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

Adrenocortical axis

A 
Hypothalamus
         I
      CRH
         I
Anterior Pituitary
         I
     ACTH
         I
Adrenal gland
         I
    Cortisol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Primary adrenal insufficiency

Pathophysiology and examples

A
  • Adrenal glands themselves are damaged, resulting in a reduction in secretion of cortisol and aldosterone
  • Most common cause is autoimmune
  • Example: Addisons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Secondary adrenal insufficiency

Pathophysiology and examples

A
  • Result of inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release
  • Due to loss or damage of the pituitary gland
  • Examples: pituitary surgical removal, infection, loss of blood flow, radiotherapy
  • Sheehan’s syndrome: massive blood loss during childbirth leads to pituitary gland necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Tertiary adrenal insufficiency

Pathophysiology and examples

A
  • Result of inadequate CRH release by the hypothalamus
  • Usually the result of long term oral steroids (>3 weeks) causing suppression of hypothalamus
  • When exogenous steroids are suddenly withdrawn, the hypothalamus does not ‘wake up’ fast enough and endogenous steroids are not adequately produced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is released by the anterior pituitary gland?

A
  • Thyroid stimulating hormone (TSH)
  • Adrenocorticotropic hormone (ACTH)
  • Follicle stimulating hormone (FSH) and luteinising hormone (LH)
  • Growth hormone (GH)
  • Prolactin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is released by the posterior pituitary gland?

A
  • Oxytocin

- Antidiuretic hormone (ADH)

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

Diabetes

What is secreted by alpha cells

A

Glucagon

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

Diabetes

What is secreted by beta cells

A

Insulin

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

Diabetes

What is secreted by D-cells

A

Somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diabetes

What is secreted by PP/F cells

A

Pancreatic polypeptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where are alpha- and beta- cells?

A

Islets of Langerhans in the pancreas

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

Basic pathology of T1DM

A

Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system
This results in an absolute deficiency of insulin resulting in raised glucose levels
Patients tend to develop T1DM in childhood/early adult life and typically present unwell, possibly in diabetic ketoacidosis

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

Basic pathology of T2DM

A

This is the most common cause of diabetes in the developed world. It is caused by a relative deficiency of insulin due to an excess of adipose tissue. In simple terms there isn’t enough insulin to ‘go around’ all the excess fatty tissue, leading to blood glucose creeping up.

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

Diagnosis of diabetes

A

Symptomatic AND one of:

  • Fasting glucose > 7.0 mmol/L
  • Random glucose > 11.1 mmol/L (or after 75 g OGTT after 2 hrs)

Asymptomatic:
- Above criteria but on two separate occasions

HbA1c:
- > 48 mmol/mol = diagnostic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diabetes

Why do you get polydipsia and polyuria

A

Osmotic effect of water being ‘dragged’ out of body due to excess blood glucose being excrete in the urine (glycosuria)

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

What can cause a misleading HbA1c result?

A

Increased red cell turnover

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

DKA

Features

A
  • Abdominal pain
  • Polyuria, polydipsia, dehydration
  • Kussmaul respiration (deep hyperventilation)
  • Acetone-smelling breath (‘pear drops’ smell)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

T1DM

Use of HbA1c

A
  • Not as useful in patients with possible/suspected diagnosis of T1DM as it may not accurately reflect a recent rapid rise in serum glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

T1DM

C-peptide

A
  • Levels are typically LOW in T1DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Diabetes

Autoantibodies

A
  • Antibodies to glutamic acid decarboxylase (anti-GAD): 80% T1DM
  • Islet cell antibodies (ICA, against cytoplasmic proteins in the beta cells): 70-80% T1DM
  • Insulin autoantibodies (IAA): 90% of young children with T1DM and 60% of older patients
  • Insulinoma-associated-2 autoantibodies (IA-2A)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

T1DM

Classic presentations

A
  • Ketosis
  • Rapid weight loss
  • Age of onset below 50 years
  • BMI below 25 kg/m²
  • Personal and/or family history of autoimmune disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How to differentiate T1DM and T2Dm if in doubt?

