Brainscape's Knowledge GenomeTM

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


See full index

Phase1c Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Metabolic ketoacidosis with normal-low glucose is associated with what?

A

Alcoholic ketoacidosis

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

Which thyroid cells form the colloid?

A

Follicular cells

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

What mineral is associated with the thyroid colloid?

A

Iodine

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

What is the function of para-follicular cells (C-cells)?

A

Produce Calcitonin

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

What is the function of follicular cells?

A

Synthesise T4 and T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the bioactive thyroid hormone?

A

T3

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

What is the main thyroid hormone produced by the thyroid gland?

A

T4

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

How is T4 transported int he blood?

A

Thyroid-binding globulin

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

What are the symptoms of hyperthyroidism?

A 
Tremor
Anxiety
Palpitations
Heat intolerance
Diarrhoea
Oligomenorrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the symptoms associated with hypothyroidism?

A 
Lethargy
Cold intolerance
Weight gain
Constipation
Menorrhagia
Decreased deep tendon reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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

What are the causes of hyperthyroidism?

A

Grave’s disease
Toxic multi-nodular goitre
Thyroiditis
Drugs (Amiodarone)

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

Which antibodies are associated with Grave’s disease?

A

Anti-TSH receptor antibodies

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

Which drug is associated with inducing hyperthyroidism?

A

Amiodarone

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

What is the most common cause of hypothyroidism?

A

Hashimoto’s thyroidits

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

Which auto-antibody is associated with Hashimoto’s thyroiditis?

A

Anti-TPO antibodies

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

What are the causes of hypothyroidism?

A

Hashimoto’s thyroiditis
Subacute thyroiditis
Drugs
Iodine deficiency -Common cause in the developing world

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

Which drugs can induce hypothyroidism (2)?

A

Lithium

Amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the most common cause of hypothyroidism in the developing world?

A

Iodine deficiency

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

What is the level of TSH in primary hyperthyroidism?

A

Low TSH

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

What is the level of TSH in primary hypothyroidism?

A

Raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is revealed in radio-scintigraphy in Grave’s disease?

A

Homogeneous increased iodine uptake

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

What is revealed in radio-scintigraphy in a toxic adenoma?

A

Hot nodule - increased iodine uptake in solitary nodule and suppressed uptake in other parts

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

What is revealed in radio-scintigraphy in a toxic multi-nodular adenoma?

A

Heterogeneous uptake

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

What is the management of hyperthyroidism?

A

Propranolol - Non cardioselective beta-blocker for symptomatic management

Carbimazole (TPO inhibitor)

Propylthiouracil

Radio-iodine

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

What are the side effects of carbimazole?

A

Agranulocytosis (No neutrophils)

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

What is the definitive management for hypothyroidism?

A

Levothyroxine

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

How common is thyroid eye disease in Grave’s patients?

A

25-50%

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

What is the most common form of thyroid eye disease in Grave’s?

A

Bilateral exophthalmos

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

What is the pathophysiology of exophthalmos in Grave’s?

A

Anti-TSH receptor antibodies binding to TSH receptors in the eyes - stimulates growth of tissue

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

What are the features of Bilateral exophthalmos in Grave’s?

A 
Diplopia 
Conjunctival oedema (chemosis)
Opthalamlgia 
Exposure keratopathy
Optic neuropathy (Blurred vision)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Due to increased sympathetic tone in Grave’s disease what features are seen in the eye?

A

Lid lag and retraction

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

What are the three specific features in Grave’s disease?

A

Bilateral exophthalmos - lid lag and retraction
Pretibial myxoedema
Thyroid acropachy (Thickening of the extremities)

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

What are the classic features of thyroid cancer?

A

Non-functional (Euthyroid), painless, rapidly growing

Solitary - Irregular (Nodular shape

Palpable nodule, hard and fixed

Hoarse voice - Tumour compression on the recurrent laryngeal nerves

Dysphagia

Haemopotysis

Airway obstruction

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

Why does a hoarse voice occur in thyroid cancer?

