Brainscape's Knowledge GenomeTM

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


See full index

Finals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is addison’s disease

A

autoimmune destruction of the adrenal glands resulting in primary hypoadrenalism
results in low cortisol and low aldosterone

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

what are the symptoms of addison’s disease

A
  • symptoms:
    • lethargy
    • weakness
    • anorexia
    • nausea & vomiting
    • weight loss,
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the signs of addison’s disease

A
  • hyperpigmentation (especially palmar creases)
    • note that secondary adrenal insufficiency does not cause hyperpigmentation
  • vitiligo
  • loss of pubic hair in women
  • hypotension
  • hypoglycaemia
  • hyperkalaemia
  • hyponatraemia
  • addisonian crisis;
    • shock
    • collapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

non-autoimmune causes of hypoadrenalism

A
  • Primary causes
    • tuberculosis
    • metastases (e.g. bronchial carcinoma)
    • meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
    • HIV
    • antiphospholipid syndrome
  • Secondary causes
    pituitary disorders (e.g. tumours, irradiation, infiltration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

management of addison’s disease

A
  • need glucocorticoid and mineralocorticoid therapy
  • hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the first half of the day
  • fludrocortisone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

patient education in addison’s

A
  • emphasise importance of not missing dose of glucocorticoid
  • give injections of hydrocortisone to be administered in the case of crisis
  • if there is intercurrent illness:
    • double the glucocorticoid dose
    • keep fludrocortisone dose the same
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the definitive diagnostic investigation for addison’s

A

ACTH stimulation test (short Synacthen test). Plasma cortisol is measured before and 30 minutes after giving Synacthen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what addison’s investigations can you do if the synacthen test is unavailable

A
  • Adrenal autoantibodies such as anti-21-hydroxylase
  • 9am serum cortisol
    • > 500 nmol/l makes Addison’s very unlikely
    • < 100 nmol/l is definitely abnormal
    • 100-500 nmol/l should prompt a ACTH stimulation test to be performed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the associated electrolyte abnormalities of addison’s

A
  • hyperkalaemia
  • hyponatraemia
  • hypoglycaemia
  • metabolic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

causes of addisonian crisis

A
  • sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison’s, Hypopituitarism)
  • Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
  • steroid withdrawal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the management of addisonian crisis?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is waterhouse-friderichsen syndrome

A

Patients with meningococcal meningitis are at risk of Waterhouse-Friderichsen syndrome (adrenal insufficiency secondary to adrenal haemorrhage).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the most common cause of cushing’s sydnrome

A

steroid therapy

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

causes of cushing’s syndrome

A
  • ACTH dependent causes
    • cushing’s disease (80%) - ACTH secreting pituitary tumour causes adrenal hyperplasia
    • ectopic ACTH production (5-10%): e.g. small cell lung cancer is the most common causes
  • ACTH independent causes
    • steroid therapy
    • adrenal adenoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is pseudo cushings

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what test for cushing’s syndrome

A
  • overnight dexamethasone suppression test
    • if a patient has cushing’s syndrome they will not have their morning cortisol spike suppressed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do you find out if the cause of cushings is ACTH dependent or independent

A

9am and midnight plasma ACTH (and cortisol) levels. If ACTH is suppressed then a non-ACTH dependent cause is likely such as an adrenal adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is MODY

A

maturity onset diabetes of the young

A group of inherited disorders that result in relatively young patients developing symptoms similar to 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
19
Q

what is LADA

A

Latent autoimmune diabetes of adults

patients often diagnosed as having type two diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the diagnostic criteria for diabetes as they relate to fasting blood glucose and HbaA1c

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does metformin work, what are he main side effects and what are the contraindications

A
  • how does it work?
    • increases insulin sensitivity
    • decreases hepatic gluconeogenesis
  • what are the main side effects?
    • lactic acidosis
    • GI upset
  • what are the contraindications?
    • eGFR <30
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How do sulfonylureas work?

