/ 1000MLs in 24hrs
Not used in subarach because it risks lowering BP which can cause vasospasm and infarction - 6What is the condition patients with a rapid drop in NA in severe hyponatraemia are at risk of?Cerebral oedema
Hypertonic saline and furosemide can be used. - 7What is pituitary apoplexy and how would it present?- Pituitary emergency - infarction/ haemaorrhage of anterior pituitary
- Presents similar to subarach + visual symptoms
- Managed with fluids and IV steroids - 8Describe the layers of the adrenal glands?Outer layer = mineral corticoids (aldosterone) - glomerulosa
Middle layer = glucocorticoids (cortisol) - fasiculata
Inner layer = adrenal adrogens - reticularis
Medulla = epinephrine and norepinephrine - 9What is the difference between primary and secondary hypocortisol/ adrenal insufficiency?Primary = failure in adrenal glands. Blood tests will show low cortisol and raised ACTH (Addisons)
Secondary = failure in hypothalamus or pituitary. Bloods will show low cortisol and low ACTH/ normal. - 10What test is used to determine if low cortisol is due to Addisons or secondary adrenal insufficiency cause ?Synacthen Test - Patients with primary Addisons will not respond to this (subnormal response). In normal patients / secondary this should stimulate the adrenal glands to produce cortisol
- 11True or False, patients with secondary cause of hypocortisol / secondary adrenal insufficiency are pigmented?False, patients with primary Addisons are pigmented due to raised ACTH which also comes with melanin.
- 12True or False, patients with Adddisons usually need replacement of mineralcorticoids and glucocorticoids?True because primary adrenal insufficiency is usually due to damage of the whole adrenal gland.
- 13Symptoms of Adrenal Crisis- Postural hypotension
- Hypoglycaemia
- Electrolyte disturbance (low Na+ and high K+)
- Malaise,
- Abdopain
- Weight loss - 14What is an adrenal crisis?Decompensated adrenal insufficiency
Treated with IM/IV steroids.
Can occur due to negative feedback of someone on long term steroid use who suddenly stops taking their steroids.
Hyponatraemia and Hyppoglycaemia - 15What is the difference between Cushings Disease and Cushings Syndrome?Disease = due to ACTH producing tumour in pituitary
Syndrome = due to other causes - 16Symptoms of Cushings?- Moon face
- Red face (plethora)
- Acne
- Hirtuism
- Diabetes/ impaired glucose tolerance
- Striae
- Weight gain
- Bruising
- Skin thinning
- proximal muscle weakness
- HTN - 17Causes of HTN- Cushings
- SIADH
- Conns
- Hyperthyroidism
- Hypothyroidism
- Phaechromocytoma
- Hyperparathyroidism
- Acromegaly - 18How to diagnose cushing?- Overnight dexamethaosne supression test. If cortisol levels stay high then the person has cushings.
- Urine free cortisol measurements and midnight cortisol measurements. - 19Causes of adrenal insufficiency / Addisons?- TB
- Autoimmune
- Waterhouse-Friderichsen Syndrome (adrenal haemorrhage secondary to meningococcal sepsis)
- Malignancy in adrenal glands - 20What are the causes of Cushings?- ACTH secreting pituitary adenoma (high levels of ACTH)
- Too many steroids
- Adrenal tumour
- Ectopic ACTH/ CRH secreting tumours - 21Difference between primary and secondary hypothyroidism?Primary = Failure of thyroid (low T3/ T4) and raised TSH
Secondary = failure of pituitary (low T3/T4) and low TSH - 22How is hypothyroidism treated?With levothyroxine.
Aim for treatment would be TSH middle of reference range in primary and T4 upper end of normal and normal T3 in secondary - 23What is a myxodema coma?Decompensated hypothyroidism. Could be due to poor compliance or failure to absorb levothyroxine. Presents with decreased mental status, hypothermia, bradycardia - treat by rewarming
- 24Causes of hyperthyroidism- Autoimmune = graves
- Toxic nodule
- Toxic multinodular goitre - 25Causes of secondary hyperthyroidism?- TSH excess
- Erratic taking of thyroid hormone
- Thyroid hormone resistance - 26What is a Thyroid storm?Decompensated hyperthyroidism. Hyperpyrexia, tachycardia, HTN, vomiting, diarrhoea.
Poor compliance, radioactive iodine surgery, infection - 27True or False pregnancy and amioderone can cause hyperthyroidism?True
- 28Causes of thyrotoxicosis?Occur without hyperthyroidism
e.g. thyroiditis - post infection/ inflammation (De Quervains) - painful goitre
Exogenous ingestion - 29What blood tests would show in subclinical hyperthroidism ?Low TSH and normal T4 and T3
- 30What happens in Hashimotos Thyroiditis?It is an autoimmune condition that causes hypothyroidism due to chronic autoimmune destruction of the thyroid gland.
Can produce a firm rubbery goitre or an atrophic gland.