A

Tumour compression on the recurrent laryngeal nerve

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

What is the most common subtype of thyroid cancer?

A

Papillary carcinoma (70%) - associated with cervical lymphadenopathy

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

What is the epidemiology of papillary carcinoma?

A

35-year old female with childhood radiation exposure

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

A circular concentric laminations in papillary carcinoma is known as what?

A

Psammoma body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What thyroid cancer is associated with a Psammoma body?

A

Papillary carcinoma

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

What is the second most common thyroid cancer?

A

Follicular carcinoma (20%) - associated with low dietary iodine intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is a rare variant of follicular carcinoma?

A

Hurthle cell carcinoma

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

Which MEN types are associated with medullary carcinoma?

A

MEN2a and MEN2B

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

What are the most aggressive thyroid cancers?

A

Anaplastic carcinomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the definitive investigation for thyroid cancer?

A

Fine needle aspirate biopsy with ultrasound

+TFTs - to exclude functional nodules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What neoplasms are associated with MEN type 1?

A 
3Ps
Pituitary tumours (Prolactinoma)

Pancreatic tumours (Insulinoma, glucagonoma, gastrinomas)

Parathyroid adenomas
(Raised Ca, and HyperPTH)

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

What are the common pancreatic tumours are associated with MEN1?

A

Insulinoma
Glucagonoma
Gastrinoma

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

What are the symptoms of hypercalcaemia?

A 
Renal colic
Abdominal pain 
Constipation 
Psychological depression
Bone pain, osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is the onset of symptoms for MEN1?

A

MEN1 mutation has high penetrance and therefore develops early in life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What investigations are performed for MEN1?

A

CT/MRI (whole-body), genetic testing

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

What is Zollinger-Ellison syndrome compared with MEN1 gastrinoma?

A

Non-MEN1 gastrinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

MEN2A and MEN2B is associated with which type of thyroid cancer?

A

Medullary thyroid cancer

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

Medullary thyroid cancer is associated with which type of cell?

A

Parafollicular C-cell - produce calcitonin

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

Which tumours are associated with MEN2A?

A

Phaeochromocytoma
Parathyroid adenoma
Medullary thyroid cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Which tumours are associated with MEN2B?

A

Phaeochromocytoma
Medullary thyroid cancer
Neuromas (Mucosal) -

Associated with Marfanoid habitus

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

What is Marfanoid habitus?

A

Including long limbs, with an arm span that is at least 1.03 of the height of the individual, and a crowded oral maxilla, sometimes with a high arch in the palate, arachnodactyly, and hyperlaxity.

Pectus excavatum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

A Marfanoid habitus is associated with which type of MEN syndrome?

A

MEN2B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What gene is associated with MEN2A and 2B in genetic testing?

A

RET oncogene

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

What blood investigation is performed in suspected medullary thyroid carcinoma?

A

Calcitonin

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

What type of tumour is carcinoid syndrome?

A

Neuroendocrine cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How does carcinoid syndrome arise to produce a symptomatic presentation?

A

The carcinoid tumour metastasises to the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What does serotonin get metabolised into by the liver?

A

5-HIAA (excreted via the urine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What hormone is raised in carcinoid syndrome?

A

Serotonin
Bradykinin
Histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the common features of carcinoid syndrome?

A

Flushing (Vasodilation due to bradykinin and histamine)

Diarrhoea (Serotonin induced effect on gut motility)

Shortness of breath

Pulmonary stenosis

Abdominal pain (Serotonin activated fibroblasts)

Itching (Histamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What hormone inhibits serotonin release?

A

Somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What investigations are performed on suspected carcinoid syndrome?

A

Urinary 5-HIAA
CT Scan
Octreotide scan - specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is octreotide?

A

A somatostatin analogue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What specific scan is performed in carcinoid syndrome?