A
  • Autoantibodies

- C-peptide

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

T2DM

Use of HbA1c

A
  • > 48 diagnostic of T2DM

- < 48 does not necessarily exclude T2DM

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

Conditions where HbA1c may not be used for diagnosis

A
  • Haemoglobinopathies
  • Haemolytic anaemia
  • Untreated iron deficiency anaemia
  • Suspected gestational diabetes
  • Children
  • HIV
  • Chronic kidney disease
  • People taking meds causing hyperglycaemia (e.g. corticosteroids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Impaired fasting glucose

A

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)

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

Impaired glucose tolerance

A

Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l

People with IFG should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn’t have diabetes but does have IGT

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

Hypertensive management in diabetes

Targets

A

Age < 80 yrs:

  • Clinic 140/90
  • ABPM 135/85

Age > 80 yrs

  • Clinic 150/90
  • ABPM 145/85
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hypertensive management in diabetes

1st line

A
  • ACE-I/ARB due to renoprotective effect in diabetes
  • ARB preferred for black African or African-Caribbean diabetic patients
  • Further management reverts back to that of non-diabetic patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Beta-blockers in diabetes

A
  • The routine use of beta-blockers in uncomplicated hypertension should be avoided, particularly when given in combination with thiazides
  • They may cause insulin resistance, impair insulin secretion and alter the autonomic response to hypoglycaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

T1DM

HbA1c target

A

48 mmol/mol or lower

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

T1DM

HbA1c
How often should it be measured

A

Every 3-6 months

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

T1DM

Patient monitoring

A
  • Measure BM QDS at least
  • Before each meal and before bed
  • More often if high frequency of hypoglycaemia episodes, e.g. illness, sport, planning pregnancy, whilst breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

T1DM

Blood glucose targets

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
34
Q

T1DM

Types of insulin

A
  • Offer multiple daily injection basal–bolus insulin regimens, rather than twice‑daily mixed insulin regimens, as the insulin injection regimen of choice for all adults
  • Twice‑daily insulin detemir is the regime of choice. Once-daily insulin glargine or insulin degludec is an alternative.
  • Offer rapid‑acting insulin analogues (insulin aspart, insulin lispro, and insulin glulisine) injected immediately before meals, rather than rapid‑acting soluble human or animal insulins, for mealtime insulin replacement for adults with type 1 diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

T1DM

When might you consider adding Metformin?

A

If BMI > 25 kg/m

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

T2DM

HbA1c targets

A

It’s worthwhile thinking of the average patient who is taking metformin for T2DM, you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%).

Once on a second drug, aim for 53 mmol/mol (7%).

If on any drug with risk of hypoglycaemia, e.g. lifestyle advice and sulfonylurea –> aim for 53 mmol/mol

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

T2DM

Dietary advice

A
  • Encourage high fibre, low glycaemic index sources of carbs
  • Low-fat dairy products
  • Oily fish
  • Discourage foods marketed specifically at diabetes
  • Initial target weight loss in obesity = 5-10%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Diabetes and ramadam

A
  • They should try and and eat a meal containing long-acting carbohydrates prior to sunrise (Suhoor)
  • Patients should be given a blood glucose monitor to allow them to check their glucose levels, particularly if they feel unwell
  • For patients taking metformin the expert consensus is that the dose should be split one-third before sunrise (Suhoor) and two-thirds after sunset (Iftar)
  • Expert consensus also recommends switching once-daily sulfonylureas to after sunset. For patients taking twice-daily preparations such as gliclazide it is recommended that a larger proportion of the dose is taken after after sunset
  • No adjustment is needed for patients taking pioglitazone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

DM

General sick day rules

A
  • Increased BM monitorign frequency
  • Increased fluid intake (3 litres in 24 hrs)
  • Sugary drinks if unable to eat
  • Box of ‘sick day supplies’
  • Access to mobile phone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

