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ENDOCRINE Flashcards

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1
Q

Give 5 parathyroid hormone actions

A
  1. Increase Ca2+ reabsorption
  2. Decrease phosphate reabsorption
  3. Increase 1 alpha-hydroxylation of 25-OH vit D
  4. Increase bone remodelling (bone resorption >bone formation)
  5. Increase Ca2+ absorption because of increase 1,25(OH)2D (no direct effect)
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2
Q

When serum calcium levels are low, what are PTH levels?

A

PTH levels are high

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3
Q

When serum calcium levels are high, what are PTH levels?

A

PTH levels are low

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4
Q

What is the effect of hyperparathyroidism on serum calcium levels?

A

Hyperparathyroidism –> hypercalcaemia

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5
Q

what are the clinical features of hyperparathyroidism?

A

SYMPTOMS

 - BONES – excess bone resorption caused by PTH Pain, fractures, osteopenia, osteomalacia, osteoporosis
  - STONES – due to excess Ca. Renal colic from renal calculi and biliary stones
  - GROANS – abdominal pain, malaise, nausea, constipation, polydipsia, polyuria, dehydration, confusion, risk of cardiac arrest
  - MOANS – depression, anxiety, cognitive dysfunction, insomnia, coma

SIGNS
hypercalcaemia

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6
Q

Give 2 causes of primary hyperparathyroidism

A
  • Parathyroid adenoma
  • Hyperplasia
  • Parathyroid cancer
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7
Q

what is the the pathophysiology of secondary hyperparathyroidism

A

Physiological compensatory hypertrophy of all parathyroid resulting in excess PTH due to hypocalcaemia
Often due to CKD and vitamin D deficiency

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8
Q

what is the pathophysiology of tertiary hyperparathyroidism?

A

Prolonged uncorrected hypertrophy - glands become autonomous producing excess PTH

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9
Q

What blood results would you see in the 3 types of hyperparathyroidism?

A

PRIMARY =

  • PTH = high
  • calcium = high
  • phosphate = low
  • alk phos = high

SECONDARY =

  • PTH = high
  • calcium = low
  • phosphate = high
  • alk phos = high

TERTIARY -

  • PTH = high
  • calcium = high
  • phosphate = high
  • alk phos = high
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10
Q

Describe the treatment for hyperparathyroidism

A
  • adenoma = surgical removal
  • hyperplasia = all 4 glands surgically removed
  • calcimimetric = ORAL CINACALET
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11
Q

How does a calcium mimetic work?

A

Increases sensitivity of parathyroid cells to calcium so less PTH secretion occurs

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12
Q

What is the affect of hypoparathyroidism on serum calcium levels?

A

Hypoparathyroidism –> hypocalcaemia

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13
Q

what are the clinical features of hypoparathyroidism?

A

SYMPTOMS:CATs go numb

  1. convulsions / seizures
  2. arrhythmias / anxious
  3. tetany / muscle spasms
  4. numbness

SIGNS:

  • CHVOSTEK’S SIGN - tap over facial nerve and look for spasm of facial nerves
  • TROUSSEAU’S SIGN - inflate BP cuff 20 mmHg above systolic for 5 mins = hand spasm - hypocalcaemia
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14
Q

what are the causes of hypoparathyroidism?

A
  • secondary to increased serum phosphate
  • severe vitamin D deficiency
  • reduced PTH function
  • drugs - calcitonin, bisphosphonates
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15
Q

What are blood results for someone with hypoparathyroidism?

A 
Calcium = Low 
PTH = Low
Phosphate = High
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16
Q

What is the treatment for hypoparathyroidism?

A 
Acute = IV calcium 
Persistant = Vitamin D analogue - ORAL ADCAL
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17
Q

what are the causes of Hypercalcaemia?

A 
Hyperparathyroidism
Malignancy
Sarcoidosis
Thyrotoxicosis
Drugs
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18
Q

What is the treatment for hypercalcaemia?

A
  • Treat underlying cause
  • increase circulation volume, increase excretion
    .- Bisphosphonates, glucocorticoids, gallium, dialysis
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19
Q

Give 2 ECG changes that you might see in someone with hypercalcaemia

A
  1. Tall T waves

2. Shortened QT interval

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20
Q

Name 3 causes of hypocalcaemia

A 
Hypoparathyroidism
Vitamin D deficiency
Hyperventilation
Drugs
Malignancy
Toxic shock
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21
Q

what are the investigations for hypocalcaemia?

A

Corrected Calcium levels,
ECG (prolonged QT)
Parathyroid function - PTH

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22
Q

what is the treatment for hypocalcaemia?

A

10ml calcium gluconate/chloride 10% slow IV,

oral calcium and Vit D

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23
Q

Give 2 ECG changes that you might see in hypocalcaemia?

A
  1. Small T waves

2. Long QT interval

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24
Q

What does the parathyroid control?

A

Serum calcium levels

A low serum calcium triggers the release of PTH and a high serum calcium triggers c-cells to release calcitonin