A

they stimulate the pancreatic beta cells to produce more insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is an example of a sulfonylurea

A

glipizide

gliclazide

glimepiride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the side effects of sulfonylureas

A

hypoglycaemia

weight gain

hyponatraemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how do Thiazolidinediones work

A

they are for treatment of diabetes

they promote adipogenesis and fatty acid uptake

e.g. pioglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is an example of a thiazolindinedione

A

pioglitazone is the only one available

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the side effects of pioglitazone

A

Weight gain
Fluid retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how do DPP-4 inhibitors work

A

they increase incretin levels which inhibit glucagon secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what do DPP-4 inhibitor drugs end in

A

-gliptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is an example of a dpp-4 inhibitor

A

sitagliptin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how do SGLT-2 inhibitors work

A

Inhibits reabsorption of glucose in the kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the main side effects of SGLT-2 inhibitors

A

urinary tract infections and weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what do the drug names of SGLT2 inhibitors end in

A

-gliflozin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is an example of an SGLT2 inhibitor

A

Dapagliflozin

Canagliflozin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how do GLP-1 antagonists work?

A

they are incretin mimetics and therefore they inhibit glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what do GLP-1 antagonist drugs end in

A

-tide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is an example of a GLP-1 antagonist

A

Dulaglutide

Exenatide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are the side effects of GLP-1 antagonists

A
  • subcut injections so side effects of sc injection
  • nausea
  • vomiting
  • pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

draw the flow chart of T2DM drug treatment

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

which antibodies may be present in T1DM

A
  • Anti-GAD
    • present in 80% T1DM patients
  • Islet cell antibodies (ICA)
    • presentin 70-80% T1DM patients
  • Insulin auto antibodies
    • found in over 90% of young children with T1DM but only 60% of older patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what are the diagnostic criteria for T1DM

A
  • fasting glucose greater than or equal to 7.0 mmol/l
  • random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

IF THE PATIENT IS ASYMPTOMATIC THEN THIS NEEDS TO BE DEMONSTRATED ON TWO SEPARATE OCCASIONS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

If there is ambiguity over whether it is T1DM or T2DM then what could you do

A

test fo c peptide and/or diabetes specific auto-antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how often should HbA1c be monitored in patients with T1DM and what should the target be

A
  • should be monitored every 3-6 months
  • adults should have a target of HbA1c level of 48 mmol/mol (6.5%) or lower
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the recommended blood glucose monitoring for T1DM

A
  • recommend testing at least 4 times a day, including before each meal and before bed
  • more frequent monitoring is recommended if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are the blood glucose targets for T1DM

A
  • 5-7 mmol/l on waking and
  • 4-7 mmol/l before meals at other times of the day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

when should you add metformin in T1DM

A

If BMI >25

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are the different types of insulin and what are their onset, peak and duration?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

two examples of rapid acting insulin

A
  • insulin aspart: NovoRapid
  • insulin lispro: Humalog
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

two examples of short acting insulin

A

Actrapid

Humulin S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

two examples of long-acting insulin

A
  • insulin determir (Levemir): given once or twice daily
  • insulin glargine (Lantus): given once daily
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

why is it important to rotate injection sites when adnministering insulin

A

to prevent lipodystrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

how do insulin pumps work

A

they deliver a continuous basal infusion and a patient-activated bolus dose at meal times.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what are the key sick day rules

A
  • increase blood glucose monitoring to four hourly
  • if struggling to eat then try sugary drinks
  • if taking oral hypoglycaemics then continue them even if you’re not eating much
    • the exception is metformin which should be stopped if the patient becomes dehydrated → renal function
  • keep a mobile phone by you
  • try and drink 3L of water per day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what are the most common precipitating factors in DKA