DM

Sick day rules on oral hypoglycaemics

A

If taking oral hypoglycaemics:

  • Continue taking
  • Stress response with increase cortisol and push sugars high even without oral itnake
  • Though stop metformin if very dehydrated (renal impairment risk)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

DM

Sick day rules on insulin

A
  • DO NOT STOP (risk of DKA)
  • Continue normal regime but check blood more frequently
  • Check ketone levels and if raised along with glucose then give corrective dose of insulin (total daily insulin divided by 6 - max dose 15 units)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

DM

Sick day rules
Factors indicating possible admission

A
  • Underlyinf illness requirign admission, e.g. MI
  • Inability to keep fluids down (> few hours)
  • Persistent diarrhoea
  • Significant ketosis in insulin dependent diabetic despite additional insulin
  • BM > 20 despite additional insulin
  • Unable to manage adjustments to usually diabetes management
  • Lack of support at home (lives alone, at risk of becoming unconscious)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Diabetes and driving - criteria for HGV licence

A
  • There has not been any severe hypoglycaemic event in the previous 12 months
  • The driver has full hypoglycaemic awareness
  • The driver must show adequate control of the condition by regular blood glucose monitoring*, at least twice daily and at times relevant to driving
  • The driver must demonstrate an understanding of the risks of hypoglycaemia
  • Tere are no other debarring complications of diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Diabetic foot disease

Causes x2

A
  • Neuropathy: resulting in loss of protective sensation, e.g. not noticing a stone in the shoe. Also Charcot’s arthropathy or dry skin.
  • Peripheral arterial disease: DM is a RF for both macro and microvascular ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Diabetic foot disease

Presentation

A
  • Neuropathy - loss of sensation

- Ischaemia - absent foot pulses, reduced ABPI, intermittent claudication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Diabetic foot disease

Complications

A
  • Calluses
  • Ulceration
  • Charcot’s arthropathy
  • Cellulitis
  • Osteomyelitis
  • Gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Diabetic foot disease

Screening

A
  • Annually (at least)
  • Screening for ischaemia: palpate dorsalis pedis pulse and posterior tibialis pulse
  • Screening for neuropathy: a 10 g monofilament is used on various parts of sole of the foot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Diabetic foot diease

Low risk

A
  • No RFs except callus alone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Diabetic foot disease

Moderate risk

A

One of:

  • Deformity
  • Neuropathy
  • Non-critical limb ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Diabetic foot disease

High risk

A

One of:

  • Previous ulceration
  • Previous amputation
  • On renal replacement therapy
  • Neuropathy and non-critical limb ischaemia together
  • Neuropathy in combination with callus and/or deformity
  • Non-critical limb ischaemia in combination with callus and/or deformity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Diabetic foot disease

Management

A

Moderate to high risk should be followed up regularly by local diabetic foot centre

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

DKA

Management

A
  • FLUIDS
  • If kid -> give fluids for 1 hr first before insulin
  • IV insulin (0.1 unit/kg/hr) of 5% dextrose
  • Correction of electrolyte disturbance (often high K+ to start but will drop with insulin so monitor and consider replacement)
  • Long-acting insulin should be continued !!! Short-term insulin should be stopped !!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

DKA

Resolution parameters

A
  • pH >7.3 and
  • Blood ketones < 0.6 mmol/L
  • Bicarbonate > 15.0mmol/L
  • Both the ketonaemia and acidosis should have resolved within 24 hours –> senior review from an endocrinologist if not
  • If above criteria met and patient is eating/drinking –> switch to SC insulin
  • Review by DM nurse prior to discharge
54
Q

DKA

Complications

A
  • Gastric stasis
  • Thromboembolism
  • Arrhythmias secondary to hyperkalaemia/ iatrogenic hypokalaemia
  • Iatrogenic due to incorrect fluid therapy (cerebral oedema (children + young adults particularly vulnerable, head CT if suspected), hypokalaemia, hypoglycaemia)
  • AKI
  • Acute respiratory distress syndrome
55
Q