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25
What hormone does the parathyroid secrete and what is its function?
PTH - secreted in response to low serum calcium
26
What is released by c-cells in the parathyroid in response to high serum calcium?
Calcitonin
27
What biochemical test might you want to do to establish the cause of hypercalcaemia?
PTH measurement
28
What disease is described as being a 'disorder of carbohydrate metabolism characterised by hyperglycaemia'?
Diabetes mellitus
29
what is T1DM?
Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.
30
what is the pathophysiology of T1DM
- autoimmune destruction of beta cells in the Islets of Langerhans by autoantibodies cause insulin deficiency and continued breakdown of liver glycogen - this causes hyperglycaemia and glycosuria
31
Is T1DM characterised by a problem with insulin secretion, insulin resistance or both?
Characterised by impaired insulin secretion - severe insulin deficiency
32
what are the risk factors for developing T1DM?
- Northern European - Family History: - HLA DR3-DQ2 or - HLA-DR4-DQ8 - Other autoimmune diseases: - Autoimmune thyroid - Coeliac disease - Addison’s disease - Pernicious anaemia
33
what are the clinical features of T1DM?
Polydipsia - Thirst (fluid and electrolyte losses) Polyuria (due to osmotic diuresis) Weight loss - usually short history of severe symptoms
34
Describe the epidemiology of T1DM
``` Onset younger (<30 years) Usually lean More Northern European ancestry ```
35
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons fasting plasma glucose be if they were diabetic?
Fasting plasma glucose >7 mmol/L
36
A diagnosis of diabetes can be made by measuring plasma glucose levels. What would a persons random plasma glucose be if they were diabetic?
Random plasma glucose >11 mmol/L
37
What might someone's HbA1c be if they have diabetes?
>48 mmol/L>6.5%
38
What happens to C-peptide in T1DM?
C-peptide reduces
39
How do you treat T1DM?
Education Glycaemic control through diet (low sugar, low fat, high starch) Insulin SC
40
Give 6 complications of Diabetes Mellitus
1. Diabetic ketoacidosis 2. Diabetic nephropathy 3. Diabetic retinopathy 4. Diabetic neuropathy 5. Hyperosmolar hyperglycaemic coma 6. Stroke, ischaemic heart disease, peripheral vascular disease
41
Give 2 potential consequences of T1DM
1. Hyperglycaemia | 2. Raised plasma ketones --> ketoacidosis
42
How is insulin administered in someone with T1DM?
Subcutaneous injections
43
Other than SC injections, how else can insulin be administered?
Insulin pump
44
what are the different types of insulin used to treat T1DM?
- short acting - 4-6hrs - short acting analogues - - long acting - 12-24hrs
45
Give 4 potential complications of insulin therapy
1. Hyperglycaemia 2. Lipohypertrophy at injection site 3. Insulin resistance 4. Weight gain 5. Interference with life style
46
What is the affect of cortisol on insulin and glucagon?
Inhibits insulin | Activates glucagon
47
Describe the pathophysiology of diabetic ketoacidosis
Results from a reduced supply of glucose and an increase in fatty acid oxidation. The increased production of Acetyl-CoA leads to ketone body production that exceeds the ability of peripheral tissues to oxidise them. Ketone bodies are relatively strong acids (pH 3.5), and their increase lowers the pH of blood it IMPAIRS THE ABILITY OF HAEMOGLOBIN TO BIND TO OXYGEN
48
Name 3 ketone bodies
1. Acetoacetate 2. Acetone 3. Beta hydroxybutyrate
49
Where does ketogenesis occur?
Liver
50
what are the clinical features of diabetic ketoacidosis?
SIGNS - Breath smells of pear drops (ketones) - Kussmaul’s breathing - deep, rapid breathing - Tachycardia - Hypotension - Reduced tissue turgor SYMPTOMS - Nausea and vomiting - Dehydration - exacerbated by vomiting - Weight loss - Drowsy/confused - Abdominal pain
51
Give 3 microvascular compilation of DM
1. Diabetic retinopathy 2. Diabetic nephropathy 3. Diabetic peripheral neuropathy
52
Give 2 macrovascular complications fo DM
CV disease | Stroke
53
What is the main risk factor for diabetic complications?
Poor glycemic control
54
What is the treatment for diabetic ketoacidosis?
- ABC - Replace fluid loss with 0.9% saline IV - IV insulin - Restore electrolytes e.g. K+
55
Give 3 endocrine diseases that can cause diabetes
1. Cushing's 2. Acromegaly 3. Phaeochromocytoma
56
What class of drugs can cause diabetes?
Steroids Thiazides Anti-psychotics
57
Is T2DM characterised by problem with insulin secretion, insulin resistance or both?
Characterised by impaired insulin secretion and insulin resistance
58
what is the aetiology of T2DM?
- Decreased insulin secretion and increased insulin resistance - No immune disturbance - No HLA disturbance but strong genetic link - Polygenic - Associated with obesity, lack of exercise, calorie and alcohol excess
59
Describe the pathophysiology of T2DM
Insulin binds normally to its receptor – insulin resistance develops post-receptor Circulating insulin levels are higher than in healthy patients but inadequate to restore glucose homeostasis Increased glucose production in liver- inadequate suppression of gluconeogenesis and there’s reduced glucose uptake in peripheral tissues Hyperglycaemia and lipid excess are toxic to beta cells - reduced beta cell mass Don’t tend to develop ketoacidosis but do get glycosuria
60
Why is insulin secretion impaired in T2DM
Due to lipid deposition in the pancreatic islets
61
what are the risk factors for T2DM?
``` Increase w/ age M > F Ethnicity: African-Carribean, Black African and South Asian Obesity Hypertension ```
62
What happens to insulin resistance, insulin secretion and glucose levels in T2DM?
Insulin resistance increase Insulin secretion decreases Fasting and post-prandial glucose increase
63
Why do you rarely see diabetic ketoacidosis in T2DM?
Insulin secretion is impaired but there are still low levels of plasma insulin Low levels of insulin prevent muscle catabolism and ketogenesis
64
By how much has the beta cell mass reduced in T2DM when diagnosis usually occurs?
50% of normal beta cell mass
65
Describe the epidemiology of T2DM
Onset older (>30) Usually overweight More common in African/Asian populations Males > Females
66
Describe the treatment pathway for T2DM
1. Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions 2. Monotherapy - Metformin 3. dual therapy 4. triple therapy i) metformin ii) DPP4 inhibitor iii) SU, gliclazide iv) SGLT-2 inhibitor v) pioglitazone vi) insulin
67
How does metformin work in treating T2DM?
Increase insulin sensitivity and inhibits glucose production
68
How does sulfonylurea work in treating T2DM?
Stimulates insulin release block ATP dependent K+ channels in beta cells -> causes depolarisations and opening of voltage gated Ca2+ channels -> stimulates insulin secretion
69
what are the side effects of Sulfonylurea?
Hypoglycaemia weight gain hyponatraemia
70
What is hypoglycaemia classified as?
Plasma glucose <3.9 mmol/L and if <3.0 mmol/L it is severe hypoglycaemia
71
Give 5 symptoms of hypoglycaemia
1. Hunger 2. Sweating 3. Tachycardia 4. Anxious 5. Shaking 6. Confusion 7. Weakness 8. Vision changes
72
Why does hypoglycaemia continuously get worse?
Glucagon is not produced so rely only on adrenaline and the threshold for adrenaline release gradually lowers after time
73
Give 6 consequences of hypoglycaemia
1. Seizures 2. Comas 3. Cognitive dysfunction 4. Fear 5. Decrease in qualitative life 6. Accidents
74
Briefly describe the treatment of hypoglycaemia
