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Phase 2A revision > Endocrine to work on > Flashcards

Endocrine to work on Flashcards

1
Q

Give 2 causes of primary hyperparathyroidism

A
  • Parathyroid adenoma
  • Hyperplasia
  • Parathyroid cancer
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2
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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3
Q

what are the signs of hypoparathyroidism?

A
  • 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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4
Q

what is chvostek’s sign?

A

sign of hypoparathyroidism

tap over facial nerve and look for spasm of facial nerves

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5
Q

what is trousseau’s sign?

A

sign of hypoparathyroidism

inflate BP cuff 20 mmHg above systolic for 5 mins = hand spasm

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6
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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7
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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8
Q

Name 3 causes of hypocalcaemia

A 
Hypoparathyroidism
Vitamin D deficiency
Hyperventilation
Drugs
Malignancy
Toxic shock
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9
Q

Give 2 ECG changes that you might see in hypocalcaemia?

A
  1. Small T waves

2. Long QT interval

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10
Q

what are the clinical features of diabetic ketoacidosis?

A

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
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11
Q

Give 3 endocrine diseases that can cause diabetes

A
  1. Cushing’s
  2. Acromegaly
  3. Phaeochromocytoma
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12
Q

Describe the treatment pathway for T2DM

A
  1. Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions
  2. Metformin
  3. dual therapy of Metformin + one of the following:
    i) DPP4 inhibitor
    ii) sulphonylureas (gliclazide)
    iii) pioglitazone
  4. triple therapy
  5. insulin
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13
Q

How does metformin work in treating T2DM?

A

Increase insulin sensitivity and inhibits glucose production

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14
Q

How does sulfonylurea work in treating T2DM?

A

Stimulates insulin release

block ATP dependent K+ channels in beta cells -> causes depolarisations and opening of voltage gated Ca2+ channels -> stimulates insulin secretion

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15
Q

what are the side effects of Sulfonylurea?

A

Hypoglycaemia
weight gain
hyponatraemia

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16
Q

Name 5 possible diseases of the pituitary

A
  1. Benign pituitary adenoma
  2. Craniopharygioma
  3. Trauma
  4. Apoplexy/Sheehans
  5. Sarcoid/TB
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17
Q

What complications are associated with acromegaly?

A

type 2 diabetes
sleep aponea
heart disease
arthritis

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18
Q

What are the investigations for acromegaly?

A

1st line = IGF-1
2nd line = oral glucose tolerance test
3rd line = pituitary function tests
4th line = MRI

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19
Q

what are the causes of Addison’s disease?

A
  • 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
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20
Q

What are the investigations for Addison’s disease?

A
  • 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
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21
Q

what are the features of addisonian crisis?

A 
Vomiting
abdominal pain
profound weakness
hypoglycaemia 
hypovolemic shock
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22
Q

What is the management of adrenal crisis?

A

Immediate IV Hydrocortisone

Fluid resuscitation - saline (IV)

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23
Q

what is the clinical presentation of grave’s dermopathy?

A

Pretibial myxoedema – raised, purple red symmetrical skin lesions over anterolateral aspects of shin

Thyroid acropachy – clubbing, swollen fingers and periosteal bone formation

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24
Q

what is pretibial myxoedema?