Diabetes insipidus

Pathophysiology
Two types

A
  • Decreased secretion of ADH from pituitary (cranial DI)
    OR
  • Insensitivity to ADH (nephrogenic DI)
56
Q

Causes of cranial DI

A
  • Idiopathic
  • Post head injury
  • Pituitary surgery or radiotherapy
  • Brain infections - meningitis/encephalitis/TB
  • Craniopharyngiomas
  • Infiltrative: histiocytosis X, sarcoidosis
  • DIDMOAD (DI, DM, optic atrophy, deafness - Wolframs syndrome)
  • Haemochromatosis
57
Q

Causes of nephrogenic DI

A
  • Genetic (affect vasopression ADH receptor)
  • Electrolytes: hypercalcaemia, hypokalaemia
  • Lithium - desensitises the kidney’s ability to respond to ADH in collecting ducts
  • Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
58
Q

DI

Features

A
  • Polyuria
  • Polydipsia
  • HYPERnatraemia
  • Dehydration
  • Postural hypotension
59
Q

DI

Investigations

A
  • High plasma osmolality
  • Low urine osmolality (> 700 mOsm/kg excludes DI)
  • Water deprivation test!
60
Q

DI

What is the water deprivation test?

A
  • Also know as desmopressin stimulation test
  • Initially avoid taking fluids for 8 hrs
  • Urine osmolality measured
  • Synthetic ADH (desmopressin) administered
  • 8 hrs later urine osmolality measured again
61
Q

Water deprivation test

Results in cranial DI

A
  • Kidneys can still respond to ADH, but aren’t getting any
  • Initially urine osmolality will remain low as continues to be diluted by excessive water, but after desmopressin –> urine osmolality is high
62
Q

Water deprivation test

Results in nephrogenic DI

A
  • Unable to respond to ADH

- Therefore urine osmolality ill remain low even after desmopressin

63
Q

What is primary polydipsia?

A

Excessive consumption of fluids leading to polydipsia and polyuria

64
Q

Water deprivation test

Results in primary polydipsia

A
  • Urine osmolality will be high even before desmopressin is given
65
Q

Management of DI

A
  • Treat underlying cause
  • Mild cases can be managed conservatively

Cranial DI:
- Desmopressin

Nephrogenic DI:

  • Thiazides
  • Low salt/protein diet
  • Sometimes higher doses of desmopressin under close monitoring
66
Q

Thyroid hormones

Functions

A
  • Food metabolism
  • Protein synthesis
  • Increased sympathetic action, e.g. CO and HR
  • Heat production
  • Needed for growth and development
67
Q

Unique features of Grave’s disease

A

All due to presence of TSH receptor antibodies

  • Diffuse goitre (without nodules)
  • Graves eye disease
  • Bilateral exophthalmos
  • Pretibial myxoedema
68
Q

Unique features of toxic multinodular goitre

A
  • Goitre with firm nodules
  • Most > 50 yrs
  • Second most common cause
69
Q

What time of lump is a solitary toxic thyroid nodules likely to be? Management

A

Benign adenoma

Surgical removal

70
Q

What is De Quervain’s thyroiditis?