A

MI

Infection

Missed insulin doses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

diagnostic criteria for DKA

A
  • glucose > 11 mmol/l or known diabetes mellitus
  • pH < 7.3
  • bicarbonate < 15 mmol/l
  • ketones > 3 mmol/l or urine ketones ++ on dipstick
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

management of DKA

A
  • Fluid replacement
    • normal saline
    • once blood glucose <15 start infusion of 5% dextrose
  • Insulin 0.1 unit/kg/hr
    • their short acting insulin should be stopped
    • their long acting insulin should be continued
  • Electrolyte correction
    • if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

how do you decide what concentration of potassium to give patients when they need replacement in DKA

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is the amount of fluid that patients in DKA typically need and how fast would you give this

A

patients in DKA are usually deplete around 5-8 litres

see picture for how fast to replace this

note that younger adults may need slower infusions as they are at greater risk of cerebral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is the definition of DKA resolution

A
  • pH >7.3 and
  • blood ketones < 0.6 mmol/L and
  • bicarbonate > 15.0mmol/L
60
Q

a HbA1c of above what is diagnostic of diabetes

A

>48 (6.5%)

note this is only the case for T2DM

should also not be used in conditions relating to increased red cell turnover such as untreated iron deficiency anaemia

61
Q

what are the HbA1c targets in a patient with T2DM

A

48

if they are on sulfonylurea then their target should be 53

if they are not meeting their target then you can up the dose of their drugs but only add another drug when the HbA1c is >58

62
Q

if triple therapy in diabetes isn’t working you can start them on combination therapy with metformin, a sulfonylurea and a glucagon-like peptide1 (GLP1) mimetic if:

A
  • BMI >= 35 kg/m² or
  • BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
  • 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 month
63
Q

give an example of an intermediate acting insulin

A
  • isophane insulin
64
Q

what is the first line antihypertensive in patients with diabetes

A
  • ACE inhibitors or angiotensin II receptor blockers (ARB) are first-line
    • an ARB is preferred if the patient has a black African or African–Caribbean family origin
65
Q

what are the blood pressure targets for people with diabetes

A

same as for patients without diabetes

66
Q

how frequently should patients with diabetes be screened for diabetic foot disease

A

annually

67
Q

what are the two types of diabetic neuropathy

A

peripheral neuropathy and autonomic neuropathy

68
Q

analgesia for diabetic neuropathy

A
  • first-line treatment: duloxetine, duloxetine, gabapentin or pregabalin
  • if the first-line drug treatment does not work try one of the other 3 drugs
  • tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
  • topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
69
Q

how frequently should patiets with diabetes be screened for nephropathy and how

A
  • screened annually using urinary albumin:creatinine ratio (ACR)
  • should be an early morning specimen
  • ACR > 2.5 = microalbuminuria
70
Q

how do you manage diabetic nephropathy

A
  • dietary protein restriction
  • tight glycaemic control
  • BP control: aim for < 130/80 mmHg
  • ACE inhibitor or angiotensin-II receptor antagonist
    • should be start if urinary ACR of 3 mg/mmol or more
    • dual therapy with ACE inhibitors and angiotensin-II receptor antagonist should not be started
  • control dyslipidaemia e.g. Statins
71
Q

how to treat hypoglycaemia in a hospital setting

A
  • If the patient is alert, a quick-acting carbohydrate may be given (as above)
  • If the patient is unconscious or unable to swallow, subcutaneous or intramuscular injection glucagon may be given.
  • Alternatively, intravenous 20% glucose solution may be given through a large vein
72
Q

how to treat hypoglycaemia in the community

A
  • a quick-acting carbohydrate may be given: GlucoGel or Dextrogel.
  • A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
73
Q

what is the pathophysiology of hyperosmolar hyperglycaemic state

A
  • severe hyperglycaemia causes diuresis and loss of Na+ and k+
  • there is increased osmolarity of the blood and associated hyperviscosity
  • the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.
74
Q

clinical features of HSS

A
  • General: fatigue, nausea and vomiting
  • Neurological: papilloedema, decreased GCS, weakness, headaches
  • Cardiovascular: dehydration, hypotension
  • Haematological: hyperviscosity may lead to MI, stroke etc
75
Q

how do you estimate serum osmolality

A

serum osmolality = 2 x Na+ + glucose + urea

76
Q

what are the rough fluid losses in HSS

A

100 - 220 ml/kg (e.g. 10-22 litres in an individual weighing 100 kg).