A

Octreotide scan - binds to neuroendocrine cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What hormone released by the hypothalamus directly controls LH/FSH secretion?

A

GnRH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Which cells respond to LH in males?

A

Leydig cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the function of Leydig cells?

A

Release testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the function of Sertoli cells?

A

Spermatogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Sertoli cells respond to which hormone?

A

FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Which hormone is secreted by theca cells?

A

Progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Which hormone is secreted by granulosa cells?

A

Oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Which gonadotrophin acts on theca cells?

A

LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is physiological hypogonadism?

A

Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is primary hypogonadism (Female)?

A

Gonadal dysfunction
-Reduced oestrogen and progesterone production

  • Turner’s syndrome (Gonadal Dysgenesis)
  • Gonadal damage
  • Primary ovarian failure
  • PCOS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the karyotype of Turner’s syndrome?

A

45X0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the causes of secondary hypogonadism?

A

Kallman syndrome
Pituitary/hypothalamic tumour (Non-functioning or prolactinoma)
Hyperprolactinaemia

Functional - Hypothalamic amenorrhoea
-Low BMI, Excess exercise, stress

Contraceptive pill use - Negative feedback signal to reduce FSH and LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What symptom is typically associated with Kallman syndrome?

A

Anosmia- Failed development migration of olfactory bundles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are functional causes of hypothalamic amenorrhoea?

A

Low BMI
Excess exercise
Stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the main causes of primary hypogonadism in Males?

A

Gonadal dysgenesis (Klinefelter’s syndrome, cryptochrodism)

Gonadal damage

Post-orchitis (Mumps)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the karyotype for Klinefelter’s syndrome?

A

47XXY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are the secondary causes of hypogonadism in Males?

A

Kallman Syndrome
Pituitary/hypothalamic tumour
Hyperprolactinaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the features of hypogonadism?

A

Delayed puberty - Primary amenorrhoea, absent sexual characteristics (absent pubic hair, delayed thelarche, micropenis, high-pitched voice, small undescended testes)

Infertility

Low libido

Female specific - Night sweats/hot flushes
-Amenorrhoea

Erectile dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the first-line investigation in females presenting with symptoms of hypogonadism?

A

Pregnancy test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What investigations are performed in hypogonadism?

A 
Pregnancy test
LH/FSH
Prolactin
Testosterone/Oestradiol
TFTs
Karyotyping 
Pituitary MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is the hormone profile in primary hypogonadism?

A

Hypergonadotrophic hypogonadism
- Raised LH/FSH/GnRH

Low tesosterone/oestrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the hormone profile in secondary hypogonadism?

A

Hypogonadotropic hypogonadism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the effects of growth hormone?

A

Increased blood glucose
Increased insulin resistance
Increased muscle growth
Increased bone thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What organs does GH have an effect on?

A

Bone
Muscle
Liver
Kidney

Releases IGF-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Growth hormone causes the release of what?

A

Insulin-like growth factor-1 (Somatomedin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the most common cause of acromegaly?

A

Pituitary adenoma of somatotrophs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the features of Acromegaly?

A 
Coarse facial features
Prognathism and large tongue
Spade-like hands and large feet
Excessive sweating
Organomegaly 
Headache
Visual disturbances
Possible: Hyperprolactinaemia, hypopituitarism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Why is gigantism?

A

Growth of long bones (Epiphyseal growth plates have no fused)

96
Q

Why is there hyperprolactinaemia in acromegaly?

A

Pituitary adenoma compression of the pituitary stalk reduces dopamine secretion -Reduces negative regulation of prolactin release from lactotrophs

97
Q

What visual defect is associated with pituitary adenomas?

A

Bitemporal hemianopia

98
Q

What are the common complications of acromegaly?

A 
Diabetes mellitus
Hypertension
Carpal tunnel syndrome
Cardiomyopathy
Colorectal cancer
99
Q

What is seen in an OGTT in acromegaly?

A

Paradoxical rise in Growth hormone

100
Q

What is the first-line investigation in acromegaly?