Oral sugar and long acting starch 50% GLUCOSE IV or IM GLUCAGON If episodes persist, suggest many small high starch meals Re-educate diabetics on insulin use
75
Why are patient with diabetes at a particular risk of hypoglycaemia?
In Diabetes there are defects in the physiological defences to hypoglycaemia and there is reduced awareness
76
What does prevention of hypoglycaemia include?
Eduction Correct choice of therapy Adjusting glucose targets in those at high risk Specialist support from a MDT
77
Is insulin secretion or insulin resistance the driving force of hyperglycaemia in T2DM?
Hepatic insulin resistance is the driving force
78
Give a potential consequence of acute hyperglycaemia
Diabetic ketoacidosis and hyperosmolar coma
79
Give a potential consequence of chronic hyperglycaemia
Mirco/macrovascular tissue complications
80
A man presents with a history of weight loss, polyuria and nocturia. He is very unwell. The GP performs a capillary blood glucose which is found to be 17.2mmol/l. What is the most likely diagnosis of this mans symptoms?
Type 1 Diabetes Mellitus
81
Name 5 possible diseases of the pituitary
1. Benign pituitary adenoma 2. Craniopharygioma 3. Trauma 4. Apoplexy/Sheehans 5. Sarcoid/TB
82
Give 3 potential consequences of a pituitary tumour
1. Pressure on local structures - e.g. optic chasm = bilateral hemianopia 2. Pressure on normal pituitary (lack of function) - Hypopituitarism 3. Functioning tumours - e.g. Cushing's, acromegaly, prolactinoma
83
Describe the growth hormone secretion from the anterior pituitary
It is secreted in a pulsatile fashion and increases during deep sleep
84
What is acromegaly?
Overgrowth of all organ systems due to excess growth hormone in adults
85
What is gigantism?
Excess GH production in children before fusion of the epiphyses of the long bones
86
what are the clinical features of acromegaly?
``` SYMPTOMS: large hands, box jaw, thick skin, arthritis, sight problems weight gain ``` ``` SIGNS: hypertension, insulin resistance, bitemporal hemiopia large tongue ```
87
what is the pathophysiology of acromegaly?
GH exerts activity indirectly through IGF-1 or directly on tissue Excessive IGF- levels mediate most of the skeletal and soft tissue growth like features of acromegaly
88
What can cause acromegaly?
- A benign pituitary adenoma producing excess GH | - rarely due to hyperplasia
89
Describe the epidemiology of acromegaly
Average age is 40 years male = female Reduces life expectancy by 10 years
90
What complications are associated with acromegaly?
type 2 diabetes sleep aponea heart disease arthritis
91
What are the investigations for acromegaly?
1st line = IGF-1 2nd line = oral glucose tolerance test 3rd line = pituitary function tests 4th line = MRI also investigate for complications
92
What is the gold standard diagnostic test for acromegaly?
Oral glucose tolerance test - failure of glucose to suppress serum GH
93
what is the management for acromegaly?
1st line = trans sphenoidal surgery 2nd line = OCTREOTIDE (somatostatin analogue) +/- CABERGOLINE (dopamine agonist) if GH secretions persist 3rd line = PEGVISOMANT (GH receptor antagonist) 4th line = radiotherapy
94
Give 3 potential complications of transsphenoidal surgical resection for the treatment of acromegaly
1. Hypopituitarism 2. Diabetes insidious 3. Haemorrhage 4. CNS injury 5. Meningitis
95
What types of medical therapy can be used to treat acromegaly?
somatostatin analogue = octreotide dopamine agonist = cabergoline GH receptor antagonist = pegvisomant
96
Give 3 advantages of using dopamine agonists in the treatment of acromegaly
1. No hypopituitarism 2. Oral administration 3. Rapid onset
97
Give 2 disadvantages of dopamine agonists in the treatment of acromegaly
1. Can be ineffective | 2. Risk of side effects
98
Name a dopamine agonist that can be used as a treatment for acromegaly
Cabergoline
99
Why can somatostatin analogues be used in the treatment of acromegaly?
They inhibit GH release
100
Why can GH receptor antagonists be used in the treatment of acromegaly?
They suppresses IGF-1
101
What is prolactinoma?
Lactotroph cell tumour of the pituitary | Prolactin secreting tumour
102
Name the 2 types of prolactinoma
1. Microprolactinoma = most common, >90% | 2. Macroprolactinoma = >10mm
103
what are the causes of prolactinoma?
1. Pituitary adenoma 2. Anti-dopaminergic drugs 3. Head injury - compression of the pituitary stalk
104
what are the clinical features of prolactinoma
``` SYMPTOMS: amenorrhea, galactorrhoea, gynaecomastia, low libido, possible cerebral symptoms ``` SIGNS: low testosterone, infertility
105
Briefly describe the pathophysiology of Prolactinoma
Increased release of prolactin can cause galactorrhoea and can inhibit FSH and LH Compression of the pituitary stalk Prevents secretion of dopamine from hypothalamus - stops inhibition of prolactin
106
what are the investigations for prolactinoma?
Serum prolactin levels - HIGH | CT head
107
What is the treatment for prolactinoma?
Dopamine agonists - cabergoline - inhibits prolactin release | Occasionally transsphenoidal pituitary resection
108
What is Cushing's Syndrome?
Chronic, excessive and inappropriate elevated levels of circulating plasma glucocorticoids (cortisol)
109
What is Cushing's Disease?
When Cushing's syndrome is caused by a pituitary tumour so excess glucocorticoids due to inappropriate ACTH secretion
110
what is the clinical presentation of Cushing's disease?
``` Central obesity Plethoric complexion Moon face Mood change Proximal muscle weakness Purple abdominal striae Gastric ulcers Osteoporosis Hirsutism ```
111
what are the causes of excess cortisol?And are they ACTH dependent or independent?
ACTH dependent: - Cushing’s disease - Ectopic ACTH production - ACTH treatment ACTH independent - adrenal adenoma - iatrogenic
112
What is a differential diagnosis of Cushing's syndrome?
Pseudo-Cushing's = excessive alcohol consumption can mimic the clinical and biochemical signs but resolved on alcohol recession
113
Describe the epidemiology of Cushing's syndrome
women > men majority diagnosed 20-50y/o most common cause is oral steroids
114
what are the investigations for Cushing's syndrome?
1. drug history - oral steroids 2. random plasma cortisol - high 3. overnight dexamethasone suppression test and urinary free cortisol (24hr) - positive (no suppression = cushings) 4. test plasma ACTH
115
How does a dexamethasone suppression test work?
Give synthetic steroids that suppress pituitary and adrenals and then measure the cortisol In Cushing's there is no suppression of cortisol
116
What is the treatment for Cushing's syndrome?
Tumours = surgical removal - pituitary adenoma = transsphenoidal surgical resection - adrenal adenoma = adrenalectomy Drugs to inhibit cortisol synthesis - metyrapone, ketoconazole
117
What are some complications associated with Cushing's Syndrome?
cardiovascular disease hypertension diabetes mellitus osteoporosis
118
What is the circadian system?
Body clock that regulates your body | Clear rhythm of cortisol production follows circadian rhythm
119
When do cortisol levels peak?
At around 8:30 am
120
What's the primary cue that synchronises an organism's biological rhythms?
Light
121
What is adrenal insufficiency?
Adrenocortical insufficiency resulting in a reduction of mineralocorticoids, glucocorticoids and androgens
122
what is Addison's disease?
Destruction of entire adrenal cortex resulting in mineralocorticoid (aldosterone), glucocorticoid and androgen deficiency