A
  • Viral infection with fever, neck pain and tenderness, dysphagia and hyperthyroidism
  • Hyperthyroidism phase is followed by a hypothyroid phase as TSH levels fall due to negative feedback
  • Self-limiting -> supportive Tx with NSAIDs and beta-blockers
71
Q

Radioactive iodine therapy

What does it involve

A
  • Drink single dose of radioactive idone

- Taken up by thyroid gland and emitted radiation destroys a proprortion of thyroid cells

72
Q

Radioactive iodine therapy

Recovery

A
  • Remission can take 6 months

- Patients can be left with hypothyroidism and require thyroxine

73
Q

Radioactive iodine therapy

Contraindications and ‘rules’

A
  • Must not be pregnant, do not get pregnant within 6 months
  • Must avoid close contact with children and pregnant women for 3 weeks
  • Limit contact with anyone for several days following the dose
74
Q

Thyroid eye disease

Pathophysiology

A
  • Autoimmune response agasint an autoantigen, possibly the TSH receptor –> retro-orbital inflammation
  • Inflammation results in glycosaminoglycan and collagen deposition in muscles
75
Q

Thyroid eye disease

Features

A
  • Eu-, hypo- or hyper- thyroid at time of presentation
  • Exopthalmos
  • Conjunctiuval oedema
  • Optic disc swelling
  • Ophthalmoplegia
  • Inability to close the eyelids –> may lead to sore, dry eyes
  • If severe and untreated, may result in exposure keratopathy
76
Q

Thyroid eye disease

Prevention

A
  • Stop smoking

- Radioiodine may increase inflammatory symptoms, prednisolone helps reduce the risk

77
Q

Thyroid eye disease

Management

A
  • Topical lubricants
  • Steroids
  • Radiotherapy
  • Surgery
78
Q

Thyroid eye disease

Need for urgent review when?

A
  • Unexplained deterioration of vision
  • Awareness of change in intensity or quality of colour vision in one/both eyes
  • Hx of eye suddenly ‘popping out’
  • Obvious corneal opacity
  • Cornea still visible when eyelids closed
  • Disc swelling
79
Q

Thyroid cancer

Papillary

A
  • 70%
  • Young females
  • Spread: lymph nodes, lung
  • Excellent prognosis
  • Surgery
80
Q

Thyroid cancer

Follicular

A
  • 20%
  • Middle-aged
  • Spread: blood to bone, lungs
81
Q

Thyroid cancer

Medullary

A
  • 5%
  • Cancer of parafollicular (C) cells
  • Secrete CALCITONIN (tumour marker)
  • Part of MEN-2
82
Q

Thyroid cancer

Anaplastic

A
  • 1%
  • Not responsive to Tx
  • Can cause pressure symptoms
83
Q

Thyroid cancer

Lymphoma

A
  • Associated with Hashimoto’s thyroiditis
  • More prevalent in females
  • STRIDOR
84
Q

What is MEN-2?

A

Multiple endocrine neoplasia type 2

  • Medullary thyroid cancer: 98% to 100% with MEN2A are affected
  • Pheochromocytoma, a typically benign (noncancerous) tumor of the adrenal glands: 50% with MEN2A affected
  • Parathyroid adenoma (a benign tumor) or hyperplasia, meaning increased size of the parathyroid gland: 5% to 10% with MEN2A affected
85
Q

Management of papillary and follicular cancer

A
  • Total thyroidectomy
  • Followed by radioiodine (I-131)
  • Yearly thyroglobulin levels to detect early recurrent disease
86
Q

Causes of gynaecomastia

A
  • Physiological in puberty
  • Testicular cancers (secrete oestrogen, hCG) - leydig cells, seminomas
  • Liver cirrhosis and failure
  • Hyperthyroidism
  • Haemodialysis
  • Other hCG secreting hormones (SCLC)

Drug causes:

  • Spironolactone (most common cause)
  • Cimetidine
  • Digoxin
  • Cannabis
  • Finasteride
  • GnRH agonists (GOSERELIN) - used in prostate cancer
  • oestrogens, anabolic steroids
87
Q

Complications of Transphenoidal surgery

A
  • Hypopituitarism
  • Diabetes insipidus
  • Haemorrhage
  • CNS injury
  • Meningitis
88
Q

Normal TSH levels

A

0.5-5.5

89
Q

Normal free T4 levels

A

9-18

90
Q

Normal total T4 levels

A

70-140

91
Q

Hypercalcaemia

At what level would you consider Tx with bisphosphonates?