A

Serum IGF-1

101
Q

What is the diagnostic investigation in confirming acromegaly?

A

OGTT

102
Q

What is the first-line definitive management of acromegaly?

A

Trans-sphenoidal surgery

  • Radiotherapy
  • Somatostatin analogues
  • Dopamine receptor agonists (Cabergoline and bromocriptine)
  • GH receptor antagonists
103
Q

What is type 1 diabetes?

A

Pancreatic islet B-cell autoimmune destruction

  • Absolute deficiency in insulin
  • Lipolysis and ketogenesis
104
Q

Which gene is associated with type 1 diabetes mellitus?

A

HLA DR3-4

105
Q

What is type 2 diabetes mellitus?

A

Reduced peripheral sensitivity to insulin , reduced insulin production over time

106
Q

What is the characteristic presentation of T1DM?

A

<20 years
Polyuria, and polydipsia (osmotic diuresis)

Weight loss and fatigue

DKA signs

FH of autoimmune disease

107
Q

What are DKA signs?

A

Nausea and vomiting
Abdominal pain
Kussmaul breathing (deep hyperventilation)
Sweet-smelling breath (ketonaemia)

108
Q

What is the characteristic features of T2DM?

A

> 40 YEARS
asymptomatic
Polyuria, polydipsia
Examination findings -acanthosis nigricans

109
Q

What are the main risk factors for T2DM?

A

Obesity
Hypertension
South Asian/Afro-Caribbean ethnicity

110
Q

What is the normal random glucose range?

A

<11.1

111
Q

What is the cut-off for fasting glucose in diabetes?

A

> 7.0

112
Q

What is the cut-off for a 2-hour post-prandial glucose?

A

> 11.1

113
Q

What is the cut-off for HbA1c diabetes diagnosis?

A

> 48 (6.5%)

114
Q

What is the pre-diabetes range for fasting glucose?

A

5.5-6.9

115
Q

What confirms the diagnosis of diabetes Mellitus?

A

symptomatic + 1 test

Asymptomatic + 2 different tests on 2 different days

116
Q

What are the specific antibodies involved in type 1 diabetes mellitus?

A

Anti-GA and islet cell antibodies

117
Q

What does a urine dip reveal in T1DM?

A

Urinary Ketones

118
Q

What is the first-line management for T1DM?

A

Basal-bolus

Long-acting and short-acting (Before meals)

119
Q

Example of long-acting insulin

A

Insulin glargine (Subcutaneous injection OD)

120
Q

Example of short-acting insulin

A

Insulin lispro

121
Q

What is basal-bolus insulin?

A

Short-acting and long-acting insulin prior to meals/

122
Q

How is T1DM measured

A

Monitored daily using capillary glucose

Over time using HbA1c

123
Q

What is the first-line management for T2DM?

A

Lifestyle modifications - diet, exercise and education

124
Q

What is step 1 of glycaemic control in T2DM?

A

Metformin if HbA1c >48 despite lifestyle advice

125
Q

What is step 2 in glycaemic control?

A

Add another drug (DPP4i, Pioglitazone, SU, SGLT-2i)

126
Q

What are the indications for starting atorvastatin in lipid management for T2DM?

A

If QRISK >10%

-Atorvastatin 20mg

127
Q

What are the indictions for 80mg OD atorvastatin in T2DM?

A

IHD, CVD and PAD

128
Q

What is the BP management in T2DM?

A

ACEi or ARB (In Afro-Caribbean Origin)

129
Q

What is step 2 in BP management?

A

Add CCB or thiazide

130
Q

What step 3 in BP management in T2DM?

A

ACEi/ARB + CCB + Thiazide

131
Q

What are the acute metabolic disturbances associated with DM?

A

Hypoglycaemia
DKA
HHS

132
Q

What glucose parameter is associated with hypoglycaemia?

