Endocrine to work on COPY Flashcards
1
Q
Name 3 causes of hypocalcaemia
A
Hypoparathyroidism Vitamin D deficiency Hyperventilation Drugs Malignancy Toxic shock
2
Q
Describe the treatment pathway for T2DM
A
- Lifestyle changes - lose weight, exercise, healthy diet and control of contributing conditions
- Metformin
- dual therapy of Metformin + one of the following:
i) DPP4 inhibitor
ii) sulphonylureas (gliclazide)
iii) pioglitazone - triple therapy
- insulin
3
Q
what are the side effects of Sulfonylurea?
A
Hypoglycaemia
weight gain
hyponatraemia
4
Q
what are the features of addisonian crisis?
A
Vomiting abdominal pain profound weakness hypoglycaemia hypovolemic shock
5
Q
Name 5 risk factors for Graves disease
A
- Female
- Genetic association
- E.coli
- Smoking
- Stress
- High iodine intake
- Autoimmune diseases
6
Q
Name 5 autoimmune diseases associated with thyroid autoimmunity
A
- T1DM
- Addison’s disease
- Pernicious anaemia
- Vitiligo
- Alopecia areata
- Rheumatoid arthritis
7
Q
what are the causes of hyperthyroidism?
A
- Grave’s disease
- Toxic multinodular goitre
- Solitary toxic nodule/adenoma - benign
- De Quervarians thyroiditis
- Postpartum thyroiditis
- Drug induced
8
Q
Give 5 side effects of anti-thyroid drugs
A
- Rash
- Arthralgia
- Hepatitis
- Neuritis
- Vasculitis
- Agranulocytosis - very serious
9
Q
What is the treatment for a thyroid crisis?
A
Large doses of oral carbimazole, oral propranolol, oral potassium iodide and IV hydrocortisone
10
Q
Name 4 causes of primary hypothyroidism
A
- autoimmune thyroiditis
- postpartum thyroiditis
- iatrogenic
- drug induced
- iodine deficiency
- congenital
11
Q
Name 4 drugs that can cause hypothyroidism
A
- Carbimazole (used to treat hyperthyroidism)
- Amiodarone
- Lithium
- Iodine
12
Q
Name 3 triggers of Hashimoto’s thyroiditis
A
- Iodine
- Infections
- Smoking
- Stress
13
Q
what are the causes of cranial DI?
A
Idiopathic Congenital defects in ADH gene Disease of hypothalamus Tumour – metastases, posterior pituitary Trauma – neurosurgery Infiltrative disease
14
Q
what are the causes of nephrogenic DI?
A
- Hypokalaemia
- Hypercalcaemia
- Drugs
- lithium chloride
- Demeclocycline
- glibenclamide - Renal tubular acidosis
- Sickle cell disease
- Prolonged polyuria of any cause
- Familial (mutation in ADH receptor)
15
Q
Give 3 possible differential diagnosis’s of DI
A
- DM
- Hypokalaemia
- Hypercalcaemia
16
Q
What is the treatment for nephrogenic DI?
A
- 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
17
Q
Give 4 causes of polyuria
A
- Hypokalaemia
- Hypercalcaemia
- Hyperglycaemia
- Diabetes insipidus
18
Q
what are the clinical features of SIADH?
A
SYMPTOMS: Nausea and vomiting Headache Lethargy Cramps Weakness Confusion / irritability
SIGNS
raised JVP
oedema
ascites
19
Q
what are the causes of SIADH?
A
brain injury infection hypothyroidism cancers lung diseases
20
Q
what are the investigations for SIADH?
A
- 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
21
Q
Describe the treatment for SIADH
A
- Restrict fluid - <1L/day
- Give salt
- Loop diuretics - furosemide
- Demeoclocycline - inhibitor of ADH
- ADH-R antagonists - vaptans - primate water excretion with no loss of electrolytes
22
Q
Give 4 local effects a pituitary adenoma
A
- Headaches
- Visual field defects - bitemporal hemianopia
- Cranial nerve palsy and temporal lobe epilepsy
- CSF rhinorrhoea
23
Q
Give 4 potential complications of untreated DKA
A
- Cerebral oedema
- Adult respiratory distress syndrome
- Aspiration pneumonia
- Thromboembolism
- Death
24
Q
Name 3 other types of diabetes other than T1DM, T2DM and DI
A
- Maturity onset diabetes of the young (MODY)
- Permanent neonatal diabetes
- Maternal inherited diabetes and deafness
25
Name 3 exocrine causes of Diabetes
1. Inflammatory - actue/chronic pancreatitis
2. Hereditary haemochromatosis
3. Pancreatic neoplasia
4. Cystic fibrosis
26
what are the clinical features of pheochromocytoma?
```
SYMPTOMS
Headache
Profuse Sweating
Palpitations
Tremor
```
```
SIGNS
Hypertension
Postural hypotension
Tremor
hypertensive retinopathy
Pallor
```
27
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
28
Give 5 risk factors for diabetic neuropathy
1. Poor glycaemic control
2. Hypertension
3. Smoking
4. High HbA1c
5. Overweight
6. Long duration DM
29
Why do isolated mononeuropathies result from in diabetic neuropathy?