77
Q

What fluid should you use in HSS

A

0.9% sodium chloride solution is already relatively hypotonic compared to the serum in someone with HHS. Therefore in most cases it is very effective at restoring normal serum osmolarity.

78
Q

Management of HSS

A
  • Normalise serum osmolality
  • Replace electrolyte loss
  • Normalise blood glucose

the above can be achieved with fluids - first line is 0.9% saline but if this is ineffective then switch to 0.45%

IV fluid replacement should aim to achieve a positive balance of 3-6 litres by 12 hours and the remaining replacement of estimated fluid losses within the next 12 hours.

insulin should NOT be used in the first instance unless there is significant ketonaemia or acidosis since rapid decline in blood glucose can be potentially harmful

RAPID CHANGES MUST BE AVOIDED - Complete normalisation of electrolytes and osmolality may take up to 72 hours.

79
Q

what is diabetes insipidus

A

either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI).

80
Q

what are the causes of cranial diabetes insipidus

A
  • idiopathic
  • post head injury
  • pituitary surgery
  • DIDMOAD is the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)
  • haemochromatosis
81
Q

causes of nephrogenic diabetes insipidus

A
  • genetic
  • lithium
    • makes the kidney less sensitive to adh
  • tubulointerstitial disease
82
Q

diagnosis of diabetes insipidus

A
  • high plasma osmolality, low urine osmolality
  • a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
  • water deprivation test
83
Q

how do you treat diabetes insipidus

A
  • nephrogenic diabetes insipidus:
    • thiazides
    • low salt/protein diet
  • central diabetes insipidus
    • desmopressin
84
Q

what are the causes of hypercalcaemia

A
  • two account for 90%
    • primary hyperparathyroidism
    • malignancy
      • commonest cause in hospitalised patients
  • other rare causes
    • sarcoidosis
      • and other causes of granuloma such as TB
    • acromegaly
    • vitamin d intoxication
85
Q

why do you get hypercalcaemia in malignancy

A
  • combination of:
    • bone mets
    • PTHrP released by tumours
    • myeloma
86
Q

What are the clinical features of hypercalcaemia

A
  • ‘bones, stones, groans and psychic moans’
  • corneal calcification
  • shortened QT interval on ECG
  • hypertension
87
Q

statin treatment in diabetics

A
  • atorvastatin 20 mg should be offered if type 1 diabetics who are:
    • older than 40 years, or
    • have had diabetes for more than 10 years or
    • have established nephropathy or
    • have other CVD risk factors
88
Q

statin treatment in ckd

A
  • atorvastatin 20mg should be offered to all patients with CKD
89
Q

when should you follow up patients on statins

A
  • in 3 months after starting a statin
  • repeat lipid profile
  • if the non-HDL cholesterol has not fallen by at least 40% increase atorvastatin dose to 80mg
90
Q

what is malignant hyperthermia

A
  • too much Ca2+ release from the sarcoplasmic reticulum
  • this causes muscle rigidity and hyperthermia
  • it is a genetic condition
    • autosomal dominant
  • it happens in response to anaesthetic agents such as suxamethonium and halothane
91
Q

how do you treat malignant hyperthermia

A

dantrolene - prevents Ca2+ release from the sarcoplasmic reticulum

92
Q

features of serotonin syndrome

A
  • neuromuscular excitation
    • rigidity
    • hyperreflexia
    • myoclonus
  • autonomic nervous system excitation
    • hyperthermia
    • sweating
  • altered mental state
    • confusion
    • agitation
93
Q

how do you treat serotonin syndrome

A
  • supportive including IV fluids
  • benzodiazepines
  • more severe cases are managed using serotonin antagonists such as cyproheptadine and chlorpromazine
94
Q

how do you tell the difference between serotonin syndrome and neuroleptic malignant syndrome