A

Low plasma glucose <3.6 mmol/L

133
Q

What are the common causes of hypoglycaemia in T2DM?

A

Inappropriate insulin regime
Missed meals
Drugs - SUs

134
Q

What are the signs of Hypoglycaemia?

A 
Palpitations
Tremor
Sweating
Pallor
anxiety
Drowsiness
Confusion
altered behaviour
COMA
135
Q

What is the management for hypoglycaemia in a conscious patient?

A

Oral glucose and complex carbohydrate

Short-acting - glucogel

136
Q

What is the management of hypoglycaemia in impaired consciousness?

A

1mg IM glucagon

137
Q

What is the triad of DKA?

A

Hyperglycaemia
Ketonaemia
Metabolic acidosis

138
Q

What is the main effect of glucose in DKA?

A

Osmotic diuresis (Polyuria) - dehydration

139
Q

What is the main effect of ketones in DKA?

A

Acid induced enzyme dysfunction - coma and death

140
Q

What is the main aim of DKA?

A

IV fluids and insulin

141
Q

What sign is not seen in HHS?

A

Abdominal pain

142
Q

What ketone parameter is indicative of DKA?

A

> 3 mmol/L

pH < 7.3

143
Q

What pH value is associated with DKA?

A

pH <7.3

144
Q

What is the pH value in HHS?

A

Normal (7.35-7.45) and normal ketones <3 mmol/L

145
Q

What is the initial management for HHS and DKS?

A

Fluids (normal saline) and potassium chloride (If K<5.5)

IV insulin after fluids and only when Potassium is not <3.5

146
Q

When is IV insulin administered in HHS?

A

After fluids and when K is not <3.5

147
Q

What is the effect of insulin on potassium?

A

Increase potassium cellular intake- risk of hypokalaemia

148
Q

What type of insulin is given in HHS and DKA?

A

Fixed-rate insulin infusion

149
Q

What signs are seen in background retinopathy on fundoscopy?

A

Blot and dot haemorrhages/hard exudates

150
Q

What is the management of background retionopathy?

A

Improve glycaemic control

151
Q

What is the management of pre-proliferative retionopathy?

A

Pan-retinal laster photocoagulation

152
Q

What fundoscopic signs are seen in pre-proliferative retionopathy?

A

Background + cotton wool spots

153
Q

What is seen in proliferative retinopathy?

A

Neovascularisation

154
Q

What is the management for maculopathy?

A

Intravitreal VEGF inhibitors

155
Q

What are the risks associated with neovascularisation in retinopathy?

A

Associated with retinal detachment and vitreous haemorrhage - visual loss

156
Q

What fundoscopic signs are seen in maculopathy?

A

Hard exudates need the macula

157
Q

What are the signs of diabetic nephropathy?

A

Oedema, polyuria, lethargy and hypertension

158
Q

What is the first-line investigations for diabetic nephropathy?

A

Urinalysis

Albumin:creatinine ratio (Raised) - Microalbuminuria

159
Q

What is the gold standard investigation for diabetic nephropahty?

A

Renal biopsy - revealing Kimmelstiel-Wilson nodules

160
Q

What nodules are seen in a renal biopsy for diabetic nephropathy?

A

Kimmelstiel-wilson nodules

161
Q

What is the definitive management for diabetic nephropathy?

A

ACEi/ARB (renoprotective)

162
Q

What is the aetiology of diabetic neuropathy?

A

Blockage of the vasa nervosum

163
Q

What is the characteristic presentation of peripheral neuropathy?

A

Glove and stocking distribution

  • Loss of sensation
  • Inspect feet

Monofilament on LL exam

Loss of ankle jerk/vibration/sense/fractures (Charcot’s joint)

164
Q

What is mononeuropathy?

A

Motor loss

-wrist drop, foot drop, 3rd nerve palsy

165
Q

What is autonomic neuropathy?

A

GI tract: Difficulty swallowing, delayed gastric emptying, bladder dysfunction

Postural hypotension

Cardiac autonomic supply

166
Q

Which neuropathic pain agents are used in DN?