123
what are the causes of Addison's disease?
- autoimmune destruction (21-hydroxylase present in 60-90%) - most common in developed countries - TB - most common in developing countries - adrenal metastases- long term steroid use
124
what are the clinical features of Addison's disease?
SYMPTOMS Fatigue Weakness Weight loss ``` SIGNS Hyperpigmentation Postural hypotension Hypoglycaemia Other signs of autoimmunity ```
125
What is the treatment for adrenal insufficiency?
Hormone replacement - any steroids ORAL HHYDROCORTISONE ORAL FLUDROCORTISONE
126
What is the pathophysiology of Addison's disease?
Destruction of the adrenal cortex results in decreased production of the hormones All steroids reduced Reduced cortisol levels = increased CRH and ACTH production through feedback
127
What are the investigations for Addison's disease?
- SynACTHen test = giving synthetic ACTH does not increase cortisol levels - Serum electrolytes = low Sodium, high Potassium - FBC: Anaemia and eosinophilia - Morning serum cortisol = Reduced - Adrenal CT or MRI
128
What investigations would you do to determine whether Adrenal insufficiency is primary or secondary?
``` Primary = adrenal antibodies, very long chain fatty acids, imaging and genetics Secondary = any steroids?, imaging and genetics ```
129
what are the features of addisonian crisis?
``` Vomiting abdominal pain profound weakness hypoglycaemia hypovolemic shock ```
130
What is the management of adrenal crisis?
Immediate IV Hydrocortisone | Fluid resuscitation - saline (IV)
131
What would sodium and potassium levels be in someone with adrenal insufficiency?
Hyponatraemia = low sodium Hyperkalaemia = high potassium Lack of aldosterone and so less sodium reabsorbed and less potassium excreted
132
Why is it important to take a drug history when speaking to someone with potential Cushing's?
To exclude steroid use as a potential cause
133
Briefly describe the mechanism of thyroid destruction
Cytotoxic (CD8+) T cell mediated thyroglobulin and Thyroid peroxidase (TPO) antibodies may cause secondary damage (alone have no effect) Antibodies against the TSH receptor may block the effect of TSH (uncommon)
134
What are the main 3 types of cells that cause thyroid destruction?
1. Cytotoxic T cells 2. Thyroglobulin 3. TPO antibodies
135
Briefly describe the pathophysiology of Grave's disease
Specific serum IgG (TSH receptor stimulating antibodies) bind to TSH receptors in thyroid Behave like TSH – stimulate T3 and T4 production This results in excess secretion and hyperplasia of thyroid follicular cells – causing hyperthyroidism and graves ophthalmopathy
136
what is the clinical presentation of Grave's opthlmopathy?
``` SYMPTOMS Eye discomfort Grittiness increased tear production Photophobia Diplopia reduced acuity ``` ``` SIGNS Exophthalmos – protruding eye Proptosis – eye protrudes beyond orbit Conjunctival oedema Corneal ulceration Ophthalmoplegia – paralysis of eye muscles ```
137
what is the clinical presentation of grave's dermopathy?
Pretibial myxoedema – raised, purple red symmetrical skin lesions over anterolateral aspects of shin Thyroid acropachy – clubbing, swollen fingers and periosteal bone formation
138
what is the treatment for Grave's ophthalmology?
Conservative treatment – smoking cessation and sunglasses | IV METHYLPREDNISOLONE and surgical decompression/eyelid surgery
139
Name 5 risk factors for Graves disease
1. Female 2. Genetic association 3. E.coli 4. Smoking 5. Stress 6. High iodine intake 7. Autoimmune diseases
140
Name 5 autoimmune diseases associated with thyroid autoimmunity
1. T1DM 2. Addison's disease 3. Pernicious anaemia 4. Vitiligo 5. Alopecia areata 6. Rheumatoid arthritis
141
What would you see histological in someone with Graves disease?
Lymphocyte infiltration and thyroid follicle destruction
142
What is goitre?
Palpabel and visible thyroid enlargement
143
Why does goitre occur and when is is most commonly found?
Due to TSH receptor stimulation resulting in thyroid growth | Seen in hypo and hyperthyroidism
144
Name 4 types of sporadic non toxic goitre
1. Diffuse --> physiological --> Graves 2. Multi nodular 3. Solitary nodule 4. Dominant nodule
145
Define hyperthyroidism
Overactivity of the thyroid gland
146
Define thyrotoxicosis
Excess of thyroid hormone in the blood (can be used interchangeably with hyperthyroidism)
147
Name the 3 mechanisms of how hyperthyroidism may come about
1. Overproduction of thyroid hormone 2. Leakage of preformed hormone from the thyroid 3. Ingestion of excess thyroid hormone
148
what are the causes of hyperthyroidism?
- Grave’s disease - Toxic multinodular goitre - Solitary toxic nodule/adenoma - benign - De Quervarians thyroiditis - Postpartum thyroiditis - Drug induced
149
Name 4 drugs which can induce hyperthyroidism
1. Iodine 2. Amiodarone 3. Lithium 4. Radioconstrast agents
150
what are the clinical features of hyperthyroidism?
``` SYMPTOMS: hot and sweaty, diarrhoea, wt. loss, anxiety/restlessness, hyperphagia ``` SIGNS: periorbital swelling, goitre, tachycardia
151
What investigations are done to diagnose hyperthyroidism?
TFTs: primary = high T3 and T4, low TSH secondary = high T3 and T4, high TSH
152
What are the thyroid function test results in primary hyperthyroidism?
high T4 high T3 low TSH
153
What are the thyroid function rests in secondary hyperthyroidism?
high T4 high T3 high TSH
154
What are the 4 main treatments for hyperthyroidism?
1. Beta blockers - PROPRANOLOL 2. Anti-thyroid drugs - CARBIMAZOLE 3. Radioiodine 4. Surgery - partial/total thyroidectomy
155
Why are beta blockers used to treat hyperthyroidism?
For rapid control of symptoms
156
Give examples of anti-thyroid drugs and why are they used?
- Carbimazole, methimazole, proplythiouracil (PTU) - (thionamides) - Decreases synthesis of new thyroid hormone by targeting thyroid peroxidase - PTU also inhibits conversion of T4 to T3
157
Give 4 poor prognostic factors of those on anti-thyroid drugs
1. Severe biochemical hyperthyroidism 2. Large goitre 3. Male 4. Young age of disease onset
158
Give 5 side effects of anti-thyroid drugs
1. Rash 2. Arthralgia 3. Hepatitis 4. Neuritis 5. Vasculitis 6. Agranulocytosis - very serious
159
Why can radioiodine be used as a treatment for hyperthyroidism?
Emit beta particle that destroy thyroid follicle and therefore reducing the production of thyroid hormones
160
Give 4 potential consequences of a partial thyroidectomy
1. Bleeding 2. Hypoglycaemia 3. Hypothyroidism 4. Recurrent laryngeal nerve palsy
161
What is a complication of hyperthyroidism?
Thyroid crisis/storm graves ophthalmopathy hypothyroidism
162
Briefly explain thyroid crisis/storm
Rapid deterioration of thyrotoxicosis | Hyperpyrexia, tachycardia and extreme restlessness Delirium --> coma --> death
163
What is the treatment for a thyroid crisis?
Large doses of oral carbimazole, oral propranolol, oral potassium iodide and IV hydrocortisone
164
Define hypothyroidism
Under-activity of the thyroid gland
165
Name the 3 types of hypothyroidism
1. Primary - absence/dysfunction of thyroid gland 2. Secondary - reduced TSH from anterior pituitary 3. Tertiary - associated with treatment withdrawal
166
Briefly describe the pathophysiology of primary hypothyroidism
Underactivity usually primary from disease of the thyroid but may be secondary due to hypothalamic-pituitary disease resulting in reduced TSH
167
Briefly describe the pathophysiology of secondary hypothyroidism
Reduced release or production of TSH so reduced thyroid hormone release