Associated with Diabetes, Downs and Turners - 31What antibodies can be detected in autoimmune thyroid conditions?TRAB = graves
Anti- TPO = hashimotos and graves - 32What is Conns Disease?It is a condition of excess aldosterone production from the adrenal glands - glomerulosa (primary aldosteronism)
- 33Screening test for Conns?aldosterone:renin ratio
Diagnosed by measuring serum aldosterone, 24hr urinary aldosterone secretion - 34Causes of primary hypogonadism?- Klinefelters = XXY
- Turners = X
- Infection, haemochromatosis, drugs, infection
- Raised LH/ FSH and low sex steroids - 35What hormone is involved in spermatogenesis and follicle developement?FSH
- 36What hormone is involved in testosterone production and ovulation?LH
- 37What are the causes of secondary hypogonadism?Opiates and obesity and drugs
Low LH/FSH - 38Prolactin is produced by the anterior pituitary, which hormone is produced by the hypothalamus to make this happen?Dopamine and SRIF/ somatostatin (growth hormone inhibiting hormone) both inhibit production of prolactin
Oestrogen positvely feedsback on this - 39What is the pathway that leads to acromegaly?GHRH secreted by hypothalamus stimulates the pituitary to secrete GH which stimulates the liver to produce IGF-1
- 40What two hormones are produced by the posterior pituitary?ADH and oxytocin
- 41How are patients managed with adrenal crisis?IM/ IV steroids and IV fluid
- 42What are the symptoms of hyponatraemia?- Non
- Headache
- Nausea
- Vomiting
- Muscle cramps
- Lethargy
- Disorientation
- Seizures
- Coma
- Cerebral oedema
- Death - 43What drugs can cause SIADH?- Anticonvulsants
- Antidepressants
- PPis
- Painkillers (opiates and Nsaids) - 44True or false, hyperglycaemia can cause pseudohyponatraemia?True
- 45How to know if hyponatraemia is emergency? How is it treated?Impaired neurological awareness
Treat with hypertonic saline
Aim for sodium increase 8-10mmol in 24hrs - 46What is hypotonic hyponatraemia?AKA hypo-osmolar hyponatraemia (dilute extracellular fluid)
- 47Which patients with hyponatraemia do you fluid restrict?- Patients with SIADH
- Patients with hypervolaemia. - 48What ECG changes can be present in patients with hypokalaemiaPR interval prolongation
Twave flattening
ST wave depression
U waves
Torsades de Pointes
Supraventricular tachycardia - 49What can cause potassium efflux out of cells?Acidosis
A-Adrenergic Agonists
Exercise - 50What can cause potassium influx into cells?Insulin
Alkalosis
B adrenergic agonists - 51True or False, Conns causes hyperkalaemia?False, causes hypokalaemia
- 52What is Gitelman's syndrome- Autosomal Recessive (family history)
- Causes defect in Na+/Cl- channel
- Increase in Na+ at distal tubule = aldosterone release and hypokalaemia - 53What is a phaeochromocytoma?Tumour of the adrenal glands
Test = metanephrine levels in blood. - 54What lab results would you expect in Conns? BP K+ Acid/alkalosis- HTN
- Hyperkalaemia
- Alkalosis
- Suppressed renin
- Elevated or inappropriately normal Aldosterone - 55What electrolyte needs to be corrected before testing for Conns?Correct the K+
Before doing aldosterone:renin ratio
Hypokalaemia can mask by inhibiting aldosterone production - 56Primary Vs Secondary AldosteronismSIADH = different disease
Secondary Aldosteronism = High aldosterone due to kidney hypoperfusion
Primary = adrenal glands producing too much aldosterone (e.g. adenoma = Conns), hyperplasia and carcinomas - 57What genes are associated with phaeochromocytomasMEN2
VHL
SDH
NF1 - 58What is the test for phaeochromocytomas?- Plasma metabolites
- 24hr urine collection
- Can be anywhere in torso (CT to check multiple tumours)
- Genetic testing needed - 59Test for primary aldosteronismSaline infusion test. To try and suppress aldosterone suppression
CT/ MRI
Adrenal vein sampling to localise source - 60Treatment of central diabetes insipidus?Desmopressin
- 61Causes of hypokalaemia?- Alkalosis
- Diuretics
- Malabsorption
- Magnesium depletion
- Conns
- Gitelmans Syndrome - 62Freatures of Hyperkalaemia on ECG?- Sinus bradycardia, slow AF
- Legnthened PR segments
- Loss of p waves
- Wide QRS
- Peaked T wavesf - 63What diseases can result from an adenoma / carcinoma of adrenal glands?Conns = primary aldosteronism
Cushings = rare - 64True or false - high cortisol can result in high levels of aldosterone? Causing conn's like disease?True
- 65What symptoms are associated with phaeochromocytomas?- Headaches
- Flushing
- Palpatations
- HTN
(emergency) - 66Test for nephrogenic vs Central diabetes insipidus?- Glucose levels = check for other diabetes
- Early morning osmolality = screen, if it is concentrated then not insipidus
- Hypertonic saline copeptine stimulation test is diagnostic (copeptine measured in replace of ADH) - normal = increased ADH, central = no increase in ADH, nephrogenic = symptoms/ polyuria + increase in ADH - 67What is the diagnostic test for diabetes?Symptoms + 1 abnormal glucose test
- >11.1 random plasma glucose
- Fasting >7
- Glucose tolerance > 11.1
- HBA1C >48
2 results in non symptomatic - 68In which patients should HBA1C not be used?- Not in children/ young people
- gestational diabetes
- Postnatal (2 months)
- Acute unwell
- Patients with recent med changes - 69What are the features of MODY?- Residual insulin secretion 3 yrs after type 1 diagnosis
- Young age at onset
- Lack of metabolic syndrome in people diagnosed with type 2
- No treatment needed - 70What are the features of glucokinase MODY?- Usually an incidental hyperglycaemia found in children
- Commonly in gestational diabetes
- Autosomal dominant
- Raised glucose persistant and fasting
- Causes threshold changes for insulin secretion. No microvascular complications - 71Features of transcription factor MODY?Genes = HNF1a = most common + HNF4a
Presents with normoglycaemic childhood worsening with age. Causes complications from high glucose.