A

Duloxetine
Pregabalin
Gabapentin

167
Q

What is the main symptom of diabetes insipidus?

A

Production of dilute urine (Hypotonic polyuria)

168
Q

What are the two types of diabetes insipidus?

A

Lack of vasopressin release from the posterior pituitary gland

Nephrogenic - Collecting ducts insensitive to vasopressin

169
Q

What are the causes of cranial DI?

A

Pituitary tumour/surgery, TBI, infection (meningitis)
Sarcoidosis/TB
SAH

170
Q

What are the nephrogenic causes of DI?

A 
Lithium therapy
Electrolyte imbalance (HyperCal, hypokal)

Ureteric obstruction
Inherited (AVPV2 gene)

171
Q

What is the presentation of DI?

A

Polyuria, nocturia
Polydipsia
Dehydration: Tachycardia/reduced tissue turgor/dry mucous membranes

Signs of the cause

172
Q

What is the diagnostic test for DI?

A

Water deprivation test

173
Q

How long is a water deprivation test carried out for?

A

8 hours or more than 3% body weight lost

174
Q

After a water deprivation test what drug is adminsitered?

A

Desmopressin

175
Q

What is the urine osmolality in diabetes insipidus during a water deprivation test?

A

Dilute - low

176
Q

What happens to urine osmolality after desmopressin administration in cranial diabetes insipidus?

A

Increases

177
Q

Management for cranial DI?

A

Intranasal desmopressin

178
Q

Management for nephrogenic DI?

A

Thiazide diuretic

179
Q

What is SIADH?

A

Excess ADH

  • Serum sodium decreases
  • Urine osmolality increases
  • Urine sodium increases
180
Q

What are the main CNS causes?

A

SAH, stroke, tumour, TB

Pulmonary: Pneumonia, bronchiectasis

Malignancy - small cell lung cancer

Drugs - Carbamazepine, SSRI

Idiopathic

181
Q

What is the management of SIADH?

A

Treat the underlying cause

Immediate fluid restriction (Hyponatremia)

If ineffective- consider oral demeclocycline (Makes collecting ducts less repsonsive to ADH)

182
Q

What are the three main causes of hypovolaemic hyponatremia?

A

Diarrhoea, vomiting, diuretics

Management is IV fluids, there is low urinary sodium (<20)

183
Q

What is the cause of euvolaemic hyponatremia?

A

SIADH
Hypothyroidism
Adrenal insufficiency

Management is fluid restriction

184
Q

What is the presentation of severe hypervolaemia?

A

Seizures, decreased consciousness

185
Q

What is the complication of administering hypertonic saline in hyponatremia (too fast)?

A

Central pontine myelionlylsis

186
Q

What are the main acquired causes of hypothyroidism?

A

Hashimoto’s thyroidits
Iatrogenic (Post-surgery, radioiodine, medication for hypertyroidism)

Severe iodine deficiency or iodine excess (Wolff-Chaikoff effect)

187
Q

What is the presentation of hypothyroidism?

A 
Cold intolerance
Lethargy
Weight gain
Constipation 
Dry skin 
Hair loss
Hoarse voice
Mental slowness, depression, dementia, cramps, ataxia, paraesthesia

Menstural disturbances (irregular cycles menorrhagia)

Myxoedema coma (severe hypothyroidism)

188
Q

What are the examination findings consistent with hypothyroidism?

A

Bradycardia, cold hands

Pale puffy face, goitre, hair loss, dry skin, vitiligo

Pericardial or pleural effusions

Ascites

Slow relaxation of reflexes

Signs of carpal tunnel syndrome

189
Q

What is subclinical hypothyroidism?

A

Normal serum free-T4 and T3, and increased TSH

190
Q

What is the management for hypothyroidism?

A

Levothyroxine

191
Q

What is the management of myxoedema coma?