168
Briefly describe the pathophysiology of tertiary hypothyroidism
Thyroid gland overcompensates until it can reestablish correct concentration fo thyroid hormone
169
Name 4 causes of primary hypothyroidism
1. autoimmune thyroiditis 2. postpartum thyroiditis 3. iatrogenic 4. drug induced 5. iodine deficiency 6. congenital
170
Give 2 examples of iatrogenic causes of hypothyroidism
1. Thyroidectomy | 2. Radioiodine therapy
171
Give an example of a transient cause of primary hypothyroidism
Post-partum thyroiditis
172
Name 4 drugs that can cause hypothyroidism
1. Carbimazole (used to treat hyperthyroidism) 2. Amiodarone 3. Lithium 4. Iodine
173
Name 3 causes of secondary hypothyroidism
1. Hypopituitarism 2. Hypothalamic disease 3. Isolated TSH deficiency
174
Why can amiodarone cause both hypo and hyperthyroidism?
Because it is iodine rich
175
what are the clinical features of hypothyroidism?
SYMPTOMS: wt. gain, depression, constipation, cold intolerance, “brain fog” SIGNS: bradycardia, delayed reflexes
176
What investigations are conducted to diagnose hypothyroidism?
Thyroid function tests | Thyroid antibodies
177
What are the TFT results for primary hypothyroidism?
High TSH | Low T4 and T3
178
What are the TFT results for secondary hypothyroidism?
Inappropriately low TSH for low T4 and T3
179
Name 3 antibodies that may be present in the serum in someone with autoimmune thyroiditis
1. TPO (thyroid peroxidase) 2. Thyroglobulin 3. TSH receptor
180
What is the treatment for primary hypothyroidism?
Thyroid hormone replacement - levothyroxine Resection of obstructive goitre
181
what are the complications of hypothyroidism?
Myxoedema coma - medical emergency heart disease pregnancy problems
182
Briefly explain a myxoedema coma
Severe hypothyroidism | Reduced level of consciousness, seizures, hypothermia IV/oral T3 and glucose infusion needed
183
What is Hashimoto's thyroiditis?
Hypothyroidism due to aggressive destruction of thyroid cells
184
Give 3 symptoms of Hashimoto's thyroiditis
1. Rapid formation of Goitre 2. Dyspnoea or dysphagia 3. General hypothyroidism symptoms
185
Name 3 triggers of Hashimoto's thyroiditis
1. Iodine 2. Infections 3. Smoking 4. Stress
186
What are the investigations for Hashimoto's thyroiditis?
TFTs - high TSH, low T3 and T4 | high TPO antibodies
187
What is the treatment for Hashimoto's thyroiditis?
Levothyroxine
188
Name a complication fo Hashimoto's thyroiditis
Hyperlipidaemia
189
what are the complications of Hashimoto's thyroiditis?
Hashimoto's encephalopathy
190
What disease would you treat with Carbimazole?
Hyperthyroidism/Graves disease
191
What disease would you treat with Levothyroxine?
Hypothyroidism
192
Name 3 disease associated with the posterior pituitary
1. Cranial diabetes insipidus - lack of ADH 2. Nephrogenic diabetes insipidus - resistance to action of ADH 3. Syndrome of antidiuretic hormone secretion - too much ADH release inappropriately
193
Define diabetes insipidus
Passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption in the kidney due to hypo secretion or insensitivity to ADH
194
Name the 2 types of DI
1. Cranial DI = reduced vasopressin (ADH) produced by hypothalamus and secreted by the posterior pituitary 2. Nephrogenic DI = impaired response of the kidney to ADH
195
what are the clinical features of DI?
SYMPTOM - Polyuria - Polydipsia - No glycosuria SIGNS - Dry mucosa - Sunken eyes - Changes in skin turgidity - Can lead to dehydration - Hypernatremia
196
what are the causes of cranial DI?
``` Idiopathic Congenital defects in ADH gene Disease of hypothalamus Tumour – metastases, posterior pituitary Trauma – neurosurgery Infiltrative disease ```
197
what are the causes of nephrogenic DI?
- Hypokalaemia - Hypercalcaemia - Drugs - lithium chloride - Demeclocycline - glibenclamide - Renal tubular acidosis - Sickle cell disease - Prolonged polyuria of any cause - Familial (mutation in ADH receptor)
198
Give 3 possible differential diagnosis's of DI
1. DM 2. Hypokalaemia 3. Hypercalcaemia
199
what are the investigations for diabetes insipidus?
- Water deprivation test - Desmopressin given and urine osmolality measured for 2-4 hrs with free fluids allowed - NDI diagnosed if urine osmolality stays the same - CDI diagnosed if urine osmolality increases by >50%ADH suppression test- shows neurogenic - Urine dip, glucose, U&E, fluid status
200
What is the treatment for cranial DI?
- Treat underlying condition - Thiazide diuretics (BENDROFLUMETHIAZIDE) - sensitise renal tubules to endogenous vasopressin - DESMOPRESSIN - high activity at V2 receptor
201
What is the treatment for nephrogenic DI?
- treat cause - thiazide diuretics - (BENDROFLUMETHIAZIDE) - Produces hypovolaemia which will encourage the kidneys to take up more Na+ and water in proximal tubule - NSAIDs - IBUPROFEN - Lower urine volume and plasma Na+ by inhibiting prostaglandin synthase. Prostaglandins locally inhibit the action of ADH
202
Do you have hyponatraemia or hypernatraemia in diabetes insipidus?
Hypernatraemia
203
Give 4 causes of polyuria
1. Hypokalaemia 2. Hypercalcaemia 3. Hyperglycaemia 4. Diabetes insipidus
204
What is SIADH?
Syndrome of inappropriate ADH secretion Continuous ADH secretion inspire of plasma hypotonicity, leading to retention of water and excess blood volume and thus hyponatraemia
205
what are the clinical features of SIADH?
``` SYMPTOMS: Nausea and vomiting Headache Lethargy Cramps Weakness Confusion / irritability ``` SIGNS raised JVP oedema ascites
206
what are the causes of SIADH?
``` brain injury infection hypothyroidism cancers lung diseases ```
207
what are the investigations for SIADH?
- ADH levels - U and Es (low sodium normal potassium), - fluid status distinguish SIADH from salt & water depletion - test with 1-2L of 0.9% saline: • Sodium depletion will respond • SIADH will NOT RESPOND
208
what is the pathophysiology of SIADH?
- Excess release of ADH will result in increased insertion of aquaporin 2 channels in apical membrane of collecting duct - Excess water retention which dilutes blood plasma - Result in hyponatremia as Na+ conc decreases
209
Describe the treatment for SIADH
1. Restrict fluid - <1L/day 2. Give salt 3. Loop diuretics - furosemide 4. Demeoclocycline - inhibitor of ADH 5. ADH-R antagonists - vaptans - primate water excretion with no loss of electrolytes
210
How do you treat asymptomatic SIADH?
Fluid restriction
211
How do you treat very symptomatic SIADH?
Give 3% saline (hypertonic)
212
Would you expect a patient with SIADH to be hypovolaemic, euvolaemic or hypervolaemic?
Euvolaemic
213
Would you associate SIADH with hyponatraemia or hypernatraemia?
Hyponatraemia - <135 mmol/L
214
Would you associate SIADH with plasma hypo-osmolality or hyper-osmolality?
Plasma hypo-osmolality - <275 mOsmol/Kg
215
Would you associate SIADH with a high to low urine osmolality?
High urine osmolality
216
Define hyponatraemia
<135 mmol/L | Biochemically severe = serum sodium <125 mmol/L
217
What stimulates the posterior pituitary to release ADH?
Osmoreceptors in the hypothalamus detect raised plasma osmolality Posterior pituitary is signalled to release ADH
218
Give 4 local effects a pituitary adenoma
1. Headaches 2. Visual field defects - bitemporal hemianopia 3. Cranial nerve palsy and temporal lobe epilepsy 4. CSF rhinorrhoea
219
What investigations are done when pituitary dysfunction is suspected?
Hormonal tests If hormonal tests are abnormal or tumour mass effect perform MRI pituitary