A

> 3

92
Q

What might be considered in a diabetic with erratic blood glucose control, bloating and vomiting?

Pathophysiology and management

A

Gastroparesis (due to neuropathy of the vagus nerve, causing abnormal gut movement)

Manage with metoclopramide, domperidone or erythromycin

93
Q

Causes of hypoglycaemia

A

EXPLAIN

  • Exogenous drugs (typically sulfonylureas or insulin)
  • Pituitary insufficiency
  • Liver failure
  • Addison’s disease
  • Islet cell tumours (insulinomas)
  • Non-pancreatic neoplasms
94
Q

Glucocorticoid SEs

A

Endocrine

  • impaired glucose regulation
  • increased appetite/weight gain
  • hirsutism
  • hyperlipidaemia

Cushing’s syndrome

  • moon face
  • buffalo hump
  • striae

Musculoskeletal

  • osteoporosis
  • proximal myopathy
  • avascular necrosis of the femoral head

Immunosuppression

  • increased susceptibility to severe infection
  • reactivation of tuberculosis

Psychiatric

  • insomnia
  • mania
  • depression
  • psychosis

Gastrointestinal

  • peptic ulceration
  • acute pancreatitis

Ophthalmic

  • glaucoma
  • cataracts
  • suppression of growth in children
  • intracranial hypertension
  • neutrophilia
95
Q

Mineralocorticoid SEs

A
  • Fluid retention

- Hypertension

96
Q

Thyroid storm

Precipitating events

A
  • Thyroid or non-thyroid surgery
  • Trauma
  • Infection
  • Acute iodine load, e.g. CT contrast media
97
Q

Thyroid storm

Features

A
  • Fever > 38
  • Tachycardia
  • Confusion and agitation
  • N+V
  • HTN
  • HF
  • Abnormal liver function - jaundice may be seen
98
Q

Thyroid storm

Management

A
  • Beta blockers
  • Propylthiouracil / Methimazole
  • Hydrocortisone
  • Dexamethasone
99
Q

Thyroid eye disease

severity of eye disease

A

NOSPECS
Best to Worst

N: No signs/symptoms
O: Only signs (e.g. upper lid retraction)
S: Signs and symptoms (including soft-tissue involvement)
P: Proptosis
E: Extra-ocular muscle involvement
C: Corneal involvement
S: Sight loss due to optic nerve involvement

100
Q

What do you need to test for in those with acromegaly and why?

A

DM, because growth hormone is anti-insulin and this leads to a state of insulin resistance and eventually diabetes

101
Q

What is the leading cause of death in those with acromegaly?

A
  • CVS disease secondary to increase in heart muscle size, HTN and insulin resistance
102
Q

What are the white patches called seen in hypothyroidism?

A

Vitiligo

103
Q

From which anatomical structure does the thyroid gland originate from before embryological descent?

A

Foramen caecum

104
Q

When do the foetal thyroid follicles and T4 develop?

A

at week 10

105
Q

Hypothyroidism

What might you see on and FBC?

A
  • Macrocytic anaemia

Pernicious anaemia

106
Q

Grave’s Disease

Three aspects that define Graves

A
  • Thyroid eye disease (ophthalmoplegia, exophthalmos, extra-ocular muscle swelling)
  • Pretibial myxoedema (mucin deposits)
  • Thyroid acropachy (clubbing, swollen fingers, toe swelling, periosteal new bone formation)
107
Q

Urine and plasma osmolalities seen in diabetes insipidus? (high/low)

A
  • urine = low

- plasma = high

108
Q

Explain how the water deprivation test allows for diagnosis of diabetes insipidus?

A

Normal response of the body is to concentrate urine and decrease urine output.

However, in DI, there is continued production of large volumes of urine with low osmolality

109
Q

What can repeated hypoglycaemic episodes lead to?