A 
Oxygen
Rewarming
Rehydration
IV T4/T3
IV hydrocortisone
192
Q

What is thyrotoxicosis?

A

A syndrome resulting from an excess of circulating free thyroxine (T4) and/or free triiodothyronine (T3).
-Due to increased thyroid hormone synthesis

193
Q

What autoantibodies are associated with Hashimoto’s thyroiditis?

A

Anti-thyroid peroxidase

194
Q

What auto-antibodies are associated with Grave’s disease?

A

TSH-receptor antibodies

195
Q

What are the features of Grave’s disease?

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

Symptoms of thyrotoxicosis

  • Heat intolerance
  • Sweating
  • Palpitations
  • Anxiety and irritability
  • Weight loss (Despite good appetite)
  • Diarrhoea, pruritus
  • Exertional dyspnoea
  • Menstural irregularities
196
Q

What is Graves opthalmopathy?

A

Blurred vision, double vision, eye grittiness, eye protrusion (Exophtalmos)

197
Q

What is the presentation of subacute thyroiditis?

A

neck pain radiating to the jaw or to the ear, inability to the swallow

  • Fever
  • Palpitations
  • Malaise
  • Tremor
  • Heat intolerance
198
Q

What is the TFT picture in subacute thyroidits?

A

Low TSH

Raised T3 and T4 due to release of pre-formed thyroid hormone in the colloid.

199
Q

What is the first-line management for subacute thyroiditis?

A

Corticosteroid

Analgesia - Ibuprofen

200
Q

What is the first-line management for controlling symptoms of thyrotoxicosis?

A

Propanolol (Beta-blockers)

201
Q

What are the symptoms of thyrotoxicosis?

A

General: Underweight, restless, irritable, sweating.
• Signs of associated autoimmune conditions – vitiligo.
• Hands: tremor, warm, moist, rapid, or irregular pulse, onycholysis, acropachy, palmar erythema.
• BP: Wide pulse pressure
• Eyes: Lid retraction and lid lag (due to increased catecholamine sensitivity of levator palpebrae superioris)

202
Q

What does a radioisotope uptake scan reveal in Grave’s disease?

A

Homogenous uptake

203
Q

What does a radioisotope uptake scan reveal in Toxic multinodular goitre?

A

Heterogenous activity - multiple areas of increased activity with suppression of uptake of the gland

204
Q

What is the first-line management of an acute thyroid crisis?

A

Beta-blockade - atenolol, propanolol

205
Q

What is the pharmacological management for thyrotoxicosis?

A

Carbimazole

Propylthiouracil

206
Q

What is a toxic multi-nodular goitre?

A

Excess production of thyroid hormones from a functionally autonomous thyroid nodules which do not require stimulation from TSH.

207
Q

What is the management of a toxic multi-nodular goitre?

A

Radioiodine therapy

208
Q

What is the presentation of thyroid storm?

A
  • Medical emergency: 50% mortality untreated.
  • Hyperpyrexia > 41 oC
  • Accelerated tachycardia/arrhythmia
  • Cardiac failure
  • Delirium/frank psychosis
  • Hepatocellular dysfunction – jaundice
209
Q

What is the management of a thyroid storm?

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

210
Q

What is the surgical management of a thyroid storm?

A

Thyroidectomy

Radiodine

211
Q

What are the side effects of thioamides?

A

Agranulocytosis (Reduction in neutrophil - neutropenia)

  • Increased sepsis risk
  • Rashes
212
Q

What is the pre-operative preparation for thyroidectomy?

A

Potassium iodide

213
Q

What effect is observed by the administration of iodine therapy in hyperthyroidism?

A

Wolff-Chaikoff effect - inhibition of thyroid hormone synthesis and secretion

214
Q

What are the main causes of Addison’s disease?