220
What do you test the thyroid axis for in pituitary disease?
Measure Free T4 and TSH
221
What is the affect of primary hypothyroidism on TSH and T4 levels?
TSH highT4 low
222
What is the effect of secondary hypopituitarism on TSH and T4 levels?
TSH low | T4 low
223
What can lead to elevated levels of prolactin?
1. Stress 2. Drugs 3. Pressure on pituitary stalk 4. Prolactinoma
224
What is the best radiological evaluation for the pituitary?
MRI - better visualisation of soft tissue and vascular structures
225
Name 3 ketone bodies
1. Beta hydroxybutyrate 2. Acetoacetate 3. Acetone
226
Does diabetic ketoacidosis occur in T1 or T2 DM?
Type 1
227
Describe the triad of DKA
1. Hyperglycaemia - blood glucose >11 mmol/L 2. Acidaemia - blood pH <7.3 or plasma bicarbonate <15 mmol/L 3. Raised plasma ketones - urine ketones >2+
228
Give 4 causes of DKA
1. Unknown 2. Infection 3. Treatment error - not administering enough insulin 4. Having undiagnosed T1DM
229
Give 5 symptoms of DKA
1. Polyuria 2. Polydipsia 3. Weight loss 4. Nausea and vomiting 5. Confusion 6. Weakness
230
Give 3 signs of DKA
1. Hyperventilation 2. Dehydration 3. Hypotension 4. Tachycardia 5. Coma
231
What is the treatment for DKA
Rehydration (3L in first 3 hours) Insulin Replacement of electrolytes - K+Treat underlying cause
232
Give 4 potential complications of untreated DKA
1. Cerebral oedema 2. Adult respiratory distress syndrome 3. Aspiration pneumonia 4. Thromboembolism 5. Death
233
In what class of drugs does metformin belong?
Biguanide
234
Give an example of a sulfonylurea
Tolazamide | Gliclazide
235
What are the physiological defences to hypoglycaemia?
Release of glucagon and adrenaline
236
What are the symptoms of hypoglycaemia?
Autonomic - sweating, tremor, palpitations Neuroglycopenic - confusion, drowsiness, incoordination Severe neuroglycopenic - convulsions, coma
237
Name 3 other types of diabetes other than T1DM, T2DM and DI
1. Maturity onset diabetes of the young (MODY) 2. Permanent neonatal diabetes 3. Maternal inherited diabetes and deafness
238
Name 3 exocrine causes of Diabetes
1. Inflammatory - actue/chronic pancreatitis 2. Hereditary haemochromatosis 3. Pancreatic neoplasia 4. Cystic fibrosis
239
Name 3 endocrine causes of Diabetes
1. Acromegaly 2. Cushing's syndrome 3. Peochromocytoma
240
What is Pheochromocytoma?
A rare catecholamine secreting tumour in the adrenal medulla (chromatin cells)
241
what are the different types of pheochromocytoma?
1. Familial type - more NAd | 2. Sporadic - more Ad
242
what are the clinical features of pheochromocytoma?
``` SYMPTOMS Headache Profuse Sweating Palpitations Tremor ``` ``` SIGNS Hypertension Postural hypotension Tremor hypertensive retinopathy Pallor ```
243
What are the investigations for pheochromocytoma?
- Plasma metanephrines and normetanephrines - 24 hour urinary total catecholamines - CT – look for tumour
244
What is the treatment for pheochromocytoma?
Without HTN crisis: 1st Line: Alpha blockers: PHENOXYBENZAMINE Most patients will eventually get the tumour removed and then managed medically. With HTN crisis: 1st Line: Antihypertensive agents: PHENTOLAMINE
245
What is the major complication of surgery on a patient with a pheochromocytoma?
Can stoke out during surgery due to rapid effect of adrenaline on the BP
246
What is the major concern in someone with pheochromocytoma?
Dangerous cause of hypertension
247
17 year old man presents with intermittent headaches and anxiety. He is sweating and vomiting. His BP is 223/159 and his pulse is 115. What is the likely cause?
Phaeochromocytoma crisis | Hypertension and tachycardia = phaeochromocytoma until proved otherwise (especially in younger patients)
248
What is the management of a phaeochromocytoma crisis?
Non-competitive alpha-blocker e.g. phenoxybenzamine Excision of paraganglioma Biochemistry: measure plasma and serum metanephrines
249
What are the 3 main sites where microvascular complications of Diabetes cause particular damage?
1. Retina = retinopathy 2. Glomerulus = nephropathy 3. Nerve sheath = neuropathy
250
How long after a young patient has been diagnosed do microvascular complications start to manifest?
10-20 years after diagnosis
251
Give 5 risk factors for diabetic retinopathy
1. Long duration DM 2. Poor glycaemic control 3. Hypertensive 4. On insulin treatment 5. Pregnancy 6. High HbA1c
252
Describe the pathophysiology of diabetic retinopathy
Micro-aneurysms --> pericyte loss and protein leakage --> occlusion --> ischaemia
253
How can diabetic retinopathy be sub-divided?
``` R1 = non-proliferative/background R2 = pre-proliferative R3 = Proliferative ```
254
What would you see in someone with an R1 retinopathy grade?
Non-proliferative/background Micro-aneurysms Intraretinal haemorrhages Exudates
255
What would you see in someone with an R2 retinopathy grade?
Pre-proliferative Venous bleeding Growth of new vessels
256
What would you see in someone with an R3 retinopathy grade?
Proliferative | New blood vessel on disc
257
What is the treatment for diabetic retinopathy?
Regular screening to assess visual acuity | Laser therapy treats neovascularisation - doesn't improve sight but stabilises
258
What are the main risks of laser treatment of diabetic retinopathy?
Loss of night vision and peripheral vision
259
What is diabetic maculopathy?
Fluid form leaking vessel is cleared poorly in macular area causing macula oedema which distorts and thickens the retina at the macula Leads to loss of central vision
260
What is the hallmark of diabetic nephropathy?
Development of proteinuria and progressive decline in renal function
261
What happens to the glomerular basement membrane in someone with diabetic nephropathy?
On microscopy there is thickening of the glomerular basement membrane
262
Give one way in which the presentation of diabetic nephropathy differs between T1 and T2DM
T1DM - microalbuminuria develops 5-10 years after diagnosis | T2DM - microalbuminuria is often present at diagnosis
263
Give 2 risk factors for diabetic nephropathy
1. Poor blood pressure | 2. Poor blood glucose control
264
Describe the treatment for diabetic nephropathy
1. Glycaemic and BP control 2. Angiotensin receptor blockers/ACE inhibitors - RAMIPRIL or CANDESARTAN 3. Proteinuria and cholesterol control
265
What is the commonest form of diabetic neuropathy?
Distal symmetrical neuropathy
266
Give 5 risk factors for diabetic neuropathy
1. Poor glycaemic control 2. Hypertension 3. Smoking 4. High HbA1c 5. Overweight 6. Long duration DM
267
Why do isolated mononeuropathies result from in diabetic neuropathy?
Occlusion of vasa nervorum - small arteries that provide blood supply to peripheral nerves
268
Why do more diffuse neuropathies arise in diabetic neuropathy?
Accumulation of fructose and sorbitol which disrupts the structure and formation of the nerve
269
Give 3 major clinical consequences of diabetic neuropathy
1. Pain 2. Autonomic neuropathy 3. Insensitivity
270
Describe the pain associated with diabetic neuropathy
Burning Paraethesia Allodynia - triggering of pain from stimuli that doesn't usually cause pain
271
What is autonomic neuropathy in relation to diabetic neuropathy?
Damage to the nerves that supply body structures that regulate function such as BP, HR, bowel/bladder emptying
272
Give 5 signs of autonomic neuropathy in diabetic neuropathy
1. Hypotension 2. HR affected 3. Diarrhoea/constipation 4. Incontinence 5. Erectile dysfunction 6. Dry skin
273