A
95
Q

what ecg changes may be seen in hypothermia

A
  • bradycardia
  • ‘J’ wave - small hump at the end of the QRS complex
  • first degree heart block
  • long QT interval
  • atrial and ventricular arrhythmias
96
Q

what temperatures constitute mild, moderate and severe hypothermia

A
  • Mild hypothermia: 32-35°C
  • Moderate or severe hypothermia: < 32°C
97
Q

dos and don’ts for hypothermia

A
  • Do:
    • Removing the patient from the cold environment and removing any wet/cold clothing,
    • Warming the body with blankets
    • Securing the airway and monitoring breathing,
    • If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient’s body
  • Don’t:
    • Don’t put the person into a hot bath
    • Don’t massage their limbs
    • Too rapid rewarming can lead to vasodilation and shock → cardiac arrest
98
Q

what is the cause of primary hyperparathyroidism

what hormone profile will you see and what clinical features will they have

A
  • cause
    • Mostly due to solitary adenoma
    • Sometimes multifocal disease occurs
    • Rarely parathyroid carcinoma in 1% or less
  • Clinical features
    • may be asymptomatic if mild
    • abdo pain
    • changes in emotional or cognitive state
  • hormone profile
    • high Ca2+
    • high PTH
    • low phosphate
    • Urine calcium : creatinine clearance ratio > 0.01
99
Q

what is the cause of secondary hyperparathyroidism

what hormone profile will you see and what clinical features will they have

A
  • Cause
    • it is the result of low calcium
    • almost always because of renal failure
  • Clinical features
    • muscle aches
    • cramps
    • spasms
    • tingling
    • may develop bone disease
  • Hormone profile
    • Ca2+ low (or normal)
    • PTH high
    • Phosphate high
100
Q

what is tertiary hyperparathyroidism

A

Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause

many will spontaneously resolve within the 12 months after surgery

101
Q

what is the hormone profile in tertiary hyperparathyroidism

A
  • Ca2+ (High)
  • PTH (Elevated)
  • Phosphate levels (Decreased)
  • Alkaline phosphatase (Elevated)
102
Q

symptoms of primary hyperparathyroidism

A

80% of patients are asymptomatic and are diagnosed on routine blood tests. The symptomatic features of primary hyperparathyroidism may be remembered by the mnemonic: ‘bones, stones, abdominal groans and psychic moans’:

103
Q

treatment for primary hyperparathyroidism

A
  • surgery - parathyroidectomy
  • conservative if they’re over 50, the hypercalcaemia is only mild and there’s no end organ damage
    • give cinacalcet, a calcimimetic
104
Q

what is primary hypoparathyroidism, what balance of calcium and parathyroid hormone would you see and what is the treatment

A
  • decrease PTH secretion
  • e.g. secondary to thyroid surgery*
  • low calcium, high phosphate
  • treated with alfacalcidol
105
Q

what are the symptoms of primary hypoparathyroidism

A
  • main symptoms are due to the symptoms of hypocalcaemia
    • 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
    • if chronic: depression, cataracts
    • ECG: prolonged QT interval
106
Q

what is pseudohypoparathyroidism, what balance of calicum, phosphate and PTH would you see

A
  • genetic
  • target cells being insensitive to PTH
  • associated with low IQ, short stature, shortened 4th and 5th metacarpals
  • low calcium, high phosphate, high PTH
107
Q

what is pseudopseudohypoparathyroidism

A

similar phenotype to pseudohypoparathyroidism with low IQ, short stature, shortened 4th and 5th metacarpals but with normal biochemistry