A
  • Primary - Autoimmune >70%
  • Infections: Tuberculosis, meningococcal septicaemia, CMV, histoplasmosis.
  • Infiltration: Metastasis (lung, breast, melanoma), lymphomas, amyloidosis.
  • Infarction: Secondary to thrombophilia.
  • Inherited: Adrenoleukodystrophy, ACTH receptor mutation.
  • Iatrogenic: Sudden cessation of long-term steroid therapy.
215
Q

What is the presentation of Addison’s disease?

A

Dizziness, anorexia, weight loss, diarrhoea, vomiting, abdominal pain

Lethargy, and weakness

Depression

Postural hypotension

216
Q

What are the examination findings associated with Addison’s disease?

A

Increased pigmentation - palmar creases, buccal mucosa

Loss of body hair in women

217
Q

What are the signs of an Addisonian crisis?

A 
Hypotensive shock
Tachycardia
Pale
Cold
Clammy 
Oliguria
218
Q

What are the consequences of adrenocortical failure?

A 
Hyponatremia
Hyperkalaemia
Hypotension
Hypoglycaemia fatigue
Hyperpigmentation
Weight loss
219
Q

What is the first-line investigation for Addison’s disease?

A

9 am cortisol - low (Diurnal rhythms exhibited by cortisol secretion)
<100

High ACTH

220
Q

What is the diagnostic investigation to confirming primary adrenal insufficiency?

A

Short synacthen test - 250ug

-There is reduced cortisol secretion - unresponsive to ACTH stimulation

221
Q

What is Waterhouse-Friderichsen syndrome?

A

Meningococcal infection precipitating adrenal haemorrhage and Addisonian crisis

222
Q

What are the precipitating factors for an Addisonian crisis?

A

Steroid withdrawal

Waterhouse-Fridericshen syndrome

Sepsis/Acute exacerbation of chronic insufficiency

223
Q

What is the first-line management of an Addisonian crisis?

A

Rapid IV infusion rehydration (0.9% saline, 1L over 30-60 minutes, 2-4L)

IV 200mg hydrocortisone bolus

224
Q

Which corticosteroid is administered first in Addison’s

A

Hydrocortisone

225
Q

What is the definitive management for Addison’s disease?

A

Hydrocortisone and fludrocortisone

226
Q

What is Cushing’s syndrome?

A

Syndrome associated with chronic inappropriate elevation of free circulating cortisol

227
Q

What are the ACTH-dependent causes of Cushings?

A

Excess ACTH secretion from a pituitary adenoma (Cushing’s disease)- Responds to High-dose dexamethasone suppression test

228
Q

What are the ACTH independent causes of Cushing’s?

A

Benign adrenal adenoma
Adrenal carcinoma
Adrenal nodular hyperplasia
Oral steroids - main cause

229
Q

Which lung is the associated?

A

Small cell lung cancer

230
Q

What is the presentation of Cushing’s?

A 
Weight gain 
Fatigue
Muscle weakness- Proximal myopathy 
Myalgia
Thin skin 
Easy bruising
Poor wound healing
Fractures
Frontal balding
Recurrent Achilles tendon rupture
231
Q

What are the examination findings are associating with Cushing’s?

A 
Moon face
Facial plethora
Interscapular fat pad- buffalo neck hump
Supraclavicular fat distribution 
Thin skin
Myopathy
Bruises
Central obesity
Striae
Kyphosis
Hypertension, ankle oedema
Pigmentation in ACTH dependent cases
232
Q

What is the first-line investigation for Cushing’s?

A

24-hour urine collection of urinary free cortisol

Late-night salivary cortisol

233
Q

What is the diagnostic investigation to differentiate between Cushing’s disease and syndrome?

A

Low-dose dexamethasone test

High-dose dexamethasone test

234
Q

What does a high-dose dexamethasone test reveal ACTH-independent Cushing’s?

A

No suppression- indicates adrenal hyperplasia

235
Q

What investigations are performed in ACTH-independent Cushing’s?

A

Low plasma ACTH

CT or MRI of adrenals

Phase1c Medicine (11 decks)

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