What are the consequences of insensitivity as a result of diabetic neuropathy?
Insensitivity --> foot ulceration --> infection --> amputation
274
Describe the distribution of insensitivity as a result of diabetic neuropathy
Glove and sticking distribution - starts in the toes and moves proximally
275
Describe the treatments for diabetic neuropathy
1. Improve glycaemic control 2. tricyclic antidepressants - AMITRIPTYLINE 3. Pain relief - PARACETAMOL and TRAMADOL
276
Give 5 ways in which amputation can be prevented in someone with diabetic neuropathy
1. Screening for insensitivity 2. Education 3. MDT foot clinics 4. Pressure relieving footwear 5. Podiatry 6. Revascularisation and antibiotics
277
What are the 4 main threats to skin and subcutaneous tissues in someone with diabetic neuropathy
1. Infections 2. Ischaemia 3. Abnormal pressure 4. Wound environments
278
Would there be increased or decreased pulses in diabetic neuropathic foot?
Decreased foot pulses
279
Peripheral vascular disease is a complication of Diabetes. Give 6 signs of acute ischaemia
1. Pulseless 2. Pale 3. Perishing cold 4. Pain 5. Paralysis 6. Paraesthesia
280
what infections can poorly controlled diabetes lead to?
1. UTIs 2. Staphylococcal infection of skin 3. Mucocutaneous candidiasis 4. Pyelonephritis 5. TB 6. Pneumonia 7. rectal abscess
281
Why does the site of insulin injection need to be varied day to day?
Can cause lipohypertrophy if the same site is used everyday
282
Name 4 non insulin treatments for diabetes
1. Metformin 2. Sulphonylurea 3. Incretin based agents 4. Thiazolidinediones (TZDs) 5. SGLT-2 inhibitors
283
Why is metformin the first line therapy for diabetes?
Associated with less weight gain and less hypoglycaemia than insulin and sulfonylurea
284
When is sulfonylurea considered as treatment for diabetes?
In individuals: - Who are not overweight (as causes weight gain) - Require rapid response due to hyperglycaemia symptoms - Are unable to tolerate metformin or where metformin is contraindicated
285
How do incretin based agents treat diabetes?
Influence glucose homeostasis via: - glucose dependent insulin secretion - postprandial glucagon suppression - slowing gastric emptying
286
Give examples of Thiazolidinediones (TZDs)
Rosiglitazone and Pioglitazone
287
How do Thiazolidinediones treat diabetes?
Effective glucose lowering agents
288
What diseases are associated with polycystic ovary syndrome?
1. Insulin resistance - T2DM 2. Hypertension 3. Hyperlipidaemia 4. CV disease
289
Give 5 symptoms of polycystic ovary syndrome
1. Amenorrhoea 2. Oligomenorrhoea 3. Hirsutism 4. Acne 5. Overweight 6. Infertility
290
What criteria can be used to make a diagnosis of polycystic ovary syndrome?
Rotterdam diagnostic criteria 1. Menstrual irregularity 2. Clinical or biochemical evidence of hyperandrogenism 3. Polycystic ovaries on USS
291
Describe the treatment for polycystic ovary syndrome
1. Hirsutism therapy - shaving/waxing excess hair OR oestrogen (e.g. OCP) 2. Menstrual disturbance therapy - cyclic oestrogen/progesterone 3. Metformin can improve hyperinsulinaemia and regulates menstrual cycle
292
A 27-year- old woman comes to see you because she is having infrequent periods (oligomenorrhoea). You note, on examination, that she has facial acne and is overweight. What is the most likely diagnosis? Give 3 other signs you might see in this patient
``` Polycystic ovary syndrome Other signs: 1. Hirsutism 2. Amenorrhoea 3. Infertility ```
293
What is Conn's syndrome?
Primary hyperaldosteronism | High aldosterone levels independent of RAAS activation - H20 and sodium retention and potassium excretion
294
What are the clinical features of Conn's syndrome?
- hypertension - nocturia and polyuria - mood disturbance - difficulty concentrating - hypokalaemia
295
A deficiency in which electrolyte causes the symptoms of Conn's syndrome?
1. Muscle weakness 2. Tiredness 3. Polyuria Due to potassium deficiency
296
What are the causes of Conn's syndrome?
``` Adrenal adenoma (2/3) Bilateral adrenal hyperplasia (1/3) ```
297
What hormone is raised in Conn's syndrome and what hormone is reduced? Where are these hormones synthesised?
1. Aldosterone is raised - synthesised in the zone glomerulosa 2. Renin is reduced - synthesised in the juxta-glomerular cells
298
What investigations might you do in someone to confirm a diagnosis of Conn's syndrome?
- first line = aldosterone renin ratio - high - increased plasma aldosterone levels that aren't suppressed with 0.9% saline infusion or fludrocortisone administration - DIAGNOSTIC - Bloods - plasma potassium = low 4. ECG - flat T waves, ST depression and long QT
299
Give 4 ECG changes you might see in someone with Conn's syndrome
1. Increased amplitude and width of P waves 2. Flat T waves 3. ST depression 4. Prolonged QT interval 5. U waves
300
What is the treatment for Conn's syndrome?
- If the cause is a single benign adrenal tumour - Unilateral adrenalectomy - If the cause is due to bilateral adrenal hyperplasia - Aldosterone antagonists (spironolactone)
301
What is adrenal hyperplasia?
Defective enzymes mediating the production of adrenal cortex products - low levels of cortisol and high levels of male hormones
302
How does adrenal hyperplasia present?
Salt loss Females - ambiguous genitalia with common urogenital sinus Males - no signs at brith, subtle hyperpigmentation and possible penile enlargement
303
Briefly describe the pathophysiology of adrenal hyperplasia
Defective 21-hydroxylase --> disruption of cortisol biosynthesis With or without aldosterone deficiency and androgen excess
304
What diagnostic test would be done to confirm adrenal hyperplasia?
Serum 17-hydorxyprogesterone (precursor to cortisol) = high
305
What is the treatment for adrenal hyperplasia?
Glucocorticoids - hydrocortisone Mineralocorticoids - control electrolytes If salt loss - sodium chloride supplement
306
What is hyperkalaemia?
Excess of potassium Serum K+ >5.5 mmol/L | Serum K+ >6.5 mmol/L = medical emergency
307
what are the clinical features of hyperkalaemia?
``` SYMPTOMS Fatigue Generalised weakness Chest pain Palpitations ``` ``` SIGNS Arrhythmias Reduced power Reduced reflexes Signs of underlying cause ```
308
what are the causes of hyperkalaemia
IMPAIRED EXCRETION - AKI and CKD - drug effect - renal tubular acidosis (T4) INCREASED INTAKE - IV therapy - increased dietary intake SHIFT TO EXTRACELLULAR - metabolic acidosis - rhabdomyolysis
309
What ECG changes might you see in someone with hyperkalaemia?
GO - absent P waves GO LONG - prolonged PR GO TALL - Tall T waves GO WIDE - Wide QRS
310
What is the treatment for hyperkalaemia?
- ABC assessment - Consider cardiac monitoring 1. Protect myocardium: 10ml, 10% calcium gluconate 2. Drive K+ intracellularly: Insulin/Dextrose, Nebulised Salbutamol
311
What is a complication for someone with hyperkalaemia?
Myocardial infarction --> death
312
What is hypokalaemia?
Deficiency in potassium Serum K+ <3.5 mmol/L Serum K+ <2.5 mmol/L = medical emergency
313
what are the clinical features of hypokalaemia?
``` SYMPTOMS: Asymptomatic Fatigue Generalised weakness Muscle cramps and pain Palpitations ``` SIGNS: Arrhythmias Muscle paralysis and rhabdomyolysis
314
Give 3 causes of hypokalaemia
- INCREASED EXCRETION - drugs e.g. thiazide, loop - renal disease - GI loss - increased aldosterone REDUCED INTAKE - dietary deficiency SHIFT TO INTRACELLULAR - drugs e.g. insulin, salbutamol
315
What ECG changes might you see in someone with hypokalaemia?