108
Q

what is first line bariatric surgery for obese patients

A

laparoscopic-adjustable gastric banding (LAGB)

offer to patients with a BMI of 30-39 early rather than as a last resort - especially if they have other conditions that are exacerbated by their obesity (such as diabetes)

109
Q

what is orlistat and how does it work

A

it is a drug for obesity - it is a pancreatic lipase inhibitor and therefore reduces absorption of fat in the diet

110
Q

what are the conditions for prescribing orlistat

A
  • BMI of 28 kg/m^2 or more with associated risk factors, or
  • BMI of 30 kg/m^2 or more
  • continued weight loss e.g. 5% at 3 months
  • orlistat is normally used for < 1 year
111
Q

what are the side effects of orlistat

A

faecal urgency/incontinence and flatulence

112
Q

when you change thyroxine dose when should you check TFTs

A

after 8-12 weeks

113
Q

what is the therapeutic goal when treating hypothyroidism

A

aim for normal range TSH

114
Q

what should women with established hypothyroidism do to their dose if they get pregnant

A

increase it due to the increased demands of pregnancy

The TSH should be monitored carefully, aiming for a low-normal value

115
Q

what are the side effects of thyroxine therapy

A
  • hyperthyroidism: due to over treatment
  • reduced bone mineral density
  • worsening of angina
  • atrial fibrillation
116
Q

non-hashimotos causes of hypothyroidism

A
  • Subacute thyroiditis (de Quervain’s)
    • associated with a painful goitre and raised ESR
  • Riedel thyroiditis
    • fibrous tissue replacing the normal thyroid parenchyma
    • causes a painless goitre
  • Postpartum thyroiditis
  • Drugs
    • lithium
    • amiodarone
  • Iodine deficiency
    • the most common cause of hypothyroidism in the developing world
117
Q

non-graves causes of hyperthyroidism

A
  • Toxic multinodular goitre
    • autonomously functioning thyroid nodules that secrete excess thyroid hormones
  • Drugs
    • amiodarone
118
Q

compare hypothyroid symptoms with hyperthyroid symptoms

A
119
Q

which abtibodies do you see in hashimotos thyroiditis

A

anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies

120
Q

clinical features seen in graves but not in other causes of thyrotoxicosis

A
  • eye signs (30% of patients)
    • exophthalmos
    • ophthalmoplegia
  • pretibial myxoedema
  • thyroid acropachy, a triad of:
    • digital clubbing
    • soft tissue swelling of the hands and feet
    • periosteal new bone formation
121
Q

which autoantibodies do you see in graves?

A
  • TSH receptor stimulating antibodies (90%)
  • anti-thyroid peroxidase antibodies (75%)
122
Q

treatment for graves

A
  • propanolol for symptoms
  • refer
  • antithyroid drugs such as carbimazole
    • either reducing regimen until they are euthyroid
    • or block and replace in combination with levothyroxine
  • radioiodine
    • second line
    • contraindicated in pregnancy
    • pregnancy avoided for 4-6 months following treatment
123
Q

what is the typical complication of carbimazole treatment

A
  • TSH receptor stimulating antibodies (90%)
  • anti-thyroid peroxidase antibodies (75%)
124
Q

what is the most important modifiable risk factor for thyroid eye disease

A

smoking

radioiodine treatment may make it worse

125
Q

features of thyroid eye disease

A
  • exophthalmos
  • conjunctival oedema
  • optic disc swelling
  • ophthalmoplegia
  • inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
126
Q

managment of thyroid eye disease

A
  • topical lubricants may be needed to help prevent corneal inflammation caused by exposure
  • steroids
  • radiotherapy
  • surgery
127
Q