A

A lack of awareness of hypoglycaemia by the body and the initial autonomic symptoms may not occur

110
Q

Advice for preventing hypos

A
  • Regular finger-prick checking
  • Never miss a meal
  • Keep emergency supply of glucose on person
  • Change insulin appropriately in response to change in diet, activity, illness
111
Q

Describe the oral glucose tolerance test

A
  • Patient fasts overnight
  • Drink containing 75 g glucose in 300 ml water is given
  • Blood glucose is measured prior to drink and then at 2 hours
  • Diabetes if > 11.1mmol/L at 2 hrs
  • Patient advised not to drink coffee or smoke in fasting period
112
Q

DKA

Bedside test to check for it once already done BM?

A

Urine dipstick for ketones

113
Q

DKA

Management

A
  • Fluid replacement (aggressively)
  • Insulin sliding scale
  • Potassium replacement
114
Q

DKA

Explain pathophysiologu

A
  • Insulin deficiency produces glucose production in the liver
  • Lipolysis occurs
  • Fatty acids are broken down to form ketone bodies
  • This produces a metabolic acidosis
  • This usually occurs in starvation periods, as breaking down ketones is less efficient
115
Q

What is the by product of ketone breakdown?

A

Acetone

116
Q

What is the hyperventilation in DKA known as?

A

Kussmaul’s respiration

117
Q

Advice for those on glucocorticoids

A
  • Never stop them suddenly
  • Carry steroid card
  • Medic alert bracelet
  • Change dose (double) when unwell
  • Carry emergency ampoule of hydrocortisone for when oral route not advisable
118
Q

Complication of parathyroid surgery?

A
  • Hypoparathyroidism

- Laryngeal nerve palsy

119
Q

What is the first type of sense to diminish in diabetic neuropathy?

A

Vibration

120
Q

What might you see in the foot of someone with diabetic neuropathy?

A
  • Charcot’s joint
  • Painless ulcers
  • High arched foot with clawing toes
  • Diminished reflexes
121
Q

Other types of neuropathy that can occur in diabetes? (other than peripheral)

A
  • Autonomic neuropathy
  • Diabetic amyotrophy
  • Mononeuropathy
  • Acute painful neuropathy
122
Q

Hypothyroidism

Pregnancy

A
  • Thyroxine is safe in pregnancy and breastfeeding
  • Increased dose during pregnancy (by up to 50% as early as 4-6 weeks in)
  • Serum TSH measured in each trimester and 6-8 weeks post-partum
123
Q

Hyperthyroidism

Pregnancy
Drug choice

A

Propylthiouracil is used in the first trimester of pregnancy in place of carbimazole, as the latter drug may be associated with an increased risk of congenital abnormalities. At the beginning of the second trimester, the woman should be switched back to carbimazole

124
Q

What is the most common thyrotoxicosis in pregnancy?

A

Graves Disease

125
Q

What are the risks of untreated thyrotoxicosis in pregnancy?

A
  • Risk of fetal loss
  • Maternal heart failure
  • Premature labour
126
Q

Hyperthyroidism

Pregnancy
TFT levels

A
  • Should be kept in upper third of normal range to avoid foetal hypothyroidism
127
Q

Hyperthyroidism

Pregnancy
Monitoring

A
  • Thyrotrophin receptor stimulating antibodies should be checked at 30-36 weeks gestation
  • Helps to determine risk of neonatal thyroid problems
128
Q

What is the risk of over-treatment with thyroxine?

A
  • Osteoporosis
  • Hyperthyroidism
  • Worsening of angina
  • Atrial fibrillation
129
Q

Interactions with levothyroxine and how to get around it?

A
  • Iron, calcium carbonate
  • Absorption of levothyroxine is reduced
  • Give at least 4 hrs apart
130
Q

1st line insulin regime in newly diagnosed T1DM?

A

Basal–bolus using twice‑daily insulin detemir

131
Q

If C-peptides are present, which type of diabetes is it?

A

T2DM

Finals (21 decks)

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