1. Increased amplitude and width of P waves 2. ST depression 3. Flat T waves 4. U waves 5. QT prolongation
316
What is the treatment for hypokalaemia?
- Potassium PO/IV - Other electrolyte replacements - Treat underlying cause
317
What are 2 possible complications of hypokalaemia?
1. Cardiac arrhythmias | 2. Sudden death
318
Name 5 types of thyroid cancer
1. Papillary - thyroid epithelium 2. Follicular - thyroid epithelium 3. Anaplastic - thyroid epithelium 4. Lymphoma 5. Medullary - calcitonin C cells
319
What types of thyroid cancers are usually asymptomatic thyroid nodule (usually hard and fixed)?
Papillary Follicular Anaplastic
320
what is the clinical presentation of thyroid cancer?
- In 90% present as thyroid nodules - Occasionally they present with cervical lymphadenopathy or with lung, cerebral, hepatic or bone mets. - If thyroid gland increases in size, becomes hard and irregular in shape think cancer - May experience dysphagia or hoarseness of voice if tumour presses on surrounding structures
321
How does a medullary cancer of the thyroid present?
Diarrhoea Flushing episodes Itching
322
Why is an anaplastic cancer of the thyroid one of the most aggressive cancers?
Cancer of the follicular cells of the thyroid but doesn't retain original cell features like iodine uptake or synthesis of thyroglobulin
323
What hormone does a medullary cancer of the thyroid produce?
Calcitonin from C cells
324
What is the most common form of thyroid cancer?
Papillary - 70%, young people, 3x more common in women | Follicular - 20%
325
What investigations can you do to confirm a thyroid cancer?
Fine needle aspiration For a Medullary cancer - elevated serum calcitonin Blood tests – check TFTs (TSH, T4, T3) – check if hyper or hypo thyroid Ultrasound - benign/malignant
326
What is the treatment for thyroid cancer?
- LEVOTHYROXINE T4 to keep TSH reduced as this is a growth factor for cancer Papillary and follicular - total thyroidectomy - ablative radioactive iodine Anaplastic and lymphoma - external radiotherapy to provide relief - largely palliative Medullary - total thyroidectomy and prophylactic central lymph node dissection
327
what is de quervain's thyroiditis?
Transient hyperthyroidism sometimes results from acute inflammation of the thyroid gland, probably due to viral infection
328
what is the clinical presentation of de quervain's thyroiditis?
Usually accompanied by fever, malaise and pain in the neck
329
what is the treatment for de quervain's thyroiditis?
Treat with aspirin and only give prednisolone for severely symptomatic cases
330
what are the side effects of metformin?
GI upset | lactic acidosis
331
what is the mechanism of action for SGLT-2 inhibitors?
inhibits resorption of glucose in the kidney
332
what are the side effects of SGLT-2 inhibitors?
UTI
333
what is the mechanism of action for glitazones?
Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
334
what are the side effects of glitazones?
Weight gain | Fluid retention
335
what is the mechanism of action for levothyroxine?
synthetic T4
336
what is the diagnostic criteria for diabetic ketoacidosis?
glucose >11mmol/L pH <7.3 bicarbonate <15mmol/L ketones >3mmol/l or ketones in urine
337
what is hyperosmolar hyperglycaemic state?
This is a life-threatening emergency characterised by marked hyperglycaemia, hyperosmolality and mild or no ketosis characteristic of uncontrolled type 2 diabetes
338
what are the risk factors for hyperosmolar hyperglycaemic state?
- infection - consumption of glucose rich fluids - concurrent medication (thiazides or steroids)
339
what is the pathophysiology of hyperosmolar hyperglycaemic state?
- Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production
340
what is the clinical presentation of hyperosmolar hyperglycaemic state?
- severe dehydration - decreased level of consciousness - hyperglycaemia - hyperosmolality - not ketones in blood or urine - stupor or coma - bicarbonate NOT LOWERED
341
what are the investigations for hyperosmolar hyperglycaemic state?
Random plasma glucose >11mmol/L Urine dipstick: glucosuria Plasma osmolality - high U+E - ↓ total body K+, ↑serum K+
342
what is the treatment for hyperosmolar hyperglycaemic state?
- Replace fluid - 0.9% saline IV - Insulin - At low rate of infusion! - Restore electrolytes - e.g. K+ - LMWH
343
what conditions is hashimotos thyroiditis associated with?
- other autoimmune conditions - coeliac disease, T1DM, vitiligo - MALT lymphoma
344
what are the side effects of levothyroxine?
- usually due to excessive doses | - GI disturbance, cardiac arrhythmias and neurological tremors
345
what is the mechanism of action for carbimazole?
prevents thyroid peroxidase from producing T3 and T4
346
what is the mechanism of action for GH receptor antagonist's e.g. pegvisomant?
blocks action of GH at GH receptor -> reduces production of IGF-1
347
what are the side effects of GH receptor antagonists e.g. pegvisomant?
- reactions at injection site - GI disturbance - hypoglycaemia - chest pain - hepatitis
348
what is the mechanism of action for vasopressin antagonists e.g. tolvaptan?
- inhibits vasopressin-2 receptor -> increases fluid excretion - causes aquaresis (excretion of H2O with no electrolyte loss) -> increased Na+
349
what are the side effect of vasopressin antagonists e.g. tolvaptan?
- GI disturbance - headache - increased thirst - insomnia
350
what is the mechanism of action for vasopressin analogues e.g. desmopressin?
binds to V2 receptors -> aquaporin 2 inserted in collecting duct which increases water reabsorption
351
what are the side effects of vasopressin analogies e.g. desmopressin?
- headache - facial flushing - nausea - seizures
352
what is the mechanism of action for metyrapone?
- blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide enzyme
353
what are the side effects of metyrapone?
- GI disturbance - headache - dizziness - drowsiness - hirsutism
354
how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?
short ACTH = no change | long ACTH = increase
355
where is the most common site for carcinoid tumours to metastasise?
liver
356
what is the most common cause of hypothyroidism in the developing world and the developed world?
developing = iodine deficiency developed = Hashimoto's thyroiditis
357
what is the levels of HbA1c in normal, pre-diabetes and diabetes?
``` normal = < 42 pre-diabetes = 42-47 diabetes = >48 ```
358
what is the difference between cushing's syndrome and cushing's disease?
``` syndrome = elevated cortisol levels disease = caused by ACTH secreting pituitary adenoma ```
359
what investigation can be used to differentiate between cushing's syndrome and cushing's disease?
dexamethasone suppression test - overnight = cushing's syndrome (including disease) is confirmed when there is no suppression - 48 hours = cushing's syndrome (not disease) = no suppression
360
which condition would cause TSH = low and T4 = high?
hyperthyroidism thyrotoxicosis graves
361
which condition would cause TSH = high T4 = normal?
subclinical hypothyroidism | poor compliance with thyroxine
362
which condition would cause TSH = high T4 = low?
primary hypothyroidism | hashimotos
363
which condition would cause TSH = low T4 = low?
secondary hypothyroidism
364
what arrhythmia is a consequence of untreated hyperkalaemia?
ventricular tachycardia - due to cell membranes becoming partially depolarised -> lower threshold potential so ventricles contract faster
Phase 2A revision
flashcards
Decks in class (38)
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