Occlusion of vasa nervorum - small arteries that provide blood supply to peripheral nerves
30
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
31
How do incretin based agents treat diabetes?
Influence glucose homeostasis via:
- glucose dependent insulin secretion
- postprandial glucagon suppression
- slowing gastric emptying
32
What diseases are associated with polycystic ovary syndrome?
1. Insulin resistance - T2DM
2. Hypertension
3. Hyperlipidaemia
4. CV disease
33
Give 5 symptoms of polycystic ovary syndrome
1. Amenorrhoea
2. Oligomenorrhoea
3. Hirsutism
4. Acne
5. Overweight
6. Infertility
34
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
35
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
36
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
37
What is adrenal hyperplasia?
Defective enzymes mediating the production of adrenal cortex products - low levels of cortisol and high levels of male hormones
38
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
39
What diagnostic test would be done to confirm adrenal hyperplasia?
Serum 17-hydorxyprogesterone (precursor to cortisol) = high
40
what are the clinical features of hyperkalaemia?
```
SYMPTOMS
Fatigue
Generalised weakness
Chest pain
Palpitations
```
```
SIGNS
Arrhythmias
Reduced power
Reduced reflexes
Signs of underlying cause
```
41
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
42
what are the clinical features of hypokalaemia?
```
SYMPTOMS:
Asymptomatic
Fatigue
Generalised weakness
Muscle cramps and pain
Palpitations
```
SIGNS:
Arrhythmias
Muscle paralysis and rhabdomyolysis
43
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
44
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
45
How does a medullary cancer of the thyroid present?
Diarrhoea
Flushing episodes
Itching
46
what are the side effects of metformin?
GI upset
| lactic acidosis
47
what is the mechanism of action for SGLT-2 inhibitors?
inhibits resorption of glucose in the kidney
48
what are the side effects of SGLT-2 inhibitors?
UTI
49
what is the mechanism of action for glitazones?
Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
50
what are the side effects of glitazones?
Weight gain
| Fluid retention
51
what are the risk factors for hyperosmolar hyperglycaemic state?
- infection
- consumption of glucose rich fluids
- concurrent medication (thiazides or steroids)
52
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+
53
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
54
what are the side effects of levothyroxine?
- usually due to excessive doses
| - GI disturbance, cardiac arrhythmias and neurological tremors
55
what is the mechanism of action for carbimazole?
prevents thyroid peroxidase from producing T3 and T4
56
what are the side effects of GH receptor antagonists e.g. pegvisomant?
- reactions at injection site
- GI disturbance
- hypoglycaemia
- chest pain
- hepatitis
57
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+
58
what are the side effect of vasopressin antagonists e.g. tolvaptan?
- GI disturbance
- headache
- increased thirst
- insomnia
59
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
60
what are the side effects of vasopressin analogies e.g. desmopressin?
- headache
- facial flushing
- nausea
- seizures
61
what is the mechanism of action for metyrapone?
- blocks cortisol synthesis by irreversibly inhibiting steroid 11 beta-hydroxide
62
what are the side effects of metyrapone?
- GI disturbance
- headache
- dizziness
- drowsiness
- hirsutism
63
how would cortisol levels react to the synacthen test if there was secondary adrenal insufficiency?
short ACTH = no change
| long ACTH = increase
64
what are the most common sites for carcinoid tumours?
```
appendix (45%)
terminal ileum (30%)
```
65
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
66
what are the investigations for carcinoid tumours?
- liver USS - confirms liver mets
- urinalysis - high conc of 5-hydroxyindolacetic acid
- CXR chest/pelvis
- MRI/CT
67
what is carcinoid crisis?
- tumour outgrows blood supply/handled too much in surgery
LIFE-THREATENING
- vasodilation, hypotension, tachycardia, bronchoconstriction, hyperglycaemia
68
what are the clinical features of Conn's syndrome?
- hypertension
- nocturia and polyuria
- mood disturbance
- difficulty concentrating
- hypokalaemia
69
give an example of a water soluble hormone
peptides - TRH, LH, FSH
70
are water soluble hormones stored in vesicles or synthesised on demand?
stored in vesicles
71
how do water soluble homrones get into cells
bind to cell surface receptors
72
give an example of a fat soluble hormone
steroids - cortisol
73
are fat soluble hormones stored in vesicles or synthesised on demand?
synthesised on demand
74
give an example of an amine hormone
noradrenaline and adrenaline
75
give the pathway for noradrenaline synthesis
phenylalanine -> L-tyrosine -> L-DOPA -> dopamine -> NAd and Ad
76
where are peptide hormone receptors located?
om cell membrane
77
where are steroid hormone receptors located?
in the cytoplasm
78
where are thyroid/vitamin A and D receptors located?
nucleus
79
what cells does FSH act on?
```
ovaries = granulosa cells
testes = sertoli cells
```
80
what cells does LH act on?
```
ovaries = theca cells
testes = leydig cells
```