how do you investigate a thyroid nodule for features of malignancy

A

ultrasound

128
Q

what is osteomalacia

A

softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content

if it happens in children it is referred to as rickets

129
Q

causes of osteomalacia

A
  • vitamin D deficiency
    • malabsorption
    • lack of sunlight
    • diet
  • chronic kidney disease
  • drug induced e.g. anticonvulsants
  • inherited: hypophosphatemic rickets (previously called vitamin D-resistant rickets)
  • liver disease: e.g. cirrhosis
130
Q

features of osteomalacia

A
  • bone pain
  • fractures
  • proximal myopathy - could lead to waddling gait
131
Q

treatment for osteomalacia

A
  • vitamin D supplmentation
    • a loading dose is often needed initially
  • calcium supplementation if dietary calcium is inadequate
132
Q

what are the causes of hypopituitarism

A
  • compression of the pituitary gland by non-secretory pituitary macroadenoma (most common)
  • pituitary apoplexy
  • Sheehan’s syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage
  • hypothalamic tumours e.g. craniopharyngioma
  • trauma
  • iatrogenic irradiation
  • infiltrative e.g. haemochromatosis, sarcoidosis
133
Q

clinical features of low ACTH from hypopituitarism

A
  • tiredness
  • postural hypotension
134
Q

clinical features of low FSH and LH from hypopituitarism

A
    • amenorrhoea
      • infertility
      • loss of libido
135
Q

what is pituitary apoplexy

A

Sudden enlargement of a pituitary tumour (usually non-functioning macroadenoma) secondary to haemorrhage or infarction.

136
Q

what are the features of pituitary apoplexy

A
  • sudden onset headache similar to that seen in subarachnoid haemorrhage
  • vomiting
  • neck stiffness
  • visual field defects: classically bitemporal superior quadrantic defect
  • extraocular nerve palsies
  • features of pituitary insufficiency
    • e.g. hypotension/hyponatraemia secondary to hypoadrenalism
137
Q

what is the typical visual field defect with pituitary apoplexy

A

bitemporal superior quadrantic defect

138
Q

how do you diagnose pituitary apoplexy

A

MRI

139
Q

What is the management of pituitary apoplexy

A
  • urgent steroid replacement due to loss of ACTH
  • careful fluid balance
  • surgery
140
Q

what are pituitary adenomas

A

benign tumours of the pituitary gland, common (10% of people), mostly asymptomatic - prolactinoma is the most common type

141
Q

what is the difference between a pituitary microadenoma and a pituitary macroadenoma

A

microadenoma is <1cm and a macroadenoma is >1cm

142
Q

which are the most common types of pituitary adenoma

A
  • prolactinoma (most common)
  • non-secreting adenomas are the next most common
  • then GH secreting
  • then ACTH secreting adenomas
143
Q

what is the first line treatment for prolactinomas

A

bromocriptine (dopamine agonist decreases prolactin secretion)

trans sphenoidal surgery if bromocriptine not tolerated

144
Q

what surgery for pituitary adenomas

A

transsphenoidal transnasal hypophysectomy

145
Q

why does magnesium affect calcium

A

Magnesium is required for both PTH secretion and its action on target tissues. Hypomagnesaemia may both cause hypocalcaemia and render patients unresponsive to treatment with calcium and vitamin D supplementation.

146
Q

in hyperparathyroidism, refer for surgery if

A
  • Any of the following:
    • Symptoms of hypercalcaemia (e.g. thirst, polyuria, constipation)
    • End-organ disease (renal calculi, fragility fractures or osteoporosis)
    • Corrected serum calcium of 2.85 mmol/L or above
147
Q

what is De Quervain’s thyroiditis

A

aka subacute thyroiditis - occurs following viral infection and typically presents with hyperthyroidism.

  • There are typically 4 phases;
    • phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
    • phase 2 (1-3 weeks): euthyroid
    • phase 3 (weeks - months): hypothyroidism
    • phase 4: thyroid structure and function goes back to normal

Finals (19 decks)

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