A

raised, purple red symmetrical skin lesions over anterolateral aspects of shin

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25
what is thyroid achropachy?
clubbing, swollen fingers and periosteal bone formation
26
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
27
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
28
Name 4 types of sporadic non toxic goitre
1. Diffuse --> physiological --> Graves 2. Multi nodular 3. Solitary nodule 4. Dominant nodule
29
what are the causes of hyperthyroidism?
- Grave’s disease - Toxic multinodular goitre - Solitary toxic nodule/adenoma - benign - De Quervarians thyroiditis - Postpartum thyroiditis - Drug induced
30
Name 4 drugs which can induce hyperthyroidism
1. Iodine 2. Amiodarone 3. Lithium 4. Radioconstrast agents
31
What are the 4 main treatments for hyperthyroidism?
1. Beta blockers - PROPRANOLOL 2. Anti-thyroid drugs - CARBIMAZOLE 3. Radioiodine 4. Surgery - partial/total thyroidectomy
32
Give 5 side effects of anti-thyroid drugs
1. Rash 2. Arthralgia 3. Hepatitis 4. Neuritis 5. Vasculitis 6. Agranulocytosis - very serious
33
Briefly explain thyroid crisis/storm
Rapid deterioration of thyrotoxicosis | Hyperpyrexia, tachycardia and extreme restlessness Delirium --> coma --> death
34
What is the treatment for a thyroid crisis?
Large doses of oral carbimazole, oral propranolol, oral potassium iodide and IV hydrocortisone
35
Name 4 causes of primary hypothyroidism
1. autoimmune thyroiditis 2. postpartum thyroiditis 3. iatrogenic 4. drug induced 5. iodine deficiency 6. congenital
36
Give 2 examples of iatrogenic causes of hypothyroidism
1. Thyroidectomy | 2. Radioiodine therapy
37
Name 4 drugs that can cause hypothyroidism
1. Carbimazole (used to treat hyperthyroidism) 2. Amiodarone 3. Lithium 4. Iodine
38
Name 3 triggers of Hashimoto's thyroiditis
1. Iodine 2. Infections 3. Smoking 4. Stress
39
what are the complications of Hashimoto's thyroiditis?
hyperlipidaemia | Hashimoto's encephalopathy
40
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
41
what are the causes of cranial DI?
``` Idiopathic Congenital defects in ADH gene Disease of hypothalamus Tumour – metastases, posterior pituitary Trauma – neurosurgery Infiltrative disease ```
42
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)
43
Give 3 possible differential diagnosis's of DI
1. DM 2. Hypokalaemia 3. Hypercalcaemia
44
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
45
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
46
Give 4 causes of polyuria
1. Hypokalaemia 2. Hypercalcaemia 3. Hyperglycaemia 4. Diabetes insipidus
47
what are the clinical features of SIADH?
``` SYMPTOMS: Nausea and vomiting Headache Lethargy Cramps Weakness Confusion / irritability ``` SIGNS raised JVP oedema ascites
48
what are the causes of SIADH?
``` brain injury infection hypothyroidism cancers lung diseases ```
49
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
50
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
51
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
52
Describe the triad of signs for 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+
53
Give 4 causes of DKA
1. Unknown 2. Infection 3. Treatment error - not administering enough insulin 4. Having undiagnosed T1DM
54
Give 4 potential complications of untreated DKA
1. Cerebral oedema 2. Adult respiratory distress syndrome 3. Aspiration pneumonia 4. Thromboembolism 5. Death
55
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
56
Name 3 exocrine causes of Diabetes
1. Inflammatory - actue/chronic pancreatitis 2. Hereditary haemochromatosis 3. Pancreatic neoplasia 4. Cystic fibrosis
57
what are the clinical features of pheochromocytoma?
``` SYMPTOMS Headache Profuse Sweating Palpitations Tremor ``` ``` SIGNS Hypertension Postural hypotension Tremor hypertensive retinopathy Pallor ```
58
what are the different types of pheochromocytoma?
1. Familial type - more NAd | 2. Sporadic - more Ad
59
What are the investigations for pheochromocytoma?
- Plasma metanephrines and normetanephrines = GOLD STANDARD - 24 hour urinary total catecholamines - CT – look for tumour
60
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
61
What is the management of a phaeochromocytoma crisis?
Non-competitive alpha-blocker e.g. phenoxybenzamine Excision of paraganglioma Biochemistry: measure plasma and serum metanephrines
62
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
63
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
64
Give 5 risk factors for diabetic neuropathy
1. Poor glycaemic control 2. Hypertension 3. Smoking 4. High HbA1c 5. Overweight 6. Long duration DM
65
Why do isolated mononeuropathies result from in diabetic neuropathy?
Occlusion of vasa nervorum - small arteries that provide blood supply to peripheral nerves
66
Describe the pain associated with diabetic neuropathy
Burning Paraethesia Allodynia - triggering of pain from stimuli that doesn't usually cause pain
67
Describe the treatments for diabetic neuropathy
1. Improve glycaemic control 2. tricyclic antidepressants - AMITRIPTYLINE 3. Pain relief - PARACETAMOL and TRAMADOL
68
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
69
How do incretin based agents treat diabetes?
Influence glucose homeostasis via: - glucose dependent insulin secretion - postprandial glucagon suppression - slowing gastric emptying
70
How do Thiazolidinediones treat diabetes?
Effective glucose lowering agents
71
What diseases are associated with polycystic ovary syndrome?
1. Insulin resistance - T2DM 2. Hypertension 3. Hyperlipidaemia 4. CV disease
72
Give 5 symptoms of polycystic ovary syndrome
1. Amenorrhoea 2. Oligomenorrhoea 3. Hirsutism 4. Acne 5. Overweight 6. Infertility
73
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
74
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