HNF1b - similar to above but with pancreatic and genitourinary abnormalities. - 72True or false, patients with HNF1a and HNF4a MODY don't need insuline?True, patients with this type of transcription factor MODY are sensitive to low dose sulphonylureas so gliclazide and glibenclamide can be used first line
HNF1B need insulin - 73True or false, autoimmunity increases risk of type 1 diabetes?True
and HLA genes - 74What can be measured years after diabeties I diagnosis to confirm?- Cpeptide (produced with insulin)
Islet autoantibodies
GaAD antibody - 75How is gestational diabetes diagnosed?- 2 Hour oral glucose tolerance test
- 76How does the parathyroid gland control calcium levels?Parathyroid hormone is released from parathyroids when low blood calcium levels are detected
- Causes reabsobion of calcium from urine and activaition of Vt D (allows calcium absorption from the gut)
- Also causes bone resorption into blood
- Increases serum clcium - 77What is the difference between osteoblasts and osteoclasts?- Osteoclasts stick to bone and secrete acid that erode the bone causing resorption (released due to PTH)
- Osteoblasts fill in the gaps and repair. Turn into osteocytes - 78Symptoms of hypercalcaemia?Moans, groans, stones adn bones
- Anorexia
- Depression
- Confusion
- Polyuria
- Thirst
- Constipation
- Weakness - 79What is the commonest cause of hypercalcaemia?Primary hyperparathyroidism.
Due to benign solitary parathyroid adenoma, parathyroid hyperplasia, parathyroid carcinoma - 80What blood results would you expect in hyperparathyroidism?- Hypercalcaemia
- Low serum phosphate
- High boney alkaline phosphate
- Raised PTH or abnormally normal PTH
- Raised urinary calcium
- Metabolic acidosis - 81How is severe hypercalcaemia treated?IV bisphosphonates and fluids
- 82True or false, PTH is raised in patients with hypercalcamia caused by malignancy?False, PTHrp is raised
- 83What are the osteolytic malgniancies?Breast
Lung
Prostate - 84What is the most common cause of hypocalcaemiaVit D deficiency
Followed by hypoparathryoidism and drugs
Renal failure
Contrast - 85What blood results would you expect in hypoparathyroidism?- Low serum calcium
- High serum phophates
- Hypomagnesaemia
low PTH - 86Symptoms of hypercalcaemia?- Paraesthesia of mouth and fingers
- Muscle twitching and leg crams
- Laryngeal stridor
- papilloedema
- prolonged QTC - 87Where do fragility fractures occur?Hip
Vertebrae
Wrist (colles)
Fall from standing height or less - 88Osteoporosis vs Osteomalacia?Osteoporosis = reduced bone mass/ mineral density but normal structure + biochemistry
Osteomalacia = change in structure of bone due to loss of mineralised component and more osteoid (flexible) - 89What are some causes of secondary osteoporosis?- Malabsorption
- Hepatic or Renal disease
- Endocrine problems - 90Diagnosis of osteoporosis?- DXA scan
- Z score (BMD copared to population)
T-score = compared to race and sex - 91What T score would give a diagnosis of osteoporosis?Less than -2.5
between -1 and -2.5 i s osteopenia - 92True or false, osteomalacia has blood results of low calcium?True. Will show raised PTH and elevated alkaline phosphatase
Linked to lack of sunlight, lack of phophates and hepatic disease.
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- 4th YEAR Flashcards on Endocrine Week Qs, created by Wannie Chisala on 28/11/2019.
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