75
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 ```
76
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
77
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
78
What is adrenal hyperplasia?
Defective enzymes mediating the production of adrenal cortex products - low levels of cortisol and high levels of male hormones
79
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
80
Briefly describe the pathophysiology of adrenal hyperplasia
Defective 21-hydroxylase --> disruption of cortisol biosynthesis With or without aldosterone deficiency and androgen excess
81
What diagnostic test would be done to confirm adrenal hyperplasia?
Serum 17-hydorxyprogesterone (precursor to cortisol) = high
82
What is the treatment for adrenal hyperplasia?
Glucocorticoids - hydrocortisone Mineralocorticoids - control electrolytes If salt loss - sodium chloride supplement
83
what are the clinical features of hyperkalaemia?
``` SYMPTOMS Fatigue Generalised weakness Chest pain Palpitations ``` ``` SIGNS Arrhythmias Reduced power Reduced reflexes Signs of underlying cause ```
84
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
85
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
86
What is a complication for someone with hyperkalaemia?
Myocardial infarction --> death
87
what are the clinical features of hypokalaemia?
``` SYMPTOMS: Asymptomatic Fatigue Generalised weakness Muscle cramps and pain Palpitations ``` SIGNS: Arrhythmias Muscle paralysis and rhabdomyolysis
88
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
89
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
90
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
91
How does a medullary cancer of the thyroid present?
Diarrhoea Flushing episodes Itching
92
what is the clinical presentation of de quervain's thyroiditis?
Usually accompanied by fever, malaise and pain in the neck
93
what is the treatment for de quervain's thyroiditis?
Treat with aspirin and only give prednisolone for severely symptomatic cases
94
what are the side effects of metformin?
GI upset | lactic acidosis
95
what is the mechanism of action for SGLT-2 inhibitors?
inhibits resorption of glucose in the kidney
96
what are the side effects of SGLT-2 inhibitors?
UTI
97
what is the mechanism of action for glitazones?
Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
98
what are the side effects of glitazones?
Weight gain | Fluid retention
99
what is the mechanism of action for levothyroxine?
synthetic T4
100
what is the diagnostic criteria for diabetic ketoacidosis?
glucose >11mmol/L pH <7.3 bicarbonate <15mmol/L ketones >3mmol/l or ketones in urine
101
what are the risk factors for hyperosmolar hyperglycaemic state?
- infection - consumption of glucose rich fluids - concurrent medication (thiazides or steroids)
102
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
103
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+
104
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
105
what conditions is hashimotos thyroiditis associated with?
- other autoimmune conditions - coeliac disease, T1DM, vitiligo - MALT lymphoma
106
what are the side effects of levothyroxine?
- usually due to excessive doses | - GI disturbance, cardiac arrhythmias and neurological tremors
107
what is the mechanism of action for carbimazole?
prevents thyroid peroxidase from producing T3 and T4
108
what are the side effects of GH receptor antagonists e.g. pegvisomant?
- reactions at injection site - GI disturbance - hypoglycaemia - chest pain - hepatitis
109
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+
110
what are the side effect of vasopressin antagonists e.g. tolvaptan?
- GI disturbance - headache - increased thirst - insomnia
111
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
112
what are the side effects of vasopressin analogies e.g. desmopressin?
- headache - facial flushing - nausea - seizures
113
what is the mechanism of action for metyrapone?
- blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide
114
what are the side effects of metyrapone?
- GI disturbance - headache - dizziness - drowsiness - hirsutism
115
how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?
short ACTH = no change | long ACTH = increase
116
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
117
what cells do carcinoid tumours originate from?
enterochromaffin cells
118
what do carcinoid tumours produce?
serotonin mainly ``` bradykinin substance P insulin glucagon ACTH ```
119
what are the most common sites for carcinoid tumours?
``` appendix (45%) terminal ileum (30%) ```
120
are carcinoid tumours malignant?
- all carcinoid tumours are considered malignant
121
what is carcinoid syndrome?
when there is hepatic involvement - hepatic metastases
122
what is the clinical presentation of carcinoid tumours?
- bluish-red flushing of face and neck(bradykinin release) - appendicitis/GI obstruction - RUQ pain (hepatic mets) - bronchoconstriction/bronchospasm with cough (bradykinin release) - congestive heart failure - diarrhoea
123
what are the investigations for carcinoid tumours?
- liver USS - confirms liver mets - urinalysis - high conc of 5-hydroxyindolacetic acid - CXR chest/pelvis - MRI/CT
124
what is the treatment for carcinoid tumours?
``` octreotide/lanreotide = somatostatin analogues cure = surgical resection ```
125
what is carcinoid crisis?
- tumour outgrows blood supply/handled too much in surgery LIFE-THREATENING - vasodilation, hypotension, tachycardia, bronchoconstriction, hyperglycaemia
126
what is the treatment for carcinoid crisis?
high dose OCTREOTIDE
127
what are the clinical features of Conn's syndrome?
- hypertension - nocturia and polyuria - mood disturbance - difficulty concentrating - hypokalaemia

Phase 2A revision (38 